Stress Proof the Heart
Ellen A. Dornelas Editor
Stress Proof the Heart Behavioral Interventions for Cardiac Patients
Editor Ellen A. Dornelas Director of Behavioral Health Programs Division of Cardiology Hartford Hospital 80 Seymour Street Hartford, CT 06102, USA
[email protected]
ISBN 978-1-4419-5649-1 e-ISBN 978-1-4419-5650-7 DOI 10.1007/978-1-4419-5650-7 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2011944506 © Springer Science+Business Media, LLC 2012 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)
To Brian with love.
Preface
In the early 1980s, as a psychology major in college, I got a part-time job as a medical assistant in a busy cardiology practice, doing electrocardiograms and preparing patients for exercise treadmill stress tests. It seemed apparent, even to a naïve college student, that many patients were deeply affected by the psychological aftermath of a heart attack. A few years later, in applying for graduate school, I stumbled across the newly developing field of health psychology and applied, looking for the academic preparation necessary to better understand the connection between the psyche and the heart. Nearly a decade later, with doctoral degree in hand, I found few advertised jobs in clinical health psychology. I came to develop a behavioral health program in a heart center by first responding to a request to develop a smoking cessation program and then later, by expanding the clinical service line to address anxiety, depression and adjustment to heart disease across the spectrum of cardiac diagnoses. In the 1990s there were almost no resources available in the field of cardiac psychology. Today, there are a growing number of books that focus exclusively on the psychological aspects of heart disease. There has been advancement of the science of practice, and more training opportunities exist. The community of clinicians and researchers focused on behavioral cardiology across the globe has increased in size as well as sophistication. Given the potential scope of practice, clinicians express again and again, the need for information on topics where the clinical research has not yet caught up with the practice. They ask questions such as: • With increasing awareness about the psychological sequelae of shock from implantable cardioverter defibrillators, why is there so little information about how to help patients with other types of arrhythmia, such as atrial fibrillation? • How is clinical practice with heart failure patients so different from treating patients with recent acute events, such as myocardial infarction? • How should cardiac patients with problems such as sleep disturbance, job stress or lack of motivation to exercise, be assessed and treated?
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There are many psychotherapists, nurses and cardiologists across the world, practicing on the front lines and devoted to providing the full spectrum of psychological care for their patients, who hunger for discussion of such issues. I am among those professionals wishing for additional resources and so I enlisted the help of some extraordinary practitioners to create an edited volume of work that provides concrete, immediately applicable, translation of clinical research into practical approaches to address the psychological needs of cardiac patients. After more than 15 years of work in a busy heart center and having already written a book on this topic, I had a pretty good idea about topics upon which little has been written. Addressing some of these areas, I hope, will help to clarify some of the confusion that many practitioners experience as they attempt to both teach themselves about a newly encountered problem and provide psychological help to a distressed patient with heart disease. Very early on in the process, I envisioned a book that would highlight how practitioners in different countries and settings approach clinical practice issues. Two years have passed since this project was initiated, and I continue to be struck by the level of innovation and depth of knowledge of the chapter authors who contributed to this volume. Our target readership is comprised of psychologists, psychiatrists, cardiologists, nurses and other cardiac professionals from around the world. I hope this book will extend knowledge about the clinical practice of behavioral cardiology and inspire research into areas that have not yet been well studied. I would be remiss if I did not point out here that there have been remarkably few clinical trials of psychological treatments for cardiac patients, particularly compared to the extraordinary numbers of studies examining the relationship between psychological factors and cardiac outcome. Throughout this book we encourage readers to be aware of results from completed clinical trials and yet not to be discouraged by the lack of consensus or guidelines for practitioners. Experts well versed in the field may wonder about choice of the topics in Stress Proof the Heart. When the project began, I never intended to exhaustively cover all clinical issues in the field but rather to provide a framework for understanding psychological aspects of cardiac disease across the spectrum in the first section and, in the second section, to include chapters with new insights about familiar topics (e.g. stress management) and to address issues that continue to vex clinicians (i.e. treatment of overcommitment and job stress). Often I included a topic because one of the participants in a continuing education workshop had asked me about it. Of course, a multitude of issues are not covered in this book, and there continues to be great need for more research focused on issues raised in this volume and more resources tailored for clinicians working in the exciting field of behavioral cardiology. Hartford, CT, USA
Ellen A. Dornelas
Acknowledgements
This book would not be possible without the extraordinary talent and commitment of the chapter authors. Their examples of ground-breaking work and program development will inform the public health and be of immense importance to practitioners. Great appreciation also goes to the many cardiac patients who have given permission to allow their information to be included as part of the clinical case examples. In all cases, identifying information has been changed to protect patient privacy but we could not convey the complexity or rewards inherent in this work without support from our patients. Special thanks are due to Edward Fischer and Jon Gallagher for their critical reviews and editorial guidance. My on-going gratitude is extended to Paul D. Thompson, MD, my cardiologist mentor and director of the Henry Low Heart Center, at Hartford Hospital, where I am employed. Without Dr. Thompson’s unfailing support, this book and indeed, the behavioral cardiology research or clinical service in our division, would not be possible. Finally, to my husband and children, I am very thankful for your love, support and patience always, but especially while this book was underway.
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Contents
Part I
Psychological Challenges of Heart Disease
1
Introduction ............................................................................................ Ellen A. Dornelas
2
Psychological Challenges of Coping with Coronary Artery Disease ........................................................................................ Lawson Wulsin
3
4
Sudden Cardiac Arrest: A Biopsychosocial Approach to Patient Management of Ventricular Fibrillation and Implantable Cardioverter Defibrillators ...................................... Kari Kirian, Samuel F. Sears, and Harry DeAntonio Atrial Fibrillation: A Biopsychosocial Approach to Patient Management.......................................................................... A. Garrett Hazelton, Samuel F. Sears, and Evelio Rodriguez
5
Psychological Management of Patients with Heart Failure ............... Jonathan Gallagher and Adam Grimaldi
6
Psychiatric Symptoms, Personality Profile, and Takotsubo Syndrome: Clinical Considerations...................................................... Ilan S. Wittstein, Riccardo Proietti, and Angelo Compare
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Psychological Aspects of Cardiac Transplantation ............................. Brigitta Bunzel
Part II 8
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45 61
93 119
Psychological Interventions for Cardiac Patients
Anxiety and Depression: Risk Factors for Cardiovascular Disease.................................................................... Angelo Compare, Riccardo Proietti, Elena Germani, and David Janeway
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Interventions in the Context of the Distressed (Type D) Personality .............................................................................. Aline J. Pelle, Krista C. van den Broek, and Johan Denollet
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Stress Management with Cardiac Patients .......................................... Carrie Lukens, Dicle Turkoglu, and Matthew M. Burg
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The Effects of Meditation and Yoga on Cardiovascular Disease .................................................................... Sonia Suchday, Maria Dziok, Miriam Katzenstein, Erica Kaplan, and Michelle Kahan
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Job Stress and Overcommitment in Cardiac Patients ........................ En-Young Nicole Cho and Roland von Känel
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Managing Sleep Problems Among Cardiac Patients .......................... Jaan Reitav
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14
Exercise as Medicine for Cardiac Patients .......................................... Beth Parker
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Approaches to Smoking Cessation in a Cardiovascular Population ............................................................ Min Sohn, Kawkab Shishani, Ayako Okada, and Erika Sivarajan Froelicher
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Advances in Cardiac Psychology: Computerized Therapies ............. Emily A. Kuhl
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Behavioral Cardiology: Toward the Development of Integrated Treatment Models ........................................................... Ellen A. Dornelas
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Index ................................................................................................................
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Contributors
Brigitta Bunzel, Ph.D. Department of Cardiac Surgery, Medical University of Vienna, Vienna, Austria Krista C. van den Broek, Ph.D. Center of Research on Psychology in Somatic diseases, Tilburg University, Tilburg, The Netherlands Matthew M. Burg, Ph.D. VA Connecticut Healthcare System, West Haven, CT, USA Yale University School of Medicine, New Haven, CT, USA Columbia University Medical Center, New York, NY, USA En-Young Nicole Cho, M.D. Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital, and University of Bern, Bern, Switzerland Angelo Compare, Ph.D. Department of Human Sciences, University of Bergamo, Bergamo, Italy Harry DeAntonio, D.O. Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA Johan Denollet, Ph.D. Center of Research on Psychology in Somatic iseases, Tilburg University, Tilburg, The Netherlands Maria Dziok, Ph.D. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA Erika Sivarajan Froelicher, R.N., M.A., M.P.H., Ph.D. Physiological Nursing Department, School of Nursing & Epidemiology & Biostatistics, School of Medicine, University of California, San Francisco, USA Jonathan Gallagher, MPsychSc Department of Psychology, Beaumont Hospital, Beaumont, Dublin, Ireland Elena Germani, Psy.D. Centro Diagnostico Italiano, Milano, Italy xiii
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Adam Grimaldi, M.D., Candidate University of Connecticut School of Medicine, John Dempsey Hospital, Farmington, CT, USA A. Garrett Hazelton, Ph.D. Department of Psychology, East Carolina University, Greenville, NC, USA David Janeway, M.D. Department of Psychiatry, New York Medical College, Valhalla, NY, USA Michelle Kahan, M.S., M.A. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA Roland von Känel, M.D. Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital, and University of Bern, Bern, Switzerland Psychocardiology Unit, Cardiac Prevention and Rehabilitation, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, and University of Bern, Bern, Switzerland Erica Kaplan, B.A. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA Miriam Katzenstein, M.A. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA Kari Kirian, M.A. Department of Psychology, East Carolina University, Greenville, NC, USA Emily A. Kuhl, Ph.D. Division of Research, American Psychiatric Association, American Psychiatric Institute for Research and Education, Arlington, VA, USA Carrie Lukens, Ph.D. VA Connecticut Healthcare System, West Haven, CT, USA Yale University School of Medicine, New Haven, CT, USA Ayako Okada, R.N., C.N.S., Ph.D.(c) College of Nursing Art and Science, University of Hyogo, Japan & Physiological Nursing Department, School of Nursing, University of California, San Francisco, USA Beth Parker, Ph.D. Henry Low Heart Center, Hartford Hospital, Hartford, CT, USA University of Hartford, Hartford, CT, USA Aline J. Pelle, Ph.D. Center of Research on Psychology in Somatic diseases, Tilburg University, Tilburg, The Netherlands Riccardo Proietti, M.D. Cardiac Electrophysiology Laboratory, Luigi Sacco Hospital, Milano, Italy
Contributors
Jaan Reitav, Ph.D., C.Psych., C.B.S.M. University Health Network, Toronto Rehabilitation Institute, Cardiac Rehabilitation and Secondary Prevention Program, Toronto, Canada Department of Clinical Diagnosis, Canadian Memorial Chiropractic College, Toronto, Canada Evelio Rodriguez, M.D. Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA Samuel F. Sears, Ph.D. Department of Psychology, East Carolina University, Greenville, NC, USA Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA Kawkab Shishani, B.S.N., Ph.D. College of Nursing, Washington State University, Yakima, WA, USA Min Sohn, R.N., A.C.N.P., M.P.H., Ph.D. Department of Nursing, Inha University, Incheon, South Korea Sonia Suchday, Ph.D. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY, USA Dicle Turkoglu, Ph.D. VA Connecticut Healthcare System, West Haven, CT, USA Yale University School of Medicine, New Haven, CT, USA Ilan S. Wittstein, M.D. Department of Medicine, Division of Cardiology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Lawson Wulsin Professor of Psychiatry and Family Medicine, University of Cincinnati, OH, USA Ellen A. Dornelas, Ph.D. Director of Behavioral Health Programs, Division of Cardiology, Hartford Hospital, Hartford, CT, USA
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Part I
Psychological Challenges of Heart Disease
Chapter 1
Introduction Ellen A. Dornelas
Stress is widely recognized as a contributor to cardiovascular illness and decreased quality of life; however, cardiac patients are often challenged in their efforts to reduce stress and change lifestyle. The clinician who specializes in this field faces the daunting task of developing an adequate fund of knowledge in both cardiovascular medicine and clinical psychology. In cardiology, the medical problems could include atherosclerotic-based disease, heart rhythm problems, heart failure, and heart transplant, as well as cardiac risk factors (e.g., cigarette smoking, hypertension, hyperlipidemia, thyroid dysfunction) and other co-occuring medical problems. In addition, the technology in cardiac medicine is ever changing; new devices, surgical techniques, and medications offer the hope of prolonging life. People with heart disease are representative of the general population in terms of mental health, but comorbid psychiatric conditions (e.g., depression, posttraumatic stress disorder, panic disorder, and adjustment reactions), personality dysfunction, and psychosocial difficulties such as job stress and overcommitment, as well as problematic behaviors (e.g., sedentary lifestyle, cigarette smoking), are all well represented within this group. Medical intervention continues to increase the number of people living with chronic heart disease, but there is a paucity of clinician-friendly books that translate the science of behavioral cardiology into practical clinical interventions. This book is designed to help to fill that void by providing the reader with an overview of the continuum of cardiac disease and its concomitant psychological ramifications, as well as illustrative examples of stress-reducing interventions for cardiac patients. To “stress-proof” the heart refers to helping the cardiac patient who seeks out or accepts behavioral intervention to become more psychologically resilient, more effective at coping with medical illness, and sometimes, but not always, to reduce risk for heart disease through lifestyle change. The assumption is that such patients E.A. Dornelas, Ph.D. (*) Director of Behavioral Health Programs, Division of Cardiology, Hartford Hospital, Hartford, CT, USA e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_1, © Springer Science+Business Media, LLC 2012
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are suffering and can be helped with behavioral and psychological interventions which might have beneficial impact on the cardiovascular system but are always aimed at improvement in psychological functioning. The spectrum of services that might be provided in a cardiac setting by a psychologist could be quite broad. There are no well-established boundaries that clearly differentiate the practice of behavioral cardiology from the ordinary delivery of mental health services. Many patients who are encountered, for example, in a medical setting such as cardiac rehabilitation, have long-standing anxiety or depression and are well served with standard psychological treatments that require no special expertise in health psychology or psychosomatic medicine. However, there are also many subgroups of cardiac patients who are best served by a therapist with specific background in behavioral cardiology. Most individuals typically view a major cardiac event, surgery, or device implantation as life changing and accordingly prefer to be treated by a clinician who has an appreciation of the psychological aspects of living with heart disease. Some cardiac conditions can cause a great deal of psychological distress; for example, it can be difficult to live with atrial fibrillation when the symptoms are not well controlled with medication or surgical intervention. A cardiac diagnosis provides a sense of urgency to making a major lifestyle change such as quitting smoking or beginning an exercise program. In addition, certain patients, for example, cardiac transplant candidates, have unique difficulties and can benefit from interventions tailored specifically for their particular circumstance. The number of permutations for how any individual patient might exhibit distress is almost overwhelming. For example, a person might present with a great deal of symptomatic distress, need help in changing deeply ingrained habits, or have problems in interpersonal relationships. Any of the difficulties that are encountered in a general psychotherapy practice might also be encountered in working with a cardiac population.
Organization of the Book This book is divided into two sections. In Part I, Psychological Challenges of Heart Disease, the continuum of heart disease is described. Lawson Wulsin, a pioneering physician in the field of behavioral cardiology, provides an overview of the psychological challenges of coping with coronary heart disease. In Chaps. 3 and 4, researchers working in the extraordinarily productive lab of Sam Sears, psychologist at East Carolina University, have written two illuminating chapters on the difficulties involved in living with life-threatening arrhythmia, surviving cardiac arrest, and adjusting to living with an implantable cardioverter defibrillator. The focus of Chap. 4 on the biopsychosocial aspects of coping with a diagnosis of atrial fibrillation is a topic of great importance in practice but is rarely receiving attention in behavioral cardiology books. Chapter 5 is an international collaboration between Irish psychologist Jon Gallagher and American physician Adam Grimaldi and focuses on the psychosocial aspects of heart failure. Chapter 6 is another example of a successful international physician-psychologist collaboration between American cardiologist
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Ilan Wittstein and Italian psychologist Angelo Compare and physician Richard Proietti who describe Takotsubo syndrome and its clinical considerations. Psychologist Brigitta Bunzel from the Medical University of Vienna wrote Chap. 7 on heart transplant, and this was translated from German by Charlotte Eckler. Bunzel’s chapter provides a thoughtful clinical perspective on working with heart transplant candidates, a topic often not covered in other books in this field. Each of the topics chosen for Part I was intended to provide a reader unfamiliar with working with a particular subgroup of cardiac patients with an overview of the patient experience of that diagnosis and its relevant psychological aspects. Part II of this book is titled Psychological Interventions for Cardiac Patients and focuses on common problems in a general cardiac population and behavioral treatment strategies. Whenever possible, illustrative case examples are included. In Chap. 8, Angelo Compare and his colleagues provide an overview of the risk factors of depression and anxiety with respect to heart disease. Aline Pelle, Krista C. van den Broek, and Johan Denollet from Tilburg University in the Netherlands have written a compelling chapter (Chap. 9) on psychological interventions in the context of type D personality. In Chap. 10, Carrie Lukens, Dicle Turkoglu, and Matthew Burg describe a comprehensive overview of stress management. Sonia Suchday and her colleagues go on in Chap. 11 to give more in-depth information about stress management, on how yoga and mindfulness meditation can be used with a cardiac population. Chapter 12 will be of great interest to readers who seek to develop interventions for patients with problems of overcommitment and work stress and is written by Swiss psychiatrists En-Young Nicole Cho and Roland von Känel from the University of Bern. Chapter 13 by Canadian psychologist Jaan Reitav addresses sleep disorders in a cardiac population, a pressing problem rarely addressed by books on this topic. Chapter 14 from exercise physiologist Beth Parker addresses the topic of exercise “as medicine” and gives clinical examples of how to improve sedentary behavior in people with heart disease. Chapter 15 is focused on smoking cessation, the primary preventable risk factor in this patient population, and also provides an important perspective in that the authors bring the nursing perspective from South Korea (Min Sohn) and North America (Kawkab Shishani, Ayako Okada, and Erika Sivarajan Froehlicher). Chapter 16 from Emily Kuhl adds a truly novel aspect to this book on the use of telehealth and computerized therapies in a cardiac population. Chapter 17 concludes the book with general principals to move the field forward toward the development of integrated models for behavioral cardiology. This book offers a global perspective on behavioral cardiology. It is only regrettable that due to limitations in scope, the perspective of scientist-practitioners from many noteworthy practice settings and laboratories across the world could not be included. However, it has been extremely rewarding to include work from authors representing Italy, Austria, Switzerland, Canada, Ireland, South Korea, and the United States. Similarly, the disciplines of psychology, psychiatry, cardiology, exercise physiology, and nursing each add a different perspective in terms of interventions to Stress Proof the Heart, and the multidisciplinary collaboration of many of the authorship teams greatly enhances the clinical relevance of the chapters. There are some topics, such as the basic anatomy and physiology of the heart, that are
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essential or are related but beyond the scope of this book, and the interested reader is referred to earlier works on this topic (Dornelas, 2008; Allen & Fischer, 2011; Molinari, Compare, & Parati, 2006).
Behavioral Cardiology as a Clinical Practice Specialty As a field of practice, clinical behavioral cardiology treats the emotional, social, and behavioral problems associated with heart disease. The development of behavioral cardiology began nearly a century ago, reflecting a recognition of the relationship between patients’ emotional state and their illness. Behavioral health specialists should be part of the multidisciplinary treatment team who work with the cardiac patients, but there are few guidelines available to aid in the delivery of behavioral health services to cardiac patients. The goal of clinical behavioral cardiology is psychological well-being. Psychological well-being is essential to good health. The ability to cope effectively with stress is a prerequisite for psychological well-being and vitally important for cardiovascular health. For much of the past 50 years, clinical interventions to reduce stress have either not often been offered to patients or been too simplistic, educational, or brief to have any significant impact. National public health agencies such as the American Heart Association have not been as proactive as necessary to spur the integration of behavioral health into the practice of mainstream clinical cardiology. However, in the past decade, as patients, cardiologists, nurses, and mental health professionals have realized the importance of stress management to heart health, the interest in effective behavioral interventions has mounted. More and more cardiac patients seek out stress management or behavioral health services each year, and there are an increasing number of books and journal articles published, aimed at a clinical audience. All people cope with some degree of stress, but a diagnosis of heart disease underscores the urgency of living life fully and with optimum psychological good health. Cardiac patients and their family members deserve information, guidance, and support about how to strive for improved psychological well-being and how to access behavioral health services. This is why Stress Proof the Heart is an important resource for cardiac professionals. Stress Proof the Heart provides the reader with examples, straight from the field, of clinical practice in this exciting field. Practitioners will benefit from the descriptions of interventions, tailored to the specific needs of each of the major subgroups of cardiovascular disease. Better integration of behavioral health into cardiac care will improve quality of life in patients, improve support for families, reduce unnecessary visits to cardiologists for mental health reasons, and, for some patients, may ultimately prove to improve cardiac morbidity and mortality. Most people will eventually have the experience coping with a cardiac event, surgery, or diagnosis either in with a family member or themselves. Patients are grateful if they encounter a hospital or health-care system where psychosocial needs are recognized and addressed. However, many people are not able to benefit from
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such support because it is not uniformly available. All practitioners can play a role in increasing public awareness of the need to address psychological factors in clinical cardiology, and mental health providers have an extraordinary opportunity to bring to bear their training and interventions to provide cardiac patients with the type of comprehensive care that they deserve.
References Allen, R., & Fischer, J. (2011). Heart and mind: The practice of cardiac psychology. Washington, DC: American Psychological Association. Dornelas, E. A. (2008). Psychotherapy with cardiac patients: Behavioral cardiology in practice. Washington, DC: American Psychological Association. Molinari, E., Compare, A., & Parati, G. (2006). Clinical psychology and heart disease. New York: Springer.
Chapter 2
Psychological Challenges of Coping with Coronary Artery Disease Lawson Wulsin
Introduction A clinically effective approach to psychological aspects of coronary disease follows an appreciation of, first, the psychological conditions associated with coronary disease and, second, the mechanisms that link them. Because the process of association often runs a circular course with causes leading to effects which further exacerbate the causes, effective treatments of psychological aspects of coronary disease must often aim for multiple targets over extended periods of time with careful monitoring and vigilant relapse prevention efforts. This chapter begins with a brief summary of coronary disease followed by a consideration of the mechanisms that link depression and anxiety to coronary disease. An understanding of the various linking pathways often guides the behavioral approach to the psychological challenges of coronary disease. Then a brief review of the epidemiologic evidence for depression, anxiety, and stress as risks for coronary disease lays the rationale for focusing behavioral treatment efforts on these conditions. Finally, general principles for treating depression and anxiety point toward specific management tips.
Coronary Disease Also called coronary artery disease or coronary heart disease, coronary disease is a chronic, progressive condition defined by the formation of plaques in the major coronary arteries. The eventual narrowing of the lumen or the development of a thrombus leads to reduced perfusion of the cardiac muscle, often chest pain (angina
L. Wulsin (*) Professor of Psychiatry and Family Medicine, University of Cincinnati, OH, USA e-mail:
[email protected];
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_2, © Springer Science+Business Media, LLC 2012
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pectoris), and ischemia or infarction of the cardiac muscle tissue. Acute coronary syndromes include unstable angina, myocardial infarction, and cardiac arrhythmias or arrest. Though the process of atherosclerosis begins in the second or third decade of life, the clinical disorder usually does not afflict men until their 40s or 50s and women about a decade later. About a third of US adults die of cardiovascular diseases, most often complications of coronary disease. In a given year, about 13 million US adults have coronary disease (www.americanheart.org). Though mortality rates from coronary disease have dropped substantially over the past 40 years because of treatment advances and public health education campaigns, incidence rates for coronary disease remain unchanged, suggesting that we have done little to prevent the onset of coronary disease. Of the six major modifiable risk factors for coronary disease (age, male gender, and family history are the three unmodifiable risk factors), any progress with reducing smoking rates has been offset by the obesity and diabetes epidemics. Hypertension, hyperlipidemia, and physical inactivity (the other three major risk factors) remain substantial public health problems. All of the six major modifiable risk factors are exacerbated by depression, anxiety, or chronic stress (Wulsin, 2007). Coronary disease results from atherosclerotic plaque formation in the walls of the coronary vessels, a process that is hastened by chronic low-grade vascular inflammation, injury to the endothelial lining of the arteries at sites of turbulent flow, and lipid deposits at these injury sites. Vasospasm and platelet aggregation, both of which may be triggered by stress, contribute to the episodic progression of coronary disease. Diagnosis of coronary disease results from a history of angina, fatigue, or weakness in the context of risk factors and confirmed by electrocardiogram evidence for ischemia or cardiac enzyme elevations. On coronary angiogram, evidence of more than 50% narrowing of the lumen of at least one major coronary artery points establishes the diagnosis of coronary disease in patients with a typical history. Prospects for people with coronary disease remain risky. One-third of those with a first MI die within an hour of the onset of symptoms. Among those who survive the first MI, one-fifth die within a year. Current treatments for acute coronary syndromes include urgent thrombolysis or revascularization by angioplasty, stent placement or coronary artery bypass graft (CABG) surgery to abort MI, b-adrenergic blockade, statin therapy to stabilize plaque, and aspirin or antiplatelet drugs. Maintenance and preventive measures include the use of aspirin as an antiplatelet drug, exercise, lipidlowering therapy with statin drugs, abstinence from or cessation of smoking, blood pressure control, and maintenance of normoglycemia (Shapiro & Wulsin, 2009).
Pathways from Negative Affect to CVD Prolonged distress or misery accelerates the development and progression of cardiovascular diseases through many pathways. The pathways from negative affect to coronary heart disease are marked by a set of behavioral and biological mechanisms associated with exposure to depression, anxiety, and acute or chronic stress on the one hand, and
2 Psychological Challenges of Coping with Coronary Artery Disease
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with the outcomes of coronary heart disease and related conditions on the other (Carney, Freedland, Miller, & Jaffe, 2002; Rozanski, Blumenthal, & Kaplan, 1999). The behavioral pathways to coronary disease include physical inactivity, smoking, social isolation, high-fat and high-carbohydrate diets, and poor adherence to medication and self-management regimens. Each of these behavior patterns is associated with exposure to clinical depression and anxiety. The biological pathways to coronary disease include sustained autonomic imbalance (sympathetic overactivity, parasympathetic underactivity), stress response dysregulation of the hypothalami pitiutary adrenal (HPA) axis, vascular inflammation, endothelial dysfunction, and increased platelet aggregation. It is also possible that negative affect and coronary disease share a set of common genetic vulnerabilities with the phenotypical expression of negative affect expressing itself usually decades before the phenotypic expression of coronary disease (McCaffery et al., 2006). The first point to note in this list of behavioral and biological precursors of coronary disease is the large number of possible mechanisms and combinations of mechanisms linking persistent exposure to negative affect with the later development of chronic pathology in the cardiovascular system. It is doubtful that any single mechanism alone could spur the onset of any chronic disease, and many people who have more than one cardiac risk factor will soon develop others. Clusters of risk factors are necessary for the development of a condition as complex and gradual in its onset as coronary disease. One such cluster, the metabolic syndrome, consisting of hypertension, dyslipidemia, hyperglycemia, and abdominal obesity, predicts increased risk of atrial fibrillation, acute coronary syndrome, sudden cardiac death, and overall mortality (Gehi et al., 2009). Persistent conditions of negative affect exert their pressure on these risk factors and the pathological processes of cardiovascular disease through disruptions in (a) the autonomic, peripheral, and central branches of the nervous system; (b) the endocrine system; (c) the immune system; and (d) the coagulation system. The behavioral and biological mechanisms can be arranged along a set of pathways that suggest some of the common sequences of events for a hypothetical patient over the decades preceding the first cardiac event. This useful oversimplification conveys some of the complexity of the process over time at all levels of the biopsychosocial model. Figure 2.1 shows three pathways by which chronic depression, anxiety, and stress may contribute to coronary disease. The first noxious effect of prolonged exposure to negative affect may take the form of behavior changes leading to high-risk patterns self-care, diet, exercise, and social contacts. Persistent patterns of high-risk behaviors then establish early biological precursors to the major risk factors for heart disease, such as hypertension, diabetes, and obesity. A second pathway from depression or anxiety to heart disease bypasses behavioral risks and directly affects biological factors that contribute to heart disease, such as inflammation (Kop & Gottdiener, 2005), autonomic imbalance (Thayer & Lane, 2007), and endothelial dysfunction. The third pathway amplifies associated forms of chronic distress, such as anxiety and exhaustion (Kop, 1999), which also exert both direct biological influences on cardiac risk factors and indirect influence via exercise and smoking.
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Psychological Factors
Behavioral Factors
Biological Factors
Early Forms of Disease
Coronary Disease
Genes
Depression 1
Smoking Physical inactivity High calorie diet High cholesterol diet Low social support
3 2 Chronic stress: poverty, hostility, job strain, marital strain, anxiety
Diabetes Obesity
High LDL cholesterol
Poor adherence to treatment regimens
Insulin resistance
Vascular Inflammation High CRP
Increased stress response and HPA activity
High blood pressure Autonomic imbalance: ↑ sympathetic, ↓ parasympathetic activity
Acute stress Anger
Exhaustion
High heart rate Low heart rate variability Endothelial dysfunction Plaque formation High platelet activity
Coronary Disease: Heart attacks, chest pain Arrhythmias Atherosclerosis Clotting Heart failure
Fig. 2.1 Plausible pathways from depression to coronary disease. Modified from Wulsin, L. R. (2007). Treating the aching heart: A guide to depression, stress, and heart disease. Figure 7.4 With permission from Vanderbilt University Press
This schematic diagram lists at least 18 variables potentially intervening between the exposures of depression or anxiety and the outcome of coronary disease. The evidence supporting the roles for these intervening mechanisms varies widely in the number of variables measured, the methods of measurement, and the duration of measurement (Carney et al., 2002; Rudisch & Nemeroff, 2003). Since no single study can hope to assess all or even most of these variables over the relevant decades of a sample, it is unlikely that a comprehensive study of this relationship could ever be done. So it is important to interpret all studies in this area in light of their potential methodologic limitations, which may include some of the following: narrow time frames for follow-up, limited measurement of the exposure to depression, exhaustion, or anxiety, and adjustment for only a few of the many potentially confounding variables. However, understanding these pathways points to several principles for behavioral treatment. First, a clear understanding of all the behavioral and biological factors contributing to cardiac risk ideally guides comprehensive treatment planning for coronary disease. Second, it is unlikely that any single treatment alone could broadly reduce all contributing factors, so collaborative care and complex treatment plans tend to be the rule for achieving effective outcomes. Third, some factors lend themselves more easily to treatment and should be the targets of early treatment efforts. Fourth, the process of developing coronary disease requires years and sometimes decades of exposure; consequently, the duration of behavioral interventions often requires many months and sometimes years to reverse these patterns of biology and behavior before consolidating new more adaptive behavior patterns.
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Depression In the good studies of community and cardiovascular samples, clinical depression is defined as a cluster of depressive symptoms for at least a week, usually associated with impaired functioning. Some retrospective studies have used a documented clinical diagnosis of depression and/or extended treatment with antidepressants or psychotherapy for depression. According to DSM IV, minor depression involves two to four depressive symptoms for at least 2 weeks, whereas major depression involves five or more symptoms for at least 2 weeks (American Psychiatric Association, 1994). Self-report measures of depression, observer ratings, and the mood modules of structured diagnostic interviews are the major methods of measuring depression. At least ten accepted self-report measures (e.g., Beck Depression Inventory, Center for Epidemiologic Studies-Depression Scale, Type D Personality), four observer ratings (e.g., Hamilton Depression Rating Scale, Montgomery-Asberg Depression Rating Scale), and five structured interviews (e.g., Structured Clinical Interview for Diagnosis, Diagnostic Interview Schedule) have been used in methodologically good studies of depression in heart disease. In the study of the many possible psychosocial risk factors for cardiovascular disease, clinical depression, more than any other psychosocial risk factor, has proven to have the strongest relationship to coronary heart disease. And this relationship holds across the spectrum of severity of clinical depression, whether the exposure is assessed by self-report measures of symptoms or by structured diagnostic interviews. That is, the dose-response relationship between depression and coronary disease is measurable and clinically significant in the range of mild depressive symptoms and minor depression, and as the severity of depression increases the cardiovascular risk increases (Lesperance, Frasure-Smith, & Talajic, 2002; Wulsin, 2004). Depression, though common in coronary disease patients, is frequently overlooked by their cardiologists and primary care physicians. Clinically significant depressive symptoms are found in 40–65% of patients following a myocardial infarction, and major depressive disorder is found in 15–25% of such patients (Rudisch & Nemeroff, 2003). Depression is often chronic: Three-fourths of the patients with major depression 2 weeks after a myocardial infarction remain depressed 3 months later (Lesperance, Frasure-Smith, & Theroux, 2000). Denollet and colleagues have examined the effect on coronary disease outcomes of “Type D Personality,” a set of traits that combine a pattern of anxious and depressive feelings with a tendency toward social inhibition and isolation (Denollet, Sys, & Brutsaert, 1995; Denollet et al., 1996). Denollet has shown in several controlled studies that people who score high on the 14-item Type D questionnaire have higher early mortality rates from coronary disease. He argues that what damages the cardiovascular system is not just depressed mood or feeling bad but the persistent pattern of feeling bad alone over many years (Denollet, Pedersen, Vrints, & Conraads, 2006). Several systematic reviews have summarized the evidence supporting the hypothesis that clinical depression increases the risk for both the development and
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the progression of CAD (Barth, Schumacher, & Herrmann-Lingen, 2004; Rugulies, 2002; van Melle et al., 2004; Wulsin & Singal, 2003). A number of large-scale, prospective, epidemiological studies included in these reviews have estimated that depression independently increases the relative risks for both the development of coronary disease and cardiac death by approximately 1.5–2.0. In the Frasure-Smith study with 6- and 18-month follow-up of MI patients, symptoms of depression and the diagnosis of major depressive disorder conferred a 3.5–6.6-fold increased adjusted relative risk of death (Frasure-Smith, Lesperance, & Talajic, 1995). The Heart and Soul Study of 1,002 stable outpatients with coronary disease showed that depression more strongly predicts impairment in quality of life and physical functioning than reduced ejection fraction or exercise-induced myocardial ischemia (Ruo, Rumsfeld, Hlatky, Browner, & Whooley, 2003). Just as the risk of incident coronary disease rises with the severity of depression, a dose-response relationship appears to exist between the severity of depression symptoms after acute MI or unstable angina and the risk of death over 5-year follow-up, even after controlling for other prognostically significant factors. This doseresponse relationship has been found in over ten methodologically sound studies and the prognostic effect size is comparable to some of the more common cardiac predictors of poor outcome, such as low ejection fraction, previous MI, and smoking (Wulsin, 2004). Severe depression 6 months after CABG surgery, or persistence of even moderate depression symptoms at 6-month postoperative follow-up, predicts increased risk of death over 12-month follow-up (Connerney, Shapiro, McLaughlin, Bagiella, & Sloan, 2001).
Psychosocial Treatments In one study of 435 post–myocardial infarction patients, a nursing-based psychosocial intervention reduced cardiac mortality at 1 year, and the incidence of recurrent myocardial infarction was significantly lower at 7-year follow-up. However, two subsequent, large, randomized trials of multimodal interventions delivered by nurses or health visitors failed to improve depression or cardiac outcomes (Taylor, Miller, Smith, & DeBusk, 1997). In the Montreal Heart Attack Readjustment Trial (M-HART), a supportive and educational home nursing intervention was provided to the most psychologically distressed post-MI patients. This rather limited intervention was compared to usual care. At 1-year follow-up, the intervention had no effect on psychological distress and no overall effect on cardiac mortality, while it was actually associated with a higher mortality rate among women (Frasure-Smith et al., 1997). However, a subgroup analysis revealed that those patients whose psychological distress did improve with treatment did have more favorable long-term cardiac outcomes. In the Enhancing Recovery in Coronary Heart Disease (ENRICHD), 2,481 recent myocardial infarction patients with depression and/or low social support randomly
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received either cognitive behavior therapy (and SSRI antidepressants if indicated) or care as usual. There was no benefit in terms of cardiac outcomes or mortality, and cardiac outcomes appeared worse for women (ENRICHD, 2003). A meta-analysis of 23 randomized controlled trials evaluated the additional impact of psychosocial treatment on rehabilitation from documented coronary disease (Dusseldorp, van Elderen, Maes, Meulman, & Kraaij, 1999). Relaxation training, stress management, and group social support were the predominant modalities of psychosocial intervention. Anxiety, depression, biological risk factors, mortality, and recurrent cardiac events were the clinical endpoints studied. These 23 studies included a total of 2,024 patients in intervention groups and 1,156 control subjects. Psychosocial treatment patients had greater reductions in emotional distress, systolic blood pressure, heart rate, and blood cholesterol level than comparison subjects. Patients who did not receive psychosocial intervention had 70% greater mortality and 84% higher cardiac recurrent event rates during 2 years of follow-up. Cardiac rehabilitation itself may reduce high levels of hostility, as well as anxiety and depression symptoms, in post-MI patients. A meta-analysis of psychoeducational programs for coronary disease patients concluded that they led to a substantial improvement in blood pressure, cholesterol, body weight, smoking behavior, physical exercise, and eating habits and to a 29% reduction in MI and 34% reduction in mortality, without achieving significant effects on mood and anxiety (Linden, Stossel, & Maurice, 1996). These programs included health education and stress management components.
Pharmacotherapy If depression lasts more than several weeks and meets diagnostic criteria for major depressive disorder, as happens in one-third or more of patients in the year after myocardial infarction, antidepressant pharmacotherapy is recommended in addition to psychotherapy. In general, SSRIs are the best first choice for the treatment of depression, and within this class, the best research has focused on sertraline and citalopram. The multicenter Canadian CREATE trial found that in 284 patients with major depression and CAD, citalopram plus clinical management was more effective for remission of depression than placebo or clinical management alone (Lesperance et al., 2007). Interpersonal therapy for depression conferred no advantage over clinical management alone. The Sertraline Antidepressant Heart Attack Randomized Trial (SADHART) was a double-blind, randomized, placebo-controlled trial of a selective serotonin reuptake inhibitor (SSRI) for major depressive disorder in patients hospitalized for myocardial infarction or unstable angina (Glassman et al., 2002). At 6-month follow-up, when compared with placebo, the more severely depressed patients who received an active drug were less depressed, although the less severely depressed patients did not show a treatment effect. The trial showed that sertraline was safe and effective for the treatment of recurrent major depression in patients with recent MI or unstable angina.
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In this study, there was a 20% reduction in life-threatening cardiac events (including nonfatal myocardial infarction and death) among those on active drug, but this difference in cardiac outcomes was not statistically significant due to the number of patients in the trial (Glassman et al., 2002). Depression is the strongest predictor of quality of life in post-MI patients, and in this study, treatment with sertraline was associated with clinically meaningful improvements in quality of life over 6 months for those with recurrent depression (Swenson, 2004). In a case-controlled study of smokers hospitalized for myocardial infarction, SSRI administration was associated with a lowered risk of recurrent myocardial infarction, suggesting that treatment of depression may reduce its negative prognostic influence on cardiac outcomes (Sauer, Berlin, & Kimmel, 2001). Thus, though it remains to be definitively demonstrated that either the pharmacologic or psychologic treatment of depression following myocardial infarction significantly improves cardiac outcomes, the rationale for treatment of depression remains strong: to reduce suffering and to improve quality of life.
Anxiety Though often confused with each other, anxiety and stress are best operationalized differently to cover the spectrum of distress. Anxiety, when applied to an enduring condition, even a brief one of several weeks or months, implies a diagnosable disorder, usually deserving treatment. Anxiety disorders may be brief, as adjustment disorders, or lifelong, as in post-traumatic stress disorder or severe forms of obsessive compulsive disorder. The five major anxiety disorders (generalized anxiety disorder, panic disorder, phobias, obsessive compulsive disorder, post-traumatic stress disorder) differ from each other in their dominant psychological features, epidemiology, biology, and response to treatments. On the other hand, stress is a more general term for the distress experienced in response to either an acute event, such as an argument or injury, or a chronic condition, such as poverty or marital conflict. The term stress has played an important role in cardiovascular research since the time of Hans Selye, and more recently in research on mental stress–induced ischemia. As with depression, the options for measuring anxiety include self-report measures (e.g., Beck Anxiety Inventory, GAD 7), observer ratings (e.g., Yale Brown Obsessive Compulsive Scale), and the anxiety disorders modules of structured diagnostic interviews. Measures of stress vary widely with the operational definitions selected, ranging from salivary cortisol levels to heart rate recovery following a mental challenge to self-reports of subjective distress. Chronic mental stress, such as job strain or marital strife, also contributes to the development and the progression of coronary disease (Albert, Chae, Rexrode, Manson, & Kawachi, 2005). In a study of over 900 men and women who returned to work after their first MI, job strain (high demand plus low decision latitude) independently doubled the risk for recurrent cardiac events in the next 6 years, in a model that adjusted for 26 confounders (Aboa-Eboule et al., 2007). In a longitudinal
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study of 812 Finnish employees over a 25-year period, those with high demands from and low levels of control over work conditions had more than double the risk for cardiovascular disease mortality (Kivimaki et al., 2002). Marital stress has been found to exert a negative prognostic influence on coronary disease in women and may be even more important than job stress for women (Orth-Gomer et al., 2000). And in the largest case control study of predictors of MI, the INTERHEART Study found that among 11,119 cases of MI in 52 countries, psychosocial factors, which included self-reports of stress and depression, ranked as the third highest predictor of MI, raising the risk for MI by an odds ratio of 2.67, similar to smoking and diabetes (Rosengren et al., 2004). Several prospective studies of initially healthy men and women found that high anxiety at baseline increased the risk for subsequent development of arteriosclerotic plaques, carotid artery intimal thickening, nonfatal myocardial infarction, and cardiac death. In the Framingham Heart Study, high levels of tension predicted increased risk for new coronary disease and anxiety predicted increased risk for mortality from all causes (Eaker, Sullivan, Kelly-Hayes, D’Agostino, & Benjamin, 2005). Another large prospective study found that high levels of phobic anxiety are associated with an increased risk of fatal coronary disease, particularly from sudden cardiac death (Albert et al., 2005). Anxiety disorders may also worsen the course of established coronary disease. In a recent meta-analysis of 12 studies, post-MI anxiety was associated with about a 40% increase in risk for impaired cardiovascular outcome (Roest, Martens, Denollet, & de Jonge, 2010). This effect, though significant, is not as large as the effect of clinical depression or Type D personality. It remains unclear whether the adverse effects of anxiety operate more through arrhythmias and suddan cardiac death than through arteriosclerosis and infarction, or both. Possible mechanisms explaining these long-term associations include sustained sympathetic nervous system upregulation with increased catecholamine production and decreased vagal activity, chronic low-grade inflammatory states, and persistent dysregulation of the stress response system, particularly the HPA axis.
Stress Acute mental stress induces arterial endothelial dysfunction, with impaired vasodilation. Paradoxically, in atherosclerotic arterial segments, stress can induce vasoconstriction or at times vasospasm. Consequently, acute mental stress may have a significant constricting effect on coronary artery blood flow in patients with preexisting coronary disease. States of fear, excitement, and acute anger reduce blood flow through atherosclerotic coronary segments, provoke coronary spasm, and are associated with abnormal left ventricular wall motion and ECG evidence of myocardial ischemia. Acute stress also increases myocardial oxygen demands as a result of its hemodynamic effects. The normal stress response increases circulating cortisol and catecholamines, which activate platelets and promote platelet aggregation and which increase cholesterol and decrease high-density lipoproteins. The net result of these
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actions is to increase cardiac demand while decreasing coronary blood supply and promoting plaque rupture and thrombus formation. Mental stress–induced ischemia is associated with increased risk of subsequent cardiac events in patients with known coronary disease and may occur even in patients who do not demonstrate evidence of ischemia during exercise stress testing. Triggering of sudden cardiac death by mental stress was demonstrated in a study of deaths in the aftermath of a major California earthquake (Leor, Poole, & Kloner, 1996). After a surge of sudden deaths on the day of the earthquake, there was a several-day period of reduced incidence of sudden cardiac death, suggesting that only those predisposed to sudden cardiac death due to underlying disease were affected by the acute stressor. Deaths were primarily associated with emotional stress rather than physical exertion. Both sudden death without antecedent angina, suggesting cardiac arrhythmia, and sudden deaths preceded by chest pain, suggesting acute coronary occlusions, were observed (Leor et al., 1996). Similar observations have been reported recently about sudden cardiac deaths in the aftermath of the destruction of the World Trade Center in New York in 2001 (Steinberg et al., 2004). Other studies have led to estimates that between 20% and 40% of sudden cardiac deaths are precipitated by acute emotional, rather than physical, stressors. Mental stress–induced ischemia occurs at lower heart rates and at lower levels of myocardial work than does exercise-induced ischemia, suggesting that decreases in myocardial perfusion may play a role in mental stress–induced ischemia. In a laboratory study of 58 patients with coronary disease and three levels of LV function (normal, mild to moderately reduced ejection fractions 30–50%, and severe or <30% ejection fractions), ischemia was induced more frequently with mental stress in those with severe LV dysfunction (50%) compared to 9% of those with normal LV function. Mental stress-induced ischemia may be most important clinically in coronary disease patients with LV dysfunction (Akinboboye et al., 2005). Mental stress–induced ischemia is more likely to be “silent,” or asymptomatic, than is ischemia induced by exercise. In one study, 83% of mental stress–induced ischemic episodes were asymptomatic. And about a third of coronary disease patients without exercise-induced ischemia experience mental stress–induced ischemia, suggesting the two forms of stress induce ischemia by different but related sets of mechanisms (Ramachandruni et al., 2006).
Treatment Laying the Groundwork The first step for the patient in the development of comprehensive care for the psychosocial aspects of coronary disease is to establish a relationship with a good primary care doctor. Reducing psychosocial risks goes hand in hand with reducing
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cardiovascular risks, which will often be directed by the primary care doctor. Most good primary care doctors will also manage the initial stages of pharmacologic trials for uncomplicated depression and anxiety. And they will often be the first to learn of relapses in either the coronary disease or the distress associated with it. The second step toward better care involves helping your patient learn his or her risks for depression, anxiety, and heart disease. This means learning a few facts and a few numbers that describe the risks. This learning process, often a late response to unwelcome symptoms, should begin early in adulthood, before habits and arteries have hardened. Until our patients learn their risk factors, they cannot hope to manage their risks, and we cannot help them much. The exercise of drawing a family tree marked with the relevant illnesses often raises useful questions for prevention and treatment planning, pointing to generational patterns related to depression, anxiety, or heart disease, like alcoholism, diabetes, high blood pressure, and obesity. After a careful review of the family history, it should become clear whether the family history contributes a low, medium, or high risk for depression, anxiety, or heart disease, or some combination. Identifying the risks for depression and heart disease means knowing a few numbers. Men in their 40s and women in their 50s should begin learning not only about their family histories but also about their cholesterol levels, blood pressure, body mass index, glucose tolerance, physical activity patterns, numbers of episodes of major depression, and current severity of depressive symptoms. Knowing the numbers makes it harder to deny the risks.
Targeted Behavior Change Once your patient has established a relationship with a primary care doctor and identified key risk factors, the next step is to pick the targets for prevention and treatment. Setting these priorities for treatment is often guided by access to treatment resources, such as cardiac rehabilitation, psychotherapy, and selected specialists. Pain or fear often lends urgency to one factor over another. People in distress may underestimate their resources and feel unnecessarily helpless when resources may be around the corner. For people with multiple risk factors, begin with the one or two targets that your patient can most easily improve. Pick your targets and be patient. It took decades to build these processes that contributed to the vicious cycle of depression and heart disease, and it usually takes several years – not days or weeks – to reverse them. One of the most important problems modern medicine has yet to solve for the management of all chronic illnesses is how to change high-risk health behaviors in large numbers of people. Sustained behavior change is tough for anyone, and, in general, doctors in the United States report low success rates in helping their patients quit smoking, lose weight, or exercise regularly. However, the “stages of change” method, originally developed by James Prochaska and his colleagues and described in their inspiring self-help book,
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Changing for Good (Prochaska, Norcross, & DiClimente, 1994), has earned the lead role among strategies for change. This model has been adopted by the Centers for Disease Control and Prevention, the National Cancer Institute, and the National Health Service of Great Britain in a wide range of programs for reducing risky behaviors. Ample studies of the stages of change method combined with motivational interviewing techniques have shown that patients, on their own and with the help of clinicians, can make sustained behavior changes that improve their health outcomes. Motivational interviewing is the counseling approach for helping people translate their particular set of arguments for and against a behavior change into a treatment plan that works. Losing weight ranks among the toughest behavior changes. For most of us losing weight is long, slow, and frustrating work. Since there is no quick fix for obesity (even bariatric or gastric bypass surgery takes about a year from start to finish), we rely on discipline, tenacity, and patience as much as any formal program or diet to achieve a stable lower weight. Losing weight is no job for the depressed mind; it is hard enough to do when we have all our wits and function at our best. Depression sabotages the best laid plans for weight loss, particularly if your patient tends to eat or drink more when depressed. The depressed mind often shifts moods and behaviors, gives up easily, grows impatient in the face of frustration, views itself as ugly, and expects failure. Before your patient launches into an ambitious diet or weight loss program, treat the depression as fully as possible and continue that regimen while working on losing weight.
Exercise Next to losing weight, increasing physical activity may be the hardest health behavior to sustain. But for people with depression or anxiety and heart disease, exercise is one treatment for two problems. What is good for the heart is good for the brain. The equivalent of three and half hours of brisk walking each week is a good place to get started. Exercise sets the range of vascular tone throughout the system, from the largest (the heart) to the smallest vessels (the arterioles where the oxygen diffuses across arteriole walls and into the tissues). Pitch exercise as a tune-up for various levels of demand on the cardiovascular system, a drill that calls into action the coordination of hormones, nerves, and the muscles in the vessel walls. The drill also tunes up the immune system and the limbic system. Once finely tuned, the rises in adrenalin, cortisol, and endorphins account for the transient good feeling, the runner’s high, that comes with exercise, often overriding the aches and the fatigue. Exercise also promotes neurogenesis or nerve cell regeneration in the hippocampus of the limbic system, the part of the brain that shrinks under prolonged stress or depression. Exercise restructures this part of the limbic system in a way that improves the functioning of the whole system. For many people, regular exercise works as an antidepressant both immediately (within minutes and lasting hours) and over the long run (lasting weeks to months).
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Studies of exercise as a treatment for heart disease show a beneficial effect for both the prevention of coronary disease and for the improvement of existing coronary disease (Taylor et al., 2004). Studies of exercise as a treatment for depression have focused mostly on mild to moderate depression and suggest that sustained regular exercise reduces depressive symptoms as much as psychotherapy or antidepressant medication, and exercise reduces the risk of relapse (Babyak, Blumenthal, Herman, & Parinda, 2000; Blumenthal et al., 1999). The levels of exercise required to reduce risk for heart disease are about the same as the levels required to reduce symptoms of depression. Thirty minutes of vigorous walking three times a week is a good goal to start with for people who usually do nothing that would pass for exercise (about half of the US population). Beyond that level the benefits increase with increasing duration and frequency up to a point. Most of the benefits can be achieved by 30–60 min of daily vigorous walking or light jogging. Any combination of exercise types and durations will do, such as several 15-min walks.
After Bypass Surgery, Angioplasty, and Stents One in five people develop major depression within weeks after the surgical correction of narrowed coronary arteries. And depression increases the risk for needing a second corrective procedure within 5 years. That is, the same or a new narrowing of the coronary artery is more likely to happen in depressed people than in those who are not depressed. And for many people, depression soon after a heart attack or unstable angina doubles or triples the risk for dying from coronary disease (Connerney et al., 2001; Sullivan, Simon, Spertus, & Russo, 2002). For these three reasons (if dodging the misery of depression is not compelling enough by itself), the first 6 months after a cardiac procedure represent a vulnerable period worthy of diligent preventive efforts. Monitoring of depressive symptoms, supportive psychotherapy, and a daily self-management plan to prevent relapse provide the best chances of avoiding complications. The pros and cons of preventive courses of antidepressants are complex and justify a psychiatric consultation.
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Leor, J., Poole, W. K., & Kloner, R. A. (1996). Sudden cardiac death triggered by an earthquake. The New England Journal of Medicine, 334(7), 413–419. Lesperance, F., Frasure-Smith, N., Koszycki, D., Laliberte, M. A., van Zyl, L. T., Baker, B., et al. (2007). Effects of citalopram and interpersonal psychotherapy on depression in patients with coronary artery disease: The Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial. JAMA, 297(4), 367–379. Lesperance, F., Frasure-Smith, N., & Talajic, M. (2002). Five-year risk of cardiac mortality in relation to initial severity and one-year changes in depression symptoms after myocardial infarction. Circulation, 105, 1049–1053. Lesperance, F., Frasure-Smith, N., & Theroux, P. (2000). Depression and 1-year prognosis in unstable angina. Archives of Internal Medicine, 160, 1354–1360. Linden, W., Stossel, C., & Maurice, J. (1996). Psychosocial interventions for patients with coronary artery disease. Archives of Internal Medicine, 156, 745–752. McCaffery, J. M., Frasure-Smith, N., Dube, M. P., Theroux, P., Rouleau, G. A., Duan, Q., et al. (2006). Common genetic vulnerability to depressive symptoms and coronary artery disease: A review and development of candidate genes related to inflammation and serotonin. Psychosomatic Medicine, 68(2), 187–200. Orth-Gomer, K., Wamala, S. P., Horsten, M., Schenck-Gustafsson, K., Schneiderman, N., & Mittleman, M. A. (2000). Marital stress worsens prognosis in women with coronary heart disease: The Stockholm Female Coronary Risk Study. JAMA, 284(23), 3008–3014. Prochaska, J., Norcross, J., & DiClimente, C. (1994). Changing for good. New York: Avon Books. Ramachandruni, S., Fillingim, R. B., McGorray, S. P., Schmalfuss, C. M., Cooper, G. R., Schofield, R. S., et al. (2006). Mental stress provokes ischemia in coronary artery disease subjects without exercise- or adenosine-induced ischemia. Journal of the American College of Cardiology, 47(5), 987–991. Roest, A. M., Martens, E. J., Denollet, J., & de Jonge, P. (2010) Prognostic association of anxiety post myocardial infarction with mortality and new cardiac events: A meta-analysis. I Am Call Cardiology, 56(1), 38–46. Rosengren, A., Hawken, S., Ounpuu, S., Sliwa, K., Zubaid, M., Almahmeed, W. A., et al. (2004). Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART Study): Case-control study. Lancet, 364(9438), 953–962. Rozanski, A., Blumenthal, J., & Kaplan, J. (1999). Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation, 99, 2192–2217. Rudisch, B., & Nemeroff, C. (2003). Epidemiology of comorbid coronary artery disease and depression. Biological Psychiatry, 54, 227–240. Rugulies, R. (2002). Depression as a predictor of coronary heart disease. American Journal of Preventive Medicine, 23, 51–61. Ruo, B., Rumsfeld, J., Hlatky, M., Browner, W., & Whooley, M. (2003). Depressive symptoms and health-related quality of life: The Heart and Soul Study. JAMA, 290, 215–221. Sauer, W., Berlin, J., & Kimmel, S. (2001). Selective serotonin reuptake inhibitors and myocardial infarction. Circulation, 104, 1894–1898. Shapiro, P. A., & Wulsin, L. R. (2009). Cardiovascular disorders. In B. J. Sadock, V. A. Sadock, P. Ruiz, et al. (Eds.), Comprehensive textbook of psychiatry (9th ed.). Philadelphia: Lippinncott, Williams & Wilkins. Steinberg, J. S., Arshad, A., Kowalski, M., Kukar, A., Suma, V., Vloka, M., et al. (2004). Increased incidence of life-threatening ventricular arrhythmias in implantable defibrillator patients after the World Trade Center attack. Journal of the American College of Cardiology, 44(6), 1261–1264. Sullivan, M., Simon, G., Spertus, J., & Russo, J. (2002). Depression-related costs in heart failure care. Archives of Internal Medicine, 162(16), 1860–1866. Swenson, J. R. (2004). Quality of life in patients with coronary artery disease and the impact of depression. Current Psychiatry Reports, 6(6), 438–445.
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Taylor, R., Brown, A., Ebrahim, S., Jolliffe, J., Noorani, H., Rees, K., et al. (2004). Exercise-based rehabilitation for patients with coronary heart disease: Systematic review and meta-analysis of randomized controlled trials. The American Journal of Medicine, 116, 714–716. Taylor, C. B., Miller, N. H., Smith, P. M., & DeBusk, R. F. (1997). The effect of a home-based, case-managed, multifactorial risk-reduction program on reducing psychological distress in patients with cardiovascular disease. Journal of Cardiopulmonary Rehabilitation, 17(3), 157–162. Thayer, J. F., & Lane, R. D. (2007). The role of vagal function in the risk for cardiovascular disease and mortality. Biological Psychology, 74(2), 224–242. van Melle, J. P., de Jonge, P., Spijkerman, T. A., Tijssen, J. G., Ormel, J., van Veldhuisen, D. J., et al. (2004). Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: A meta-analysis. Psychosomatic Medicine, 66(6), 814–822. Wulsin, L. R. (2004). Is depression a major risk factor for coronary disease? A systematic review of the epidemiologic evidence. Harvard Review of Psychiatry, 12, 79–93. Wulsin, L. R. (2007). Treating the aching heart: A guide to depression, stress, and heart disease. Nashville: Vanderbilt University Press. Wulsin, L., & Singal, B. (2003). Do depressive symptoms increase the risk for the onset of coronary disease? A systematic quantitative review. Psychosomatic Medicine, 65, 201–210.
Chapter 3
Sudden Cardiac Arrest: A Biopsychosocial Approach to Patient Management of Ventricular Fibrillation and Implantable Cardioverter Defibrillators Kari Kirian, Samuel F. Sears, and Harry DeAntonio
Introduction Sudden cardiac arrest remains the single most common cause of death for adults in the Western world. Sudden cardiac arrest (SCA) affects approximately 350,000 Americans annually and is a significant health concern and risk (The American Heart Association 2007). These potentially life-threatening arrhythmias often begin as ventricular tachycardia (VT), a dangerously fast heart rhythm that originates in one of the ventricles that may decompensate into ventricular fibrillation (VF). Treatment for VF usually includes high-energy defibrillation from either an automatic external defibrillator (AED) or an implantable cardioverter defibrillator (ICD) that restores proper heart rate and rhythm using high-energy electrical shock. Randomized controlled clinical trials have demonstrated superior mortality benefits of ICDs compared to medications for both primary and secondary prevention for patients at risk for VT/VF. The patient experiences of both spontaneous life-threatening arrhythmias and the treatment via high-energy shock from the ICD have prompted significant clinical and research attention to psychosocial factors (Stutts, Cross, Conti, &
K. Kirian, M.A. Department of Psychology, East Carolina University, 215 Rawl Hall, Greenville, NC 27858, USA S.F. Sears, Ph.D. (*) Department of Psychology, East Carolina University, 215 Rawl Hall, Greenville, NC 27858, USA Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA e-mail:
[email protected] H. DeAntonio, D.O. Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_3, © Springer Science+Business Media, LLC 2012
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Sears, 2007). Biopsychosocial approaches to understanding and managing the risk of sudden cardiac arrest have included examination of psychosocial factors both as antecedents and as consequences to the experience of VF and the subsequent treatment by the ICD. The purpose of this chapter is to review the medical manifestation of ventricular fibrillation and the psychosocial factors of ventricular fibrillation and its treatment and suggest psychological intervention approaches for patients with VF/ICDs.
Connection Between the Heart and Psychological Factors of Sudden Cardiac Arrest and Ventricular Fibrillation (VF) Sudden cardiac arrest and death can result in as short as 4 min (Kenny, 2006) from ventricular fibrillation. Ventricular fibrillation (VF) is a rapid and disorganized rhythm that prohibits normal blood flow throughout the body and cardiac output drops to zero. VF is self-sustaining, rapid, and irregular electrical activity that manifests in heart rates from 200 to 300 bpm (Burstein, Comtois, & Nattel, 2008). VF has a number of possible causes but most often includes the overall process of ischemic damage, but there remain many unknowns regarding the occurrence, timing, and predictability of VF events. Investigators have long postulated that an association exists between emotional states and ventricular arrhythmia (Engel, 1971). Recent epidemiological studies have demonstrated that strong negative emotions, such as stress and anger, have arrhythmogenic effects in patients at risk of arrhythmic events (Lampert, 2010). Studies have shown significant increases in episodes of ventricular arrhythmia and sudden cardiac death in people after situations of war, natural disaster, and terrorist attacks in locations both near and distant from the attack site (Leor, Poole & Kloner, 1996; Meisel et al., 1991; Steinberg et al., 2004; Shedd et al., 2004). Psychological stress is more likely to affect persons who are at risk of cardiac events such as those with anatomical abnormalities of the heart (e.g., CAD or scars from previous MIs). Lampert et al., (2000) demonstrated that patients engaged in mental stress (completing mental arithmetic and recalling an episode in which they were angry), who were induced via noninvasive programmed stimulation to experience VT, achieved the arrhythmia significantly quicker, and it was more difficult to terminate. Additionally, 40% of patients who underwent mental stress required shock in order to terminate the arrhythmia. In a follow-up investigation, Lampert et al., (2002) utilized a mood-state diary for patients with ICDs in which the patients recorded their emotions for the 15-min and 2-h periods prior to having received an ICD shock. Significant associations were shown between the preshock mood state of anger and the delivery of an ICD shock, suggesting that anger may be a trigger in ventricular arrhythmic events (VF) in a group of patients with a known arrhythmic risk. Other variables of negative affect such as depression have been linked as risk markers for shorter time to first shock and increased frequency of shock in prospective studies (Whang et al., 2005).
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Physiological Pathways of Psychological States in Ventricular Arrhythmias While the physiological substrates of the effect of emotions on VF are not completely known, it has been theorized that arrhythmias are caused by the arousal of the sympathetic system, but in a fashion that differs from the pathway in which exercise-induced arrhythmias occur (Kop et al., 2004). Additionally, the VT cycle length is altered, which results in acceleration of the VT rhythm and/or causing the rhythm to be more difficult to terminate. This recalcitrance to termination facilitates the progression from ventricular tachycardia into ventricular fibrillation (Lampert et al. 2000, 2002). More recently, it has been revealed that anger can actually increase T-wave alternans (TWA) (Kop et al., 2004; Lampert et al., 2009). T-wave alternans is the periodic beat-to-beat variation in the amplitude of successive T waves (Shusterman, Goldberg, & London, 2006). The T wave represents the repolarization or recovery of the ventricles. T-wave alternans have been shown to occur prior to the initiation of ventricular arrhythmias and “establish a mechanism linking T-wave alternans of the ECG to the pathogenesis of sudden cardiac death” (Pastore, Girouard, Laurita, Akar, & Rosenbaum, 1999, p. 1385; Shusterman, Goldberg, & London, 2006; Gehi, Stein, Metz, & Gomes, 2005). Evidence from TWA studies suggest that increases in TWA correlated with increases in catecholamines, which are hormones released in response to stress that are known to be linked with arrhythmogenesis (Lampert et al., 2009). Furthermore, these increases in catecholamine levels are associated with increases in the variability and instability/alteration of repolarization, as measured by TWA. In sum, strong negative emotions are capable of increasing TWA and triggering potentially fatal arrhythmias in at-risk patients (Lampert, 2005; Lampert, 2010). Additional research in this area is indicated to further delineate the circumstances of risk, the predictions of risk, and possible preventive approaches to mitigate risk that both TWA can provide.
Medical Treatment of VF VF is a fatal arrhythmia and, as such, requires swift and effective treatment in order to avert sudden cardiac arrest and almost certain death. ICDs have shown a clear mortality advantage in randomized clinical trials comparing antiarrhythmic medications vs. ICDs in patients at risk for potentially life-threatening arrhythmias. The ICD is a surgically implanted medical device whose purpose is to terminate potentially life-threatening ventricular arrhythmias by administering a jolt of electricity, or a “shock,” to the heart. A review of randomized controlled trials in both primary and secondary prevention categories examined the results of eight trials, including 4,909 patients. The summarized findings indicated that ICDs significantly reduced SCA compared with usual care and antiarrhythmic drugs (Ezekowitz, Armstrong, &
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McAlister, 2003). As a result of these trials, ICDs are considered the “gold standard” for treatment of VF and prevention of SCA. While ICDs were originally indicated for secondary prevention (involving patients who have been resuscitated post cardiac arrest), they are now indicated prophylactically for primary prevention in people who are at high risk of SCD. Pharmacological interventions remain a valuable adjunctive therapy to reduce arrhythmic burden, and cardiologists employ antiarrhythmic medications, such as ACE inhibitors, beta blockers, and calcium channel blockers, and other antiarrhythmics and functions to reduce ventricular arrhythmias and stabilize the heart muscle tissue (Domanski, Zipes, & Schron, 1997). Modern ICDs allow for greater levels of customization in programming, functionality, and treatment aspects involving the use of antitachycardia pacing (painless attempts to terminate arrhythmias), dual chamber monitoring (both atrial and ventricular leads for discrimination of rhythms), biventricular pacing (aka: resynchronization therapy for congestive heart failure), fluid monitoring, and remote monitoring using home-based connectivity to upload cardiac data.
Implantable Cardioverter Defibrillators (ICD) The implantable cardioverter defibrillator (ICD) is a small battery-powered device that is about the size of a deck of cards and weighs between 40 and 82 g (Wilkoff & Thal 2008; Wang, Al-Ahmaid, Hsia, & Zei, 2008). Due to the small size, the device can usually be implanted below the clavicle in the left pectoral region. Depending on the frequency of ICD shocks, the battery life generally lasts 5–7 years in the newest devices (Zimetbaum and Josephson 2009). The actual device is a titanium exoskeleton, housing complex circuitry that detects and records arrhythmic events 24 h a day, 365 days per year. The conduits for electricity are silicone-encased transvenous electrode leads. ICDs may be single-, dual-, or triple-lead devices anchoring in up to three of the chambers of the heart, depending on the medical indication for use. The primary lead winds down a vein into the right chambers of the heart, with the end of the ventricular lead being anchored in the apex of the right ventricle of the heart, in the optimal case (Kenny, 2006). The device is designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) in which the heart beats too fast or erratically, respectively (Connolly, Dorian, Roberts et al., 2006). Ventricular tachycardia may be corrected with electrical pacing, known as antitachycardia pacing. This function is similar to that of a traditional pacemaker. This occurs when a precisely timed impulse is administered, in order to increase the pace of the heart faster than its normal rate to disrupt the tachycardia before it progresses into VF. Pacing therapy is painless and is considered the first line of ICD therapy. Sustained VF is the most dangerous type of arrhythmia and occurs when the chambers of heart quiver uncontrollably and are unable to coordinate contraction. In this instance, blood is not circulated through the body and death will occur in a matter of minutes unless the dangerous rhythm is converted through shock (Turhakia & Tseng, 2007). The shock restores the normal contraction of the heart and allows the delivery of oxygen-rich blood to the vital organs.
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The Patient Experience of VF and/or ICD Patients who experience an episode of sustained VF without an ICD are at great risk of death. In fact, only 5% of people survive such an episode of VF (The American Heart Association 2007). Regardless of the possible reversible nature of the VF, it is recommended that patients receive an ICD for secondary prevention of SCA, after a cardiac arrest event. Patients with an ejection fraction of >35% are also medically indicated to receive an ICD, which is considered primary prevention of SCA (Moss et al., 1996). The experience of living with an ICD is a highly unique and personal experience. The patient’s reasoning and understanding of ICD therapy can differ widely, and ICD type and individualized programming can also differ substantially. Regardless, the common factor across ICD care is the capability of delivering a high-energy, life-saving shock. While this fantastic capability is certainly a boon from the medical perspective, it can also be experienced as a burden by the patient. The energy required to shock the heart back into normal sinus rhythm is significant and usually involves the delivery of shock up to 35–40 J in high-energy devices (Zimetbaum and Josephson, 2009). Patients have described the experience of shock as a swift kick in the chest and have rated it as a “6” on a 0–10 pain scale (Ahmad, Bloomstein, Roelke, Bernstein, & Parsonnet, 2000; Pelletier, Gallagher, Mitten-Lewis, McKinley, & Squire, 2002). It is considered an uncomfortable and nearly always surprising experience. Most patients report feeling that shocks are completely unpredictable with no noticeable precipitating events or indicators that a shock is pending. This lack of ability in predicting shocks can result in a profound sense of helplessness and anxiety in patients with ICDs, as patients can do nothing to prevent a shock if one is indicated. It should come as no surprise then, that psychological ramifications of shock can be deleterious. The experience of shock and even the ever-present possibility of shock may elicit anxiety, avoidance behaviors, decrements in quality of life, and depression. Risk factors for psychosocial adjustment difficulties have been established and include young age (<50 years of age), female sex, shock history, poor understanding of condition and device, previous psychological history, and severe comorbid medical history (Sears, Matchett, & Conti, 2009). Below, we review these common psychosocial and behavioral responses to the potential of life-threatening VF and ICD therapy.
Quality of Life The quality of life (QOL) studies of ICD patients have deduced that the QOL of these patients is at least equal to, or better than, those taking antiarrhythmic medications (Sears et al., 2005). However, those patients who avoid behaviors associated with shock may eventually come to avoid many daily activities inadvertently compromising the quality of their life. Additionally, the occurrence of shock has been associated with changes in QOL in ICD patients. The effect of shock on QOL
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appears to depend in large part on the frequency of shocks. Passman et al. (2007) found that ICD patients are able to endure one to five shocks without clinically meaningful differences in QOL, but when shocks exceed five, clinically and statistically significant changes in QOL are evidenced, consistent with previous research. More recently, QOL was studied in 2,521 patients with stable heart failure in the SCD-HeFT trial (Bardy et al., 2005), and results indicated that the ICD patient group had significantly improved psychological QOL at 3 and 12 months postimplantation, when compared to patients who were treated with medications alone (Mark et al., 2008). However, there were no differences between groups at 30 months in patient reported QOL. Importantly, the deleterious effects of an ICD shock were noted on a host of QOL subscales if the shock had occurred within 30 days of the sampling. Collectively, desirable QOL can be expected for most ICD patients with the caveats of limitations associated with exposure to repeated ICD shocks and the overall management of the disease substrate that prompted ICD implantation such as congestive heart failure or cardiomyopathy.
Anxiety Anxiety is a common psychological side effect of having an ICD, and ICD recipients are at risk of experiencing anxiety (Bilge, Ozben, Demircan, et al., 2006); Hegel, Griegel, Black, et al., 1997; Pauli, Wiedemann, Dengler, et al., 1999). In fact, anxiety disorders are experienced by between 13% and 38% of ICD recipients (Sears, Todaro, Saia et al., 1999). It is also important to bear in mind the possible psychologic effect of shock, principally because shocks are emotionally disconcerting and physically uncomfortable reminders of one’s cardiac condition and mortality. Recent research indicates that patients who have been shocked are significantly more likely to suffer from anxiety than those who have never received a shock (Jacq et al., 2009; Spindler, Johansen, Andersen, Mortensen, & Pedersen, 2009). While not all ICD patients go on to experience symptoms of anxiety, many do. The experience of anxiety may vary from general anxiety, more specific anxiety surrounding the fear of shock and death, and even posttraumatic stress (Ladwig, Baumert, & Marten-Mittag, 2008; Matchett, Kirian, Hazelton, Brumfield, & Sears, 2009; Sears, Kirian, Matchett, Benton, & Nekkanti, 2011; Kapa et al., 2010).
Avoidance Avoidant behavior in cardiac patients frequently results from a self-protective response to avoid situations where increased heart rate and demand may occur. For ICD patients, avoidance may occur because patients want to avoid even the chance that shock could occur. Approximately 55% of ICD patients regularly avoid people, places, and activities in an attempt to avoid shock (Lemon, Edelman, & Kirkness, 2004).
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Based on this finding, the implications for decreased quality of life in ICD patients are significant, as the result of the fear is a decrease in the likelihood that the person will participate in that behavior in the future. Often, ICD patients are shocked while engaging in some sort of activity and may go on to avoid activities for a number of reasons. First, shocked patients may attempt to create reason from randomness and, henceforth, become reticent to participate in activities in which they were shocked. These patients often incorrectly believe that the activity caused the shock. In turn, they believe that they can avoid shock by simply avoiding those activities. Learning theory may also help to explain how shocked ICD patients come to exhibit behavioral avoidance and how those behaviors are maintained. Classical conditioning and operant conditioning have been posited as explanations of behavior after shock (Sears et al., 1999). Classical conditioning describes how an object or event that was previously neutral (unconditioned stimulus) can become a conditioned stimulus once paired with an aversive stimulus (i.e., shock) and can result in a conditioned response. When applied to ICD patients, this theory may elucidate why patients may avoid behaviors they were engaging in prior to shock. The behavior or the activity becomes associated with shock, whether it is reading a book on the couch or going on a jog. The result of this conditioned fear is behavioral avoidance or a decrease in the likelihood of participating in that activity again in the future. Operant conditioning, another type of learning, can assist in explaining the maintenance of the behavioral avoidance. Negative reinforcement is the removal of something that results in an increased response. For example, if an ICD patient engages in a sedentary activity, such as sitting on the couch, and is not shocked, the patient may be more likely to perform that behavior again.
Depression The rates of depression in ICD patient populations have been comparable to those of other cardiac patients, but continue to be a sizeable concern, particularly since depression can affect all aspects of coping, adjustment, and disease management (Sears & Conti, 2003; Matchett et al., 2009). Symptoms of depression have been reported in 24–33% of patients with ICDs (Sears, Todaro, Saia, Sotile, & Contiet, 1999) and even as high as 41% (Bilge et al., 2006). Akin to QOL, shock has also been implicated in the contribution to depressive symptomatology. Results from the Triggers of Ventricular Arrhythmias (TOVA) study indicated that risk of shock was associated with depression whereby increased depression severity was associated with increased frequency of shock (Whang et al., 2005). Implantable cardioverter defibrillators have demonstrated clear life-saving benefits in multiple randomized trials for patients at risk for potentially life-threatening arrhythmias. We suggest that a biopsychosocial conceptualization of patient care fits well with the potential patient adjustment challenges that the conditions of VT/ VF and the impact of the ICD prompt. This suggests the need for routine intervention to facilitate positive biopsychosocial outcomes.
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Clinical Psychology
• Anxiety • Depression • PTSD
A N X I E T Y
• Patient acceptance • Shock anxiety • Death anxiety • Shock phobia • Avoidance
Cardiac Psychology
Fig. 3.1 Convergence of clinical and cardiac psychology
Table 3.1 Device-specific measures for ICD patients Measure Florida Shock and Anxiety Scale (FSAS) (Kuhl et al., 2006) Florida Patient Acceptance Scale (FPAS) (Burns, Serber, Keim, & Sears, 2005) Avoidance behaviors in patients with ICDs (Lemon et al., 2004) Implanted Cardioverter Defibrillator Concerns Questionnaire (ICDC) (Frizelleet al., 2006) Implanted Device Adjustment Scale (IDAS) (Beery, Baas, Matthews, Burroughs, & Henthorn, 2005) Self-Efficacy Expectations and Outcome Expectations After ICD Implantation Scales (Dougherty, Johnston, & Thompson, 2007)
Construct assessed Anxiety related to ICD shock Patient acceptance of a cardiac device Behavioral avoidance Acuteness and degree of ICD patient concerns Adjustment to an implanted device Perceptions of one’s ability to manage common problems encountered after surviving sudden cardiac arrest
The importance of device-specific constructs in the ICD patient population cannot be underestimated. As you can see in Fig. 3.1, there is some overlap between clinical psychology and cardiac psychology as they relate to anxiety, but the psychologic needs of ICD patients are considerably different than those patients struggling with traditional clinical anxiety. For this reason, we strongly advocate that psychologic constructs be assessed with device-specific measures. ICD patient scores should not be compared to those of their nondevice harboring counterparts. These patients require measures whose norms were standardized solely on ICD patients in order to avoid the tendency for providers to overpathologize ICD patients based on general measures, as ICD patients tend score higher on such measures due to the contextual factors of chronic disease and a possible near death experience. To increase clinical precision, measures have been developed for use specifically with this population. To date, assessment tools have been developed to measure anxiety, patient acceptance, ICD knowledge, behavioral avoidance, patient concerns, and adjustment in the ICD patient population (see Table 3.1).
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Psychological Treatment of Patients with Arrhythmias In some cases, the optimization of medical treatment may be all that is required to alleviate psychological concerns. For example, a patient who has recently experienced an ICD shock and receives changes in ICD programming and antiarrhythmic medication may feel adequately relieved about the reduced potential for future shocks. However, some arrhythmia patients may continue to experience psychological distress even after medical therapy is optimized, and those patients often warrant referral for specialty mental health care. Facilitating referrals from cardiology groups has been addressed elsewhere (Sears, Matchett, & Conti, 2009). Routine and continuous consultation and availability by mental health professionals emphasizing screening approaches, key signs and symptoms of distress sampling psychosocial risk factors, risk behaviors, behavioral observations, and affective assessment can be achieved in cardiac clinics. Living with spontaneous, potentially life-threatening arrhythmias and the ICD can be challenging for ICD patients, and a variety of treatment programs have been developed to address this issue. While the programs vary in format, content, and administration, they share some demonstrated efficacy in decreasing psychological distress and improving physiological functioning postimplant (Carlsson, Olsson, & Hertervig, 2002; Chevalier et al., 2006; Dunbar et al., 2009; Dougherty, Thompson, & Lewis, 2005; Fitchet et al., 2003; Frizelle et al., 2004; Kohn, Petrucci, Baessler, Soto, & Movsowitz, 2000; Lewin, Coulton, Frizelle, Kaye, & Cox, 2009; Sears et al., 2007; Kuhl, Sears, Vazquez, & Conti, 2009; Edelman, Lemon, & Kirkness, 2007; Vazquez, Conti, & Sears, 2010). Meta-analytic reviews of ICD psychosocial treatment studies have indicated a wide range of effect sizes for reductions of anxiety ranging from .14 for a peer-led support group to 1.79 for multidisciplinary cognitive-behavioral therapy combined with exercise (Pedersen, Van Den Broek, & Sears, 2007). Collectively, these studies provide promising results that patients can benefit from a biopsychosocial model of care.
Cognitive-Behavioral Therapy (CBT) Recent reviews of CBT for ICD patients have been somewhat encouraging. Salmoirago-Blotcher and Ockene (2009) reviewed 12 studies employing psychosocial interventions to improve the emotional distress of patients after ICD implantation. Overall, the most effective technique utilized in the studies was cognitive-behavioral therapy (CBT), and the results evidenced decreases in anxiety and depression as a result (see Table 3.2). Multiple CBT techniques have proven efficacious with ICD patients and with cardiac patients in general. Our focus will include cognitive, behavioral, and other methods including psychosocial education and emotional support.
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Table 3.2 ICD intervention studies in the last 10 years First author Intervention components Carlsson et al. (2002) ICD-specific education Social/group support Chevalier et al. (2006) Relaxation and stress management Cognitive-behavioral techniques Dougherty et al. ICD-specific education (2004, 2005) Social/group support Shock planning
Dunbar et al. (2009)
ICD-specific education Relaxation and stress management Cognitive-behavioral techniques Shock planning Symptom management Edelman et al. (2007) ICD-specific education Shock planning Fitchet et al. (2003)
Frizelle et al. (2004)
Kohn et al. (2000)
Kuhl et al. (2009)
ICD-specific education Relaxation and stress management Cognitive-behavioral techniques Exercise ICD-specific education Relaxation and stress management Cognitive-behavioral techniques Social/group support Exercise Relaxation and stress management Cognitive-behavioral techniques
ICD-specific education Relaxation and stress management Cognitive restructuring Social/group support Shock planning Lewin et al. (2007) ICD-specific education Relaxation and stress management Cognitive-behavioral techniques Social/group support Sears et al. (2007) ICD-specific education Relaxation and stress management Cognitive-behavioral techniques Social/group support Shock planning Vazquez et al. (2010) ICD-specific education Relaxation and stress management Cognitive-behavioral techniques tailored to women (e.g., body image issues, family relationships) Shock planning
Significant findings ↓ Sleep disturbances ↓ Anxiety ↓ Physical symptoms ↓ State anxiety ↓ Fear of dying ↑ Self-efficacy ↑ Patient knowledge ↓ Anxiety ↓ Depression ↓ Health care utilization ↓ Sick/disability days No significant improvements on anxiety, depression, hostility, or stress ↓ Anxiety ↓ Depression ↑ Exercise time ↓ Anxiety ↓ Depression ↓ Patient concerns ↑ Perceived health status ↑ Quality of life ↑ Physical function ↓ Depression ↓ Sexual problems ↓ Anxiety ↑ Patient adjustment ↑ Patient knowledge
↓ Physical limitations ↓ Unplanned hospitalization Admissions ↑ Quality of life ↓ Psychological anxiety ↓ Physiological anxiety ↑ Patient acceptance
↓ Shock anxiety ↑ Patient acceptance
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Cognitive Methods Cognitive Restructuring Cognitive restructuring refers to the process of helping patients recognize and change maladaptive thoughts in order to produce salutary effects on feelings and behaviors (Wright, Basco, Thase, 2006). The premise behind cognitive therapy methods is that changes in behavior and affect result from cognitive changes (DeRubeis, Webb, Tang, & Beck, 2010). Often, people in distress experience negative automatic thoughts and do not stop to challenge or critically examine those thoughts (see Fig. 3.2).
Behavioral Methods Shock Planning All ICD patients, regardless of shock history, can benefit from shock planning. Education around shock and what to do after receiving a shock is desired because there is a known probability of ICD patients being shocked, and the event of shock has the potential to cause psychologic ramifications. Additionally, patients (and families) who are prepared for what to do postshock may be more likely to cope in a more optimal and effective manner. Behavioral and affective preparedness can be achieved if the clinician discusses a shock plan with the patient at each visit, such as the plan outlined in the patientfriendly Cardiology Patient Page by Sears, Shea, & Conti (2005). In this plan, the patient is instructed what to do based on the number of shocks received and how the patient feels. For example, if the patient receives one shock in a 24-h period and is
Event Palpitation
Automatic Thought “I just felt a funny beat. My heart must be acting up. I am having a heart attack and am going to die!”
Fig. 3.2 Automatic thought progression
Anxiety
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feeling fine, the patient is encouraged to call their cardiologist to inform them of the event and arrange follow-up if deemed necessary by the physician. The other end of the spectrum should also be addressed, whereby if a patient receives two or more shocks in a 24-h period, they are advised to seek immediate medical attention, regardless of how they are feeling.
Activity Scheduling As a result of distress and concerns about their cardiac or ICD functioning, many patients find themselves no longer participating in activities that they once enjoyed, such as playing golf, going shopping, or traveling. These drops in activities may be due to many reasons. Some common reasons for cardiac patients are concern that their medical condition will limit them, fear that the activity may put them at risk for injury (i.e., cause a shock), or a general loss of interest. It is important for these patients to return to living their lives. Cardiac psychologists may employ activity scheduling as a way to improve the patient’s quality of life. In activity scheduling, a list of pleasurable activities is generated (new or tried-and-true) and the patient chooses which activity he or she would like to perform during the following week. Scheduling the activity will increase the likelihood of follow-through on the part of the patient. Once the patient is able to initiate pleasant activities spontaneously, this practice may be ceased. Activity scheduling has a dual purpose – to increase the probability that the patient will engage in the activities that he or she has been avoiding and to eliminate any decision-making process that may have served as a barrier to participation (DeRubeis et al., 2010).
Relaxation Training Prior to the initiation of relaxation training, a rationale is presented for using relaxation training and the empirical evidence supporting the methods. Multiple types of relaxation training that have been proven effective in producing beneficial psychological and physiological responses in various patient populations including progressive muscle relaxation, diaphragmatic breathing, and guided imagery. These techniques have demonstrated significant success in promoting relaxation, improving stress management, and decreasing negative emotional states if used regularly. Progressive muscle relaxation (PMR) is a technique used to reduce muscle tension by increasing the patient’s awareness of the feelings of tension and relaxation. This is accomplished by leading a patient through an exercise in which they consciously tense certain muscle groups, monitor the tension, and then relax the muscles. This is repeated systematically through the major muscle groups in the body in a directed sequence. PMR has been shown to decrease state and trait anxiety
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(Dehdari, Heidarnia, Ramezankhani, Sadeghian, & Ghofranipour, 2009), improve quality of life (Yu, Lee & Woo, 2009), and decrease blood pressure (Chesney, Black, Swan, & Ward, 1987) in cardiac patients post-CABG, hypertensive patients, and patients with CHF (Dehdari et al., 2009; Chesney et al., 1987; Yu et al., 2009). Diaphragmatic breathing is a type of breathing retraining performed to increase the amount and reach of oxygen to the lungs. Patients are taught to slowly breathe in through the nose and out through the mouth. They are also taught to breathe using the diaphragm, rather than the chest wall muscles. In this exercise, the diaphragm is extended as oxygen is inspired deeply into the lungs in contrast to short shallow breaths that usually accompany feelings of anxiety. Multiple studies have confirmed the physiologic benefits of diaphragmatic breathing, including improvements in heart rate variability, glycemic index, exercise capacity, dyspnea, respiratory rate, oxygen saturation, and lung volume (Kulur, Haleagrahara, Adhikary, & Jeganathan, 2009; Laoutaris et al., 2007; Lewis, Williams, & Olds, 2007). These benefits have been found in a wide variety of patient populations, including diabetic, ischemic heart disease, CHF, and respiratory disease patients. Guided imagery is yet another technique used to allow patients to take a “mental vacation” from stress, worry, and distress. Certain calming mental images can assist in relaxation and may be suggested by the therapist or determined by the patient (e.g., sitting on a warm beach). Mental imagery can assist in reaching a deeper level of relaxation and providing the patient something to focus on instead of worrisome thoughts. It can be viewed as a healthy form of daydreaming. A calm, even, soothing, and genuine vocal tone is used during these exercises. Guided imagery studies have demonstrated effectiveness in increasing self-report relaxation and decreasing heart rate and pain among other benefits (Urech et al., 2010; Baird, Murawsi, & Wu, 2010; Lahmann et al., 2010).
Other Psychological Treatment Psychosocial Education Patients often desire additional information about their cardiac condition or their device. Cardiac psychologists have training in cardiac anatomy, functioning, and pathophysiology and are able to provide patients with information in way that is easy to understand. Most ICD programs utilize a psychosocial education component to help improve patient understanding and promote acceptance of their condition and new lifestyle. An additional rationale may be that “knowledge is power,” and information helps to improve psychological outcomes. Patient-focused materials are often available via cardiology journals that can aid in instructing patients about the management of shocks, recalls, or spouse and family problems (Sears et al. 2005, Kirian, Sears, & Shea, 2009, Hazelton, Sears, Kirian, Matchett, & Shea, 2009).
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Emotional Support Emotional support tends to be the primary function when people think of psychologists and what psychologists provide. While only a facet of the care that a cardiac psychologist can provide, emotional support is a very important one. Validation of the patient’s unique experience, recognizing that living with arrhythmic problems is difficult and requires adaptability, strength, and courage. Emotional support may be provided in an individual format or in via support groups. Support groups offer a setting in which people with similar cardiac issues can get together and provide and receive support and understanding. The power of feeling understood and being part of group are important and can demonstrate improvements in psychological distress and physiological functioning including increased social support, self-efficacy, and exercise and decreased pain and healthcare utilization (Hilding and Fridlund 2003, 2004; Parry and Watt-Watson 2010). Moreover, the research is also clear that patients with no or low social support have higher rates of cardiac and all-cause mortality (Barth, Schneider, & von Känel, 2010). ICD patient support groups have been quite successful around the United States for creating an additional support system for patients. In addition, web-based support groups focused on ICD patient issues are also actively engaged in emotional support.
Comprehensive Psychosocial Care for Shocked ICD Patients Psychological consultation following an ICD shock is a common event. Limited research on treatment of shock-specific anxiety is available and may require much more clinical care than any one of the aforementioned cognitive or behavioral strategies to promote patient acceptance and decrease possible psychologic sequelae related to the device and the event of shock. This may be particularly true if they have experienced a multiple shock experience. Such patients may require a comprehensive treatment such as that created and implemented by Sears et al. (2007) with 30 ICD patients who had previously experienced one or more shocks. The content of the Shock and Stress Management Program (SSMP) included the four domains of ICD-specific education, relaxation and stress management training, cognitivebehavioral techniques, group discussion, and social support. All participants had experienced shock at least once in the previous year. Sears and colleagues found that both psychological anxiety and physiological markers of anxiety (salivary cortisol levels) were significantly reduced (P < 0.05; P = 0.05), and patient acceptance was significantly increased (P < 0.01) in these patients.
Conclusions The modern care of the ventricular arrhythmias using ICDs prompts a biopsychosocial model for ICD patients and families to achieve the full benefits of improved longevity and desirable quality of life. Sudden cardiac arrest remains the leading
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cause of death in the United States and requires a broad conceptualization to fully address prevention and treatment. Research has demonstrated that negative emotional states can be both antecedents and consequences of possibly deadly arrhythmias like VF. The realistic application of biopsychosocial care remains limited by the relatively little specific training in most training programs for mental health professionals about how each of the domains of medical, nursing, engineering, psychological, pharmacological, behavioral, physiology, and social aspects of care can be integrated. This theoretical and practical collision cannot be delayed if the goal of patient outcomes is truly improved longevity and optimal quality of life. The present chapter has attempted to advance the dialogue of achieving the goals of biopsychosocial outcomes.
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Chapter 4
Atrial Fibrillation: A Biopsychosocial Approach to Patient Management A. Garrett Hazelton, Samuel F. Sears, and Evelio Rodriguez
Introduction Atrial fibrillation (AF) is by far the most common arrhythmia in clinical practice, affecting approximately 2.2 million Americans, with an incidence rate of 160,000 new cases per year (Lloyd-Jones et al., 2009). It is estimated that by the year 2050, AF will affect 5.6 million Americans. The cost of managing AF and its associated complications in Medicare patients has been estimated to be $15.7 billion per year (Lee et al., 2008). The mortality and morbidity effects of AF are significant (Benjamin et al., 1994, 1998). AF independently doubles the risk of all cause mortality, as determined by the Framingham study (Kannel, Abbott, Savage, & McNamara, 1982; Kannel, Wolf, Benjamin, & Levy, 1998). AF patients also have a four- to fivefold increase in the rate of stroke (Wolf, Abbott, & Kannel, 1991), which could be significantly decreased when patients are properly anticoagulated with warfarin (commonly referred to as a blood thinner). Different risk models have been used to estimate the risk of stroke in patients with AF based on their comorbidities. Lifelong anticoagulation with
A.G. Hazelton, Ph.D. Department of Psychology, East Carolina University, 215 Rawl Hall, Greenville, NC 27858, USA S.F. Sears, Ph.D. (*) Department of Psychology, East Carolina University, 215 Rawl Hall, Greenville, NC 27858, USA Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA e-mail:
[email protected] E. Rodriguez, M.D. Department of Cardiovascular Sciences, East Carolina Heart Institute, East Carolina University, Greenville, NC, USA E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_4, © Springer Science+Business Media, LLC 2012
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warfarin is associated with risk of significant bleeding of approximately 1% per year. The need for warfarin is one of the biggest sources of dissatisfaction for patients with AF, significantly affecting their quality of life. In addition to anticoagulation, clinicians taking care of AF patients have concentrated their efforts in controlling the patient’s heart rate and occasionally rhythm (i.e. conversion into sinus rhythm) using one or many of the following options: antiarrhythmic medications, electrical cardioversion, catheter ablation with or without a pacemaker, and/or surgical ablation. For the most part, clinicians have not paid attention to the potential biopsychosocial factors responsible for AF and, thus, have not tried to modify psychosocial factors as part of a comprehensive treatment for patients with AF. The purpose of this chapter is to review a biopsychosocial model of AF and provide a guide for the clinical management of psychological distress in patients with AF. We begin by briefly describing the physiology of AF in terms of subtypes, causes, and symptoms. Next, we describe the patient experience in terms of the potential ways in which psychological factors can interact with AF. Finally, we demonstrate the application of clinical health psychology in the AF population despite limited interventional research. These behavioral treatment options are primarily based on clinical experience and research from similar medical populations. We hope to demonstrate areas for potential research and needed clinical trials while also justifying the importance of appropriately managing distress in this population until such evidence based treatments exist.
Understanding Atrial Fibrillation Cardiac arrhythmias are passive or active arrhythmias. Passive arrhythmias are often seen through disturbances in the conduction between the atria and ventricles, known as atrioventricular (AV) blocks. Active arrhythmias are further divided into abnormal impulse formation and reentry. AF, an active arrhythmia, is by far the most common in clinical practice and can present in the form of lone AF in relatively healthy people who have a structurally normal heart. Concomitant AF refers to patients with AF and structural heart abnormalities (e.g. valvular or coronary artery disease). The majority of patients with AF have other associated cardiovascular diseases such as hypertension, coronary artery disease, and/or diabetes (Aldhoon, Melenovsky, Peichl, & Kautzner, 2010). AF occurs when the atria (upper chambers of the heart) beat irregularly and rapidly, often surpassing 350 beats each minute. Electrical impulses are conducted from the atria to the ventricles (lower chambers of the heart) over an electrical bridge called the AV node. Fortunately, the AV node slows the transmission of many of these impulses; however, the ventricular rate can still be quite rapid (more than 100 beats per minute) and, if left untreated, can result in the development of what is known as “tachycardia-induced” cardiomyopathy or heart failure.
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AF has recently being classified as (Calkins et al., 2007; Fuster et al., 2007): 1. Paroxysmal: recurrent episodes that self-terminate in less than 7 days 2. Persistent: recurrent episodes lasting more than 7 days 3. Long-standing persistent: AF episode ongoing for more than 1 year Causes of AF are not completely understood; however, causes of AF can be generally classified as either cardiac or noncardiac. Examples of cardiac causes include valvular diseases, left ventricular hypertrophy, coronary heart diseases, sick sinus syndrome, and pericarditis. Some noncardiac examples include hypothyroidism, alcohol use, a pulmonary embolism, and pneumonia. AF may be due to wandering, disorganized electrical waves that circulate throughout the atria. In others, a single rapidly firing electrical spot that is usually located around one of the pulmonary veins in the left atrium may cause it. AF results from a complex interaction between substrate, mechanisms, and triggers responsible for atrial changes (Aldhoon et al., 2010). AF diagnosis tends to be problematic because many patients are asymptomatic (approximately 65% of episodes). However, AF can cause a range of symptoms including dizziness, palpitations, reduced exercise tolerance, shortness of breath, and other signs of heart failure (Kannel et al., 1998). Some people are unaware of their AF, whereas others are immediately aware of the change in their heart’s rhythm. It is unclear why some people experience symptoms while in AF and others do not. In many patients, the symptoms are related to a rapid ventricular response. If medications effectively slow the rate, the symptoms tend to disappear. Other patients continue to have symptoms, even if the heart rate is not fast. Occasionally, symptoms are due to a heart rate that is too slow. The patient perception of symptoms remains a variable of keen interest because perceived symptoms prompt patients to access medical care and the initiation of pharmacological, catheter-based, and/or surgical interventions. Patients complaining of symptoms may be more likely to seek and receive treatment, and therefore, the interrelationship between the physical and psychological experience in this population is clear. The diagnosis of AF can occur during routine exams by checking pulse or listening to the heart with a stethoscope. Usually, if there is suspicion of arrhythmia, an electrocardiogram (ECG or EKG) is used detect and confirm the presence of AF. Skin electrodes record the electrical activity of the heart. If there is suspicion of AF, and ECG does not detect arrhythmia during examination, a portable ECG monitor, or Holter monitor, can record events of the heart over a longer time (Table 4.1).
Medical Interventions As mentioned in the introduction, AF management can vary greatly due to factors such as age, comorbidities, and AF severity (i.e. type of AF or symptoms). Clinicians have routinely guided their therapy based on symptom severity. However, as mentioned above, approximately 65% of AF episodes do not produce perceptible symptoms.
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Table 4.1 Biopsychosocial management of atrial fibrillation – quick reference AF category Key terms Definitions/examples Etiology Cardiac For example, coronary heart disease Noncardiac For example, alcohol use Subtypes Paroxysmal Spontaneous termination within 7 days Persistent Episodes lasting more than 7 days, requires cardioversion and/or antiarrhythmic drugs to restore sinus rhythm Long-standing persistent Episode duration for more than 1 year Symptom presentation Symptomatic Patient experiences physical symptoms Asymptomatic Patient unaware of atrial arrhythmia Electrical disease Lone Structurally normal heart Concomitant Associated with structural heart disease Diagnosis Checking pulse General physical exam Stethoscope General physical exam EKG or ECG Electrode-based detection of arrhythmia Holter monitor Portable EKG often for home monitoring Interventions Anticoagulation Prevents potential stroke Heart rate control Prevents elevated heart rates Heart rhythm control Restores sinus rhythm Electrical cardioversion Restores sinus rhythm Catheter ablation Isolation of arrhythmogenic pathways Medications Beta-blockers Block norepinephrine and epinephrine; HTN Calcium channel blockers Decrease rate of aberrant pacemaker firing; HTN Warfarin Thins blood; reduces risk of clotting/stroke Amiodarone Antiarrhythmic for tachyarrhythmias Dronedarone Antiarrhythmic specific to AF Tikosyn Maintenance of, and conversion to, normal sinus rhythm Sotalol Dual action, potassium channel blocker and beta-blocker Lifestyle adjustments Medication management Taking exactly as directed Diet Avoid alcohol, caffeine, etc., as directed Exercise and activity More is better, unless directed otherwise Psychosocial factors Anxiety Antecedent or consequence of AF Depression Antecedent or consequence of AF Anger/hostility Can trigger arrhythmias Personality More likely to experience negative affect Behavioral medicine Clinical interviewing Assess AF knowledge, AF symptoms, and distress Psychoeducation Relationship of disease, distress, thoughts, and behavior Stress management PMR; diaphragmatic breathing; imagery Cognitive restructuring Reframing; thought records Problem solving Nonjudgmental brainstorming to solution Relapse prevention Understanding and coping with triggers for distress
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Table 4.2 CHADS2 criteria C H A D S2
Risk factors Congestive heart failure Hypertension history Age ³ 75 years Diabetes mellitus history Stroke symptoms or TIA
49 Points 1 1 1 1 2
AF type could also be misleading as the sole indication for treatment. For example, the risk of stroke was not different in patients with paroxysmal versus persistent or long-standing persistent AF (Hohnloser et al., 2007). Therefore, most medical practitioners utilize risk assessment scores in order to guide their management for stroke prevention in patients with AF. One of the most important treatment strategies in stroke prevention is anticoagulation. AF increases the risk of blood clots in the atria since blood does not flow normally during arrhythmia. During atrial fibrillation, blood is not effectively ejected into the ventricles, and some of the blood may become stagnant and begin to clot. The left atrial appendage appears to be the most likely site for blood clots to form in patients with AF. These blood clots could break loose and travel to the brain causing a stroke. The specific risk of stroke increases as patients get older, and the risk of stroke in patients over 80 years old is approximately 25%. The CHADS2 score is the most commonly used tool to assess the risk of stroke in patients with AF in order to determine the need for anticoagulation. Table 4.2 describes the CHADS2 scoring system. If a patient has a CHADS2 score ³ 2, then warfarin anticoagulation is recommended regardless of AF symptoms or AF type. Besides stroke prevention, the medical management of AF patients includes rate control or rhythm control. Rate control refers to the strategy of using medications such as beta-blockers, calcium channel blockers, and digitalis, among others, to help slow conduction of electrical impulses over the AV node to maintain the ventricular response around 80 beats per minute at rest. This strategy reduces ventricular response in order to decrease symptoms (e.g. palpitations) and to potentially prevent tachycardia-induced cardiomyopathy. Heart rhythm control refers to the strategy of sinus rhythm or “normal heartbeat” restoration. Restoration of a normal heartbeat is often attempted for those individuals with more symptomatic AF who have failed rate control strategies. Medications called antiarrhythmic drugs (e.g. sotalol, tikosyn, propafenone, amiodarone, dronedarone) are used to stabilize the electrical activity in the atria in an attempt to restore sinus rhythm. If AF is persistent and does not stop by itself, electrical cardioversion can be performed to restore the normal rhythm. Electrical cardioversion is a procedure whereby a brief electrical current (shock) is delivered through the chest wall to the heart in order to interrupt the abnormal electrical circuit(s) in the heart to restore the normal sinus rhythm. Although cardioversion works immediately, it does not prevent the AF from recurring; medications, ablation, and surgery are potential treatments to try to prevent AF from recurring.
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The most extreme form of ventricular rate control is AV node ablation. Using catheters with small electrodes able to deliver radiofrequency energy, the AV is ablated and thus unable to conduct electrical impulses from the atrial chambers. Therefore, these patients will require a permanent pacemaker in order to maintain adequate ventricular rhythm. The patients remain in AF and have the same risk of thromboembolic events. More invasive therapies to restore sinus rhythm in patients with AF are based on the Cox-MAZE cut and sew surgical procedure. Dr. James Cox developed this procedure, which by making strategically placed incisions in both right and left atria resulted in the interruption of the macroreentrant circuits responsible for AF (Cox et al., 1991; Cox, 2004). This procedure became the “gold standard” for sinus rhythm restoration in patients with AF. However, it was not widely adopted because it was thought to be too complex and associated with a high morbidity rate. Technological advances have allowed for use of different energy sources (e.g. radiofrequency, cryoablation, laser, high-frequency ultrasound) to create linear lesions mimicking the Cox-MAZE III lesion set. Using these energy sources, physicians can use percutaneous (i.e. catheter-based) or surgical techniques to perform the MAZE procedure. Using current catheter techniques, electrophysiologists are able to create most of the atrial lesions described by Dr. Cox. The difficulty with being able to create all lesions described in the Cox-MAZE procedure with the current catheter ablation technology has been blamed to be the cause for the rates of sinus rhythm restoration being less than those described in Dr. Cox’s series. The success rates of catheter ablation depend on the type of AF. They are better for paroxysmal patients with short histories of AF and not severely enlarged left atria. Surgical ablation techniques allow the surgeon to completely reproduce the CoxMAZE III lesion set (Gaynor et al., 2004). The surgical procedures that reproduce the entire lesion set as described by Dr. Cox are associated with the best rates of sinus rhythm restoration. Some centers have attempted to use less invasive surgical techniques to recreate some of the lesions; however, their results have been similar to those of catheter ablation. Some surgical teams reproduce the entire lesion set using minimally invasive or robotic-assisted techniques via a right mini thoracotomy using cryoablation (e.g. East Carolina Heart Institute). Diet, medication management, and physical activity are each important aspects of disease self-management for AF. Physicians and other medical providers will develop particular regimens for these important areas. For example, patients who take warfarin may need to monitor intake of foods high in vitamin K, which is used by the liver to prevent excessive bleeding. Given the cooccurrence of hypertension and hyperlipidemia with AF, physicians often recommend limiting the use of sodium and fat. Physicians also recommend limiting alcohol, caffeine, and nicotine given their potentially arrhythmia-inducing effects. Patients who adhere to medication regimens are less likely to experience the negative effects of AF (McCabe, 2008). Regular physical activity is another important area for adherence, and medical providers can help develop patient-specific regimens. Cardiovascular rehabilitation is a proven way for patients to improve health via physical activity in a structured format.
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The Patient Experience The challenges seen in the patient experience of atrial fibrillation (AF) roughly estimate the level of medical severity and a patient’s ability to cope with their disease (Sears et al., 2005). Symptoms of AF overlap and are sometimes indistinguishable from the physiological response to anxiety, anger, and depression. For example, transtelephonic monitoring showed 69% of symptomatic calls were associated with AF recording, and 31% of calls demonstrated normal sinus rhythm (Bhandari et al., 1992). This data suggests that 31% of calls were complaints of anxiety or hypervigilance to possible or perceived symptoms of AF that were not objectively verified. Palpitations, which may be evidence of either AF or psychological distress, have been shown to be the only symptom that occurred with greater frequency during AF versus sinus rhythm (67% vs. 24%) but were still not a perfect distinguishing factor by any means (Gerstenfeld et al., 1999). Patients with AF can present with various symptoms that overlap psychological distress and AF symptoms. The research remains unclear as to exactly how psychological distress plays a role in (1) the etiology, (2) how it coincides, and (3) how it may exacerbate AF. We are also unsure as to whether the (4) development of AF can lead to anxiety or other forms of psychological distress. These are all interesting questions in need of further exploration. The following reviews attempt to address these questions with the limited available literature. Psychological factors clearly intertwine in the patient experience of AF. Recent research demonstrates how arrhythmias can be both antecedent to and consequence of psychological and emotional factors (i.e. Lampert, 2010), and an in-depth review of psychological distress (anxiety, depression, anger) in AF patients is available (McCabe, 2010). Evidence of a relationship between anxiety and AF was shown in 240 intermittent AF patients (Suzuki & Kasanuki, 2004), where nearly 29.5% of AF patients experienced panic with or without agoraphobia. Anxiety greatly affected both quality of life and AF, and interestingly, the presence of anxiety made AF symptoms worsen. As reported in McCabe’s, 2010 excellent review, anxiety is particularly interesting because symptoms can increase adrenaline function, which can initiate and perpetuate AF in at-risk patients. AF can initiate anxiety if patients perceive risk, and AF can perpetuate anxiety if patients fear future AF episodes. Patients can also confuse symptoms of AF and anxiety because many symptoms can be strikingly similar (see Table 4.3).
Psychological Factors and Patient Perception of AF Symptoms Psychological factors increase an unhealthy awareness of AF symptoms. Individuals who experience AF symptoms (1) that readily notice symptoms (2) and are concerned about symptoms may result in symptoms that are more poignant and perceived as
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Table 4.3 Symptom overlap and differentiation – AF and anxiety AF symptoms Anxiety symptoms Shared symptoms • Palpitations • Palpitations • Irregular heartbeat • Pounding heart • Chest pain • Accelerated heart rate • Chest discomfort • Chest pain • Difficulty breathing • Chest discomfort • Shortness of breath • Sensations of shortness of breath • Dizziness • Sensation of smothering • Lightheadedness • Feeling dizzy • Fatigue • Feeling lightheaded • Weakness • Feeling unsteady • Feeling faint • Being easily fatigued Unique symptoms • Heart failure • Chills or hot flashes • Dizziness while exercising • Sweating • Shortness of breath while exercising • Trembling or shaking • Pain while exercising • Feeling of choking • Nausea or abdominal distress • Feelings of unreality • Fear of losing control • Fear of dying • Numbness or tingling sensations • Restlessness; keyed up; on edge • Difficulty concentrating • Irritability • Muscle tension • Sleep disturbances
less tolerable. Research among patients who experience similar sets of AF symptoms demonstrated that patients endorsed high variations in report of anxiety (Ong et al., 2006). A propensity for anxiety may lead to greater distress related to AF symptoms. This study suggests that psychological features may predict outcomes as symptom attention predicted worse mental and physical QOL. An interesting note is that optimism predicted better mental QOL, but not physical QOL. Internal health locus of control (looking toward self as primarily responsible to one’s health) was also demonstrated to have a moderating effect on the relationship between uncertainty and appraisal of danger among patients with atrial fibrillation (Kang, 2009). This evidence may indicate that a subset of patients experience vague symptoms as dangerous after the diagnosis of AF. These patients may also be more likely to seek treatment due to fear of symptoms. With patient perception being a key to the experience of patients with AF, it may be that those who have greater psychosocial distress are more likely to receive or request medical treatment such as catheter ablation therapy.
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Psychological Factors as an Antecedent to AF According to patient report, stress may be the most common trigger to the experience of AF. Hansson, Madsen-Hardig, and Olsson (2004) studied 100 intermittent AF patients to identify triggers associated with AF symptoms, and the report of stress was the most common trigger among 54% of patients, followed by physical exertion (42%), tiredness (41%), coffee (25%), and infections (22%) (Hansson et al., 2004). This data is important because patients themselves believe that stress is an important trigger, regardless of actual directionality. Nonetheless, recent analyses utilizing data from the Framingham Offspring Study demonstrated a predictive relation between anger/hostility in the development of AF in men. As for supraventricular arrhythmias, anger, hostility (Eaker, Sullivan, Kelly-Hayes, D’Agostino, & Benjamin, 2004), and tension (Eaker, Sullivan, Kelly-Hayes, D’Agostino, & Benjamin, 2005) were found to predict the 10-year occurrence of AF among males. Similarly, recent experience of acute stress was identified as an independent risk factor for the development of acute lone AF (Mattioli, Bonatti, Zennaro, Melotti, & Mattioli, 2008). Interestingly, patients that developed AF after an acute stress were more likely to have spontaneous conversion of arrhythmia. Depressed mood may also be a significant predictor of AF recurrence. Specifically, AF recurred in 85% of depressed versus 39% of patients who did not endorse depression (Lange & Herrmann-Lingen, 2007). The authors suggested results were indicative of depressed mood, increasing risk for recurrence of AF after electrical cardioversion. Specifically, depressive symptoms may bring about heightened adrenergic tone and a proinflammatory state that are possible mechanisms responsible for the observed association. However, directionality remains elusive as patients who experience AF recurrence and/or more provision of medical care may be more likely to experience symptoms of depression.
Psychological Factors as a Consequence of AF As many patients with AF become more anxious and vigilant to cardiac functioning, depression may result from a perceived lack of control over their health. In fact, depression symptoms are also common in AF. Thrall, Lip, Carroll, and Lane (2007) found in a sample of AF patients that 38% had depressive symptoms and 38% had anxiety symptoms (Thrall et al., 2007). At 6 months, there were no significant changes in symptoms. As has been seen in other cardiac populations, depression symptoms predicted QOL. Women had worse QOL, which insinuates a stronger reaction to AF symptoms among women. Patients who experience AF symptoms may eventually feel a loss of control over their illness, especially when considering the often unpredictable nature of AF. The diagnosis of AF in a cohort of 70 was associated with the onset of anxiety (Lane, Langman, Lip, & Nouwen, 2009), and interestingly, those who attributed anxiety symptoms to AF reported lower healthrelated quality of life.
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Research suggests that the perception of distress related to AF is related to psychological factors. Collectively, the clinical scenario of patient and treatment factors associated with AF indicate that the biopsychosocial model that addresses the dynamic interaction of biological, psychological, and social factors may have utility in explaining the antecedents and consequences of AF presentations. Cognitive and behavioral (CBT) interventions are clearly necessary for patients diagnosed with AF.
Cognitive and Behavioral Interventions In addition to the clear indication of CBT being effective in other cardiac populations (Sears et al., 2007), psychological interventions as a precursor to surgical intervention may be a cost-advantageous and risk-reducing strategy for a subset of patients. While behavioral research is extremely limited for patients experiencing AF, the following review utilizes empirical work from other cardiac disease states as well as clinical experience. Clinicians who use this chapter as a resource will have the tools to (1) discern etiology of comorbid psychological and AF symptoms, (2) provide education to patients who may confuse these symptoms, (3) treat psychological distress that exacerbates AF, and (4) provide behavioral intervention for distressed AF patients. While prevention of AF development through primary prevention strategies (e.g. smoking cessation) is ideal, the objective of this section is to provide a rationale for the importance of psychological intervention in patients diagnosed with AF. The triggers of AF are still being investigated, but the available data suggests that stress is a likely contributor, with approximately 54% of patients with intermittent AF citing psychological stress as the most common trigger (Hansson et al., 2004). However, stress is probably one of many factors to prompt AF. Like patients with other cardiac problems, patients with AF can benefit from understanding the role emotional distress plays in their ability to manage their illness. The following is a suggested protocol for managing distress associated with AF that warrants additional research investigation but can serve as a useful clinical heuristic.
Assessment Step 1: Assessment of AF knowledge and psychological factors • Does the patient have a history of psychological morbidity? • Is the patient’s AF symptomatic, and if so, what are the symptoms? • What symptoms are more associated with AF and what symptoms are more associated with distress?
Psychological distress in AF patients is complex, and we suggest screening during routine visits to health-care providers. If distress is noted, the patient should be
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referred for an intake to a licensed mental health provider. An AF specific quality of life measure exists (Badia, Arribas, Ormaetxe, Peinado, & de Los Terreros, 2007) that would be an appropriate tool to consider throughout treatment. The clinical interview is the opportunity to find out what a patient knows about AF, as well as how they feel AF affects their life. The clinician needs to gain insight into the patient’s perception of the threat of AF symptoms. This is important because AF symptom tolerance can vary dramatically between individuals. It is also important to understand the patient’s history of psychological distress and any significant stressors in their life. Understanding patterns of distress can helpfully tailor cognitive and behavioral treatment by identifying triggers for AF and associated distress. Psychoeducational considerations should be made after assessing patient understanding of both AF and psychological distress.
Psychoeducation Step 2: Education of AF and the relationship with distress • Explain how AF works, why symptoms are present, and the interaction between AF, emotion, social factors, and behavior • Explain that AF is not an immediately dangerous condition, but the ability to communicate symptoms can improve physician’s ability to provide medical treatment
Providing disease and psychological information is a key to providing care for AF patients, and when the provider can conceptualize and describe the specific interaction between the medical, psychological, social, and behavioral factors in AF, patients are on the way toward coping better with their disease. A patient with a proficient understanding of AF allows communication of needs, especially when interacting with health-care providers. The AF AWARE group conducted a study that highlights the need for improved education for AF patients (Aliot et al., 2010). Among 825 patients with AF and 810 cardiologists, this group surveyed perceptions, communicating information, and burden of AF. Physicians were more likely to worry about stroke and hospitalization than patients, while patient concerns were about potential mortality. Roughly 25% of patients were unable to effectively explain AF and 33% were anxious as a result of AF. Patients and physicians agreed of the negative effects that AF has on patient quality of life. Education is an important stress-reducing and quality of life–improving strategy, as patients gain greater insight into the interplay between psychological symptoms and the perception of symptoms of AF. Patients can feel a sense of empowerment once they understand their condition. As a mental health provider for AF patients, there is clear importance (e.g. building rapport, accurate cognitive reframing) in understanding the physiology of AF in terms of subtypes, causes, and arrhythmogenesis.
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Stress Management Step 3: Provide a tool kit for managing stress • When appropriate, encourage pleasurable activities that include physical activity and relaxation • Provide a rationale for why stress management is important for stress and AF • Demonstrate techniques and have patient practice in session • Be aware that some patients experience a paradoxical increase in anxiety • Emphasize continued practice during anxiety and when feeling calm
Feelings of depressed mood or anxiety can lead to feelings of lack of control of the management of AF. To break the cycle, a deliberate plan is needed in which the patient schedules pleasant events and has tools to help gain some control over thoughts and physiological reactivity to distress. Reducing autonomic arousal may limit the occurrence of AF. For example, clinical hypnosis has been effectively utilized in an inpatient sample (n = 50) to reduce AF after coronary artery bypass graft surgery (Novoa & Hammonds, 2008). Diaphragmatic breathing is often a first line of defense when combating anxiety and controlling autonomic arousal. When a patient is experiencing AF symptoms, they may begin to view the event as lifethreatening even though immediate harm is unlikely. While the effectiveness of diaphragmatic breathing has not been assessed in the AF population, the technique may reduce arousal and related distress. Theoretically, reducing sympathetic arousal through diaphragmatic breathing may even help prevent or terminate AF episodes. Progressive muscle relaxation (PMR) may also be useful as PMR can reduce tension and arousal by training patients to systemically tense and release muscle group with the idea that tension will swing like a pendulum and invoke relaxation. Many cardiac patients benefit from guided imagery, which serves as a distraction from arousal by replacing anxious thoughts with a mental setting of relaxation. The therapist initially acts as a guide to help patients focus on various sights, smells, sounds, tastes, and/or feeling, and eventually, patients use the strategy in natural settings.
Cognitive Restructuring Step 4: Challenging negative thoughts • Teach patient about common thought traps and automatic negative thoughts • Ask patient to describe their thoughts during AF • Help patient identify their negative thoughts and replace them with factual information about AF and heart disease • Teach patient thought stopping
Many AF patients believe that they are the only ones who are experiencing worry or anticipatory fear. However, most AF patients experience at least some periods of fear and depression. Merely discussing the facts about AF can help to rectify false beliefs and unrealistic cognitions (Sears, Shea, & Conti, 2005). Sometimes, the only
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medicine needed is knowledge. For many patients, thoughts about their condition continue to be exaggerated and inconsistent from the reality of their condition. When negative automatic thoughts are present, patients must actively confront these thoughts and try to replace them with cognitions that are more realistic. The education of step 2 can come back into play, and the mental health provider who is comfortable with the facts of AF can appropriately demonstrate and differentiate realistic and unrealistic thoughts.
Problem Solving Step 5: Application of problem solving • Discuss the differences between solvable and unsolvable problems • Encourage the patient to put it on paper: Identify problem, generate possible solutions, evaluate alternatives, decide on a plan, engage in plan, and evaluate outcome • Explain that AF is not an immediately dangerous condition, but the ability to communicate symptoms can improve physician’s ability to provide medical treatment
Patients who have an ability to systemically process their experiences as they relate to AF are more likely to seek help when necessary, feel confident in time of uncertainty, and make appropriate lifestyle changes when medical changes require them to do so. Patient will thrive if they know when to seek their physician versus seek ways to reduce their arousal. Problem solving can help patients gain an ability to manage roadblocks in medication management, social support, diet changes, physical activity, and sleep. As sleep difficulties are common in AF patients, this may be a great place to start the application of problem solving. In fact, studies have shown autonomic dysregulation may connect sleep apnea and AF. The body responds to apnea by increasing sympathetic tone to the peripheral vasculature and parasympathetic tone to the heart, resulting in a decrease in myocardial oxygen demand and thereby improving the chances for cardiac survival (Asirvatham & Kapa, 2009). Exploring sleep hygiene with the patient may serve as a foundation for problem solving, as it is a concrete example to begin utilizing this technique.
Relapse Prevention Step 6: Preventing reemergence of distress • The goal is to help make a formal plan to cope with future triggers of distress • Help the patient develop a stress management plan • Help the patient develop a medical plan for when they need to seek their physician or emergency services
Relapse prevention is typically considered for addiction treatment, but the idea of prevention is being utilized in to treat many forms of distress. Applying relapse prevention may be important for AF patients because symptoms can be confusing
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and going back to previous ways of functioning is natural. Patients who have a clear plan for managing distress and managing their disease are more likely to feel empowered and think clearly during a real emergency.
Conclusion This chapter presented a biopsychosocial model of AF as a guide for allied and mental health professionals who work with patients who have AF accompanied by psychological distress. AF remains one of the most common, most costly, and most burdensome cardiac conditions in medical practice. While behavioral research is ongoing and is lacking in interventional studies, we have sampled research from other disease states, where possible, to meet the unique needs of patients managing AF. This chapter serves as a rationale for screening and providing treatment for the psychological symptoms in patients with AF. We also hope to encourage researchers to continue to develop a better understanding of the AF/distress relationship and explore evidence based treatment options through randomized controlled trials.
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description of the electrophysiologic basis of atrial flutter and atrial fibrillation. The Journal of Thoracic and Cardiovascular Surgery, 101, 406–426. Eaker, E. D., Sullivan, L. M., Kelly-Hayes, M., D’Agostino, R. B., Sr., & Benjamin, E. J. (2004). Anger and hostility predict the development of atrial fibrillation in men in the Framingham Offspring Study. Circulation, 109, 1267–1271. Eaker, E. D., Sullivan, L. M., Kelly-Hayes, M., D’Agostino, R. B., Sr., & Benjamin, E. J. (2005). Tension and anxiety and the prediction of the 10-year incidence of coronary heart disease, atrial fibrillation, and total mortality: The Framingham Offspring Study. Psychosomatic Medicine, 67, 692–696. Fuster, V., Ryden, L. E., Cannom, D. S., Crijns, H. J., Curtis, A. B., Ellenbogen, K. A., et al. (2007). ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation–executive summary. Circulation, 114, e257–e354. Gaynor, S. L., Diodato, M. D., Prasad, S. M., Ishii, Y., Schuessler, R. B., Bailey, M. S., et al. (2004). A prospective, single-center clinical trial of a modified cox maze procedure with bipolar radiofrequency ablation. The Journal of Thoracic and Cardiovascular Surgery, 128, 535–542. Gerstenfeld, E. P., Hill, M. R., French, S. N., Mehra, R., Rofino, K., Vander Salm, T. J., et al. (1999). Evaluation of right atrial and biatrial temporary pacing for the prevention of atrial fibrillation after coronary artery bypass surgery. Journal of the American College of Cardiology, 33, 1981–1988. Hansson, A., Madsen-Hardig, B., & Olsson, S. B. (2004). Arrhythmia-provoking factors and symptoms at the onset of paroxysmal atrial fibrillation: A study based on interviews with 100 patients seeking hospital assistance. BMC Cardiovascular Disorders, 4, 13. Hohnloser, S. H., Pajitnev, D., Pogue, J., Healey, J. S., Pfeffer, M. A., Yusuf, S., et al. (2007). Incidence of stroke in paroxysmal versus sustained atrial fibrillation in patients taking oral anticoagulation or combined antiplatelet therapy: An ACTIVE W substudy. Journal of the American College of Cardiology, 50, 2156–2161. Kang, Y. (2009). Role of health locus of control between uncertainty and uncertainty appraisal among patients with atrial fibrillation. Western Journal of Nursing Research, 31, 187–200. Kannel, W. B., Abbott, R. D., Savage, D. D., & McNamara, P. M. (1982). Epidemiologic features of chronic atrial fibrillation: The framingham Study. The New England Journal of Medicine, 306, 1018–1022. Kannel, W. B., Wolf, P. A., Benjamin, E. J., & Levy, D. (1998). Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: Population-based estimates. The American Journal of Cardiology, 82, 2N–9N. Lampert, R. (2010). Anger and ventricular arrhythmias. Current Opinion in Cardiology, 25(1), 46–52. Lane, D. A., Langman, C. M., Lip, G. Y., & Nouwen, A. (2009). Illness perceptions, affective response, and health-related quality of life in patients with atrial fibrillation. Journal of Psychosomatic Research, 66, 203–210. Lange, H. W., & Herrmann-Lingen, C. (2007). Depressive symptoms predict recurrence of atrial fibrillation after cardioversion. Journal of Psychosomatic Research, 63, 509–513. Lee, W. C., Lamas, G. A., Balu, S., Spalding, J., Wang, Q., & Pashos, C. L. (2008). Direct treatment cost of atrial fibrillation in the elderly American population: A medicare perspective. Journal of Medical Economics, 11, 281–298. Lloyd-Jones, D., Adams, R., Carnethon, M., De Simone, G., Ferguson, T. B., Flegal, K., et al. (2009). Heart disease and stroke statistics–2009 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation, 119, 480–486. Mattioli, A. V., Bonatti, S., Zennaro, M., Melotti, R., & Mattioli, G. (2008). Effect of coffee consumption, lifestyle and acute life stress in the development of acute lone atrial fibrillation. Journal of Cardiovascular Medicine (Hagerstown, MD), 9, 794–798. McCabe, P. J. (2008). Self-management of atrial fibrillation: A new frontier for nursing research. Progress in Cardiovascular Nursing, 23, 37–40.
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McCabe, P. J. (2010). Psychological distress in patients diagnosed with atrial fibrillation: The state of the science. The Journal of Cardiovascular Nursing, 25(1), 40–51. Novoa, R., & Hammonds, T. (2008). Clinical hypnosis for reduction of atrial fibrillation after coronary artery bypass graft surgery. Cleveland Clinic Journal of Medicine, 75(Suppl 2), S44–S47. Ong, L., Cribbie, R., Harris, L., Dorian, P., Newman, D., Mangat, I., et al. (2006). Psychological correlates of quality of life in atrial fibrillation. Quality of Life Research, 15, 1323–1333. Sears, S. F., Serber, E. R., Alvarez, L. G., Schwartzman, D. S., Hoyt, R. H., & Ujhelyi, M. R. (2005). Understanding atrial symptom reports: Objective versus subjective predictors. Pacing and Clinical Electrophysiology: PACE, 28, 801–807. Sears, S. F., Jr., Shea, J. B., & Conti, J. B. (2005). Cardiology patient page. How to respond to an implantable cardioverter-defibrillator shock. Circulation, 111, e380–e382. Sears, S. F., Sowell, L. D., Kuhl, E. A., Kovacs, A. H., Serber, E. R., Handberg, E., et al. (2007). The ICD shock and stress management program: A randomized trial of psychosocial treatment to optimize quality of life in ICD patients. Pacing and Clinical Electrophysiology, 30, 858–864. Suzuki, S., & Kasanuki, H. (2004). The influences of psychosocial aspects and anxiety symptoms on quality of life of patients with arrhythmia: Investigation in paroxysmal atrial fibrillation. International Journal of Behavioral Medicine, 11, 104–109. Thrall, G., Lip, G. Y., Carroll, D., & Lane, D. (2007). Depression, anxiety, and quality of life in patients with atrial fibrillation. Chest, 132, 1259–1264. Wolf, P. A., Abbott, R. D., & Kannel, W. B. (1991). Atrial fibrillation as an independent risk factor for stroke: The Framingham Study. Stroke, 22, 983–988.
Chapter 5
Psychological Management of Patients with Heart Failure Jonathan Gallagher and Adam Grimaldi
Introduction Heart failure (HF) is a complicated clinical syndrome that is progressive in nature and restrictive of physical independence. This disease presents with an array of psychosocial challenges. Patients must adapt to a new way of living and learn to cope with HF and its clinical course, which is characterized by uncertainty. Adjustment to this condition is very difficult for many patients, and as a result, professional intervention is often indicated. A significant proportion of patients with HF suffer from depression and anxiety as they grapple with a life-changing diagnosis. From the perspective of the medical team, such comorbidities can lead to worsened clinical outcomes and poorer quality of life in patients with HF, but too often these conditions are overlooked and patients remain untreated. The present chapter will present some key pathophysiology and the epidemiology of HF and review what is currently known about the psychosocial experience of patients with this condition. The clinical implications of addressing the psychological needs in this population – for achieving improvements in quality of life and overall improved patient outcome – will also be discussed.
J. Gallagher, MPsychSc (*) Department of Psychology, Beaumont Hospital, Beaumont, Dublin 9, Ireland e-mail:
[email protected] A. Grimaldi, M.D. Candidate University of Connecticut School of Medicine, John Dempsey Hospital, 263 Farmington Avenue, Farmington, CT 06030, USA E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_5, © Springer Science+Business Media, LLC 2012
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Background of Heart Failure In order to appreciate the challenges faced by the heart failure patient and the underlying pathophysiology of this disease, one must first understand the basics of the heart as a muscular pump. The cardiovascular system is arranged such that blood is pumped from high to low pressures. The heart is the organ which ensures this circulation of blood to the many different areas of the body. It performs this duty by functioning as a pump whereby the heart fills with blood at low pressure during diastole and then contracts, generating high pressure, to eject blood during systole. The heart is furthermore divided into right and left sides. The right ventricle accepts deoxygenated blood from systemic venous return and pumps this blood through the low resistance of the pulmonary vasculature. The left ventricle of the heart receives oxygenated blood from pulmonary venous return and pumps this blood out into systemic circulation against relatively higher resistance. When gauging the overall performance of the heart hemodynamically, cardiologists analyze stroke volume (SV) (the volume of blood ejected in a beat to beat basis from the heart), cardiac output (CO) (the volume of blood ejected from the heart in 1 min), and ejection fraction (EF) (the fraction of blood at the end of diastole that is ejected during each contraction of the heart). The latter, EF, is the most informative to cardiologists in evaluation of the heart’s efficiency in pumping blood. A normal EF is between 50% and 70% (Veronique, 2010). Disruptions in the normal physiology of the heart as a muscular pump can result in inadequate perfusion of body tissues as well as buildup of metabolic waste products. HF results when the heart is damaged or overworked and can no longer pump efficiently. Consequently, it is unable to supply adequate blood to meet the metabolic demands of the body (Lilly, 2007; Piano, Bondmass, & Schwertz, 1998). In 2005, the American Heart Association (AHA) defined HF as “a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood” (Hunt, 2005). This broad definition illustrates the extensive pathophysiology underlying HF. This inability of the heart to pump blood can be isolated to either the right or left ventricle or can even be a failure of both. When the left ventricle is affected, blood entering systemic circulation is reduced, and thus a reduction in SV, CO, and EF is observed. This can lead to congestion of blood in the pulmonary vasculature and over time can eventually impact the right side of the heart. When the right ventricle fails, this leads to congestion of systemic veins. The AHA goes on to emphasize that a diagnosis of HF is also reliant on patient history and physical examination (Hunt, 2005). As diagnosis of HF weighs heavily upon physical examination data and patient report, understanding the clinical manifestations of this syndrome is crucial. So important are symptoms and physical examination findings that they are used to stratify HF patients into different classes of disease severity. The New York Heart Association (NYHA) classification is based on the relationship between physical exertion and HF symptoms. Patients are categorized into one of four classes (classes I–IV) according to how limited their physical activity is by their disease (Vader &
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Drazner, 2009). Dyspnea is the most common symptom experienced by patients with HF, with other common signs associated with this condition being fatigue and swelling (edema), and an inability to lie down (orthopnea) (Barnes et al., 2006). Additional symptoms of HF recognized by other studies include chest pain, memory loss, sleeplessness, and palpitations (Barnes et al., 2006). Depending on disease severity, each patient with HF will present with one or a combination of these symptoms. Studies investigating the symptomatology of HF have determined that approximately 90% of patients will report some degree of dyspnea, with this shortness of breath frequently being so severe in later stages of the disease that up to half of HF patients will experience these symptoms at rest (Vader & Drazner, 2009). With respect to physical examination data, the most useful aid to bedside diagnosis of HF is jugular venous pressure (JVP) measurement (Vader & Drazner, 2009). In a study of 1,000 patients with chronic HF, JVP was able to identify elevated left ventricular filling pressures in 80% of patients (Drazner et al., 1999), strongly attesting to the clinical utility of simple physical examination techniques for accurately diagnosing HF. Other physical exam findings include peripheral edema (estimated to occur in two-thirds of HF patients) and the patient’s extremities being cool to the touch (Vader & Drazner, 2009). Depending on disease severity, physical exam findings will vary from patient to patient, and identifying an individual with HF can be as challenging for the clinician as it is frustrating for the undiagnosed patient. HF can occur as a result of any form of heart disease. It may be due to poorly controlled hypertension, an MI, valvular disease, a virus, prolonged alcohol abuse, or even kidney disease. In some cases, the cause is undetermined (idiopathic HF). The condition may develop suddenly following an acute event, or it may come about slowly, over a period of weeks or months. Sometimes, the patient may have a history of angina, medical management, revascularization, repeat heart attacks, and then progress to HF. HF can be due to systolic dysfunction (abnormal emptying of the ventricle) and/ or diastolic dysfunction (abnormal relaxation or filling of the ventricle) (Lindenfield, 2010). Approximately two-thirds of patients with HF are affected by systolic dysfunction, with the remaining third suffering from diastolic dysfunction (Chatterjee & Massie, 2007). As a progressive condition, HF frequently begins with stress or injury to the heart which ultimately sets in motion cellular changes resulting in dilation or hypertrophy of the ventricle, or both. Some of the major pathophysiologic processes that cause HF are loss of cardiac muscle, pressure overload, volume overload, and restrictive filling of the ventricle (Parmley, 1985). Of these, the most common cause of HF is coronary artery disease (CAD), whereby an acute ischemic event to the myocardium results in loss of contractile tissue (Francis, 2001). As indicated earlier, this ischemic event results in cellular changes which progress to HF. Following an acute myocardial infarction, interstitial fibrosis develops as diseased myocardium becomes replaced with noncontractile tissue; later, the ventricle becomes hypertrophic as the heart attempts to compensate for the loss of contractile tissue (Francis, 2001). This compensatory response is initially beneficial as cardiac output is maintained, but these changes ultimately weaken the heart muscle further. There is now a strain placed on the myocardium; more tissue begins to deteriorate
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and die, thus resulting in the clinical manifestation of HF (Simmonds, Franklin, & Birch, 2006). If treated effectively, this deterioration can be slowed down, but the precise mechanism of how ventricular remodeling occurs in HF patients is as yet unclear and the subject of ongoing research. Patients with viral infections or valvular-based HF are typically young adults who are shocked to discover that they have acquired a debilitating condition, expected to deteriorate and reduce their life expectancy. However, it is the aging cardiovascular system which has become established as a major contributing factor in HF (Thomas & Michael, 2007), with more than three-quarters of patients with HF aged over 65 (Forman et al., 2009). Specific age-related changes of the aging cardiovascular system that contribute to HF include increased systemic vascular resistance (caused by increased connective tissue deposition in arteries) and impaired endothelial function resulting in reduced dilatory response of coronary arteries (Thomas & Michael, 2007). Together, these age-related processes contribute to the findings that the incidence of HF increases with age and remains predominantly a condition of the elderly. It has been estimated that the incidence of HF in people aged 65 or greater is 10 per 1,000 (Cheng & Nayar, 2009). Treatment of HF is focused on symptom management, improving quality of life, slowing down the progression of disease, and facilitating patient self-management (e.g., diet and fluid restrictions, tailored physical activity) (Lindenfield, 2010). While the multifaceted treatment plan may achieve its objectives, implementation can be difficult for the patient to sustain, and failure to do so can result in symptom exacerbation and rehospitalization (Lindenfield, 2010).
Epidemiologic Data and Patient Outcomes Clearly, HF remains a condition common to an aging population. In the United States, life expectancy has increased such that the number of people 65 and older will increase in the coming years. Estimates suggest that over the next 25 years, the population of elderly (aged ³ 65) will double to 70 million (Thomas & Michael, 2007). Additionally, as therapies have improved for related cardiovascular diseases such as hypertension and myocardial infarction, the proportion of patients surviving from these conditions has increased. Consequently, an increasingly aging population, in combination with improved mortality rates from other related conditions, has ensured that the number of HF cases in the United States is expected to increase dramatically. There are approximately 5.7 million patients with HF in the United States, with the number of new cases diagnosed per year contributing a further 550,000 patients to this growing population (Cheng & Nayar, 2009). As HF currently remains the most frequent cause of hospitalization in people 65 years and older (Veronique, 2010), it is anticipated that HF will continue to pose a large resource and financial burden to the medical system. Recent projections in 2009 for both the direct and indirect care costs of HF in the United States were estimated at $37.2 billion (Cheng
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& Nayar, 2009). An average hospital stay for HF patients lasts 7–10 days and can exceed $10,000 (Stull, Starling, Hass, & Young, 1999). With current data indicating an increase in this population, HF will clearly strain the United States health-care system for the foreseeable future. In addition to HF being a growing epidemic, this chronic condition has a poor prognosis. After initial diagnosis, it is estimated that only 50% of these patients will survive after 5 years and only 10% of patients survive 10 years (Veronique, 2010). Compared to the general population, the risk of sudden death in HF patients is fivefold greater (Mosterd et al., 2001), and outcome studies indicate better survival rates for women than men, with median survival following diagnosis being 3.2 years longer for women (Stromber-Stromberg & Martensson, 2003). The poor expected outcome following diagnosis can contribute greatly to the psychological impact of HF on patients.
Depression in the Patient with HF Dealing with a physically debilitating disease, with an uncertain prognosis, together with a complex medical regimen can all contribute to a potentially depressing reality for the patient with HF. While depression is indeed very common in HF, it is important to note that the majority of patients with HF do not present with major depression, despite their challenging circumstances. The prevalence of depression in patients with HF can depend on a number of factors including age, severity of illness, method of assessment (questionnaire self-report versus clinical interview), and even the time point at which it is assessed. What is not in doubt is that the trajectory of illness in HF lends itself to depressed mood, and depression and HF seem to operate synergistically to bring about both poorer medical outcomes and reduced quality of life in patients with HF. Studies investigating the incidence of major depression in HF patients have found that approximately one-third of patients suffer from depression (Freedland et al., 2003; Rutledge, Reis, Linke, Greenberg, & Mills, 2006; Dekker, Peden, Lennie, Schooler, & Moser, 2009), with up to 40% of depressed HF patients remaining depressed 1 year later (Dekker et al., 2009). With regard to symptom severity in HF, several studies have a found a direct relationship between a patient’s depressive symptoms and HF stage (Freedland et al., 2003; Rutledge et al., 2006; Azevendo et al., 2008), indicating that as the patient continues to deteriorate, depressive symptoms are more prevalent during advanced stages of the disease. A recent meta-analysis indicated that the prevalence of depression was twice as high among the most severely ill patients with HF (Rutledge et al., 2006), while other investigators have observed that as many as two-thirds of patients under 60 in class NHYA-IV present with major depression (Freedland et al., 2003). The course of depression in this population is by no means certain, however, and symptoms of depression can fluctuate in terms of their timing and severity. While Koenig (2006) reported that half of depressed HF patients at baseline had remitted within 6 months, conversely, Havranek, Spertus, Masoudi, Jones, and Rumsfeld
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(2004) observed that 21% of patients without depression at baseline had developed significant symptoms a year later. Such findings underline the importance of screening for depression in HF at multiple time points. Further studies have examined the role that depression plays in the prognosis of the patients with HF. In a prospective study with 165 patients with HF, Song, Lennie, and Moser (2009) demonstrated that moderate and severely depressed HF patients had a higher incidence and rate of rehospitalization, while Sherwood, Blumenthal, Hinderliter et al., (2011) showed that worsening of depressive symptoms was associated with adverse clinical outcomes compared to those whose symptoms remained stable for the preceding year. Depressive symptoms would also appear to be the most significant predictor of quality of life in patients with HF. HF-ACTION, a large-scale study of 2,322 HF patients, found a strong association between depression and reduced quality of life (Gottlieb et al., 2009). Furthermore, in a study of 206 HF patients, Faller et al., (2009) demonstrated that while HF on its own only affected the physical domain, depression influenced both the mental and physical components of quality of life. While depression is related to clinical severity in HF, its impact on adverse clinical outcomes remains when HF disease biomarkers such as BNP, LVEF, and other established risk factors are controlled for (Sherwood et al., 2007; Jiang et al., 2007; Pelle, Gidron, Szabó, & Denollet, 2008; Sherwood, Blumenthal, Hinderliter et al., 2011). Depressed patients with HF are less adherent with medical treatment (Pelle et al., 2008) and less likely to engage in exercise (Van der Wal et al., 2006) when compared to their nondepressed counterparts, and also less likely to consult their health-care provider when experiencing heart failure symptoms, frequently delaying to the point that they require rehospitalization (Song et al., 2009; Pelle et al., 2008). From both a medical and psychosocial standpoint, depression clearly plays an important role in the quality of life and clinical outcomes of HF patients. Therefore, assessment of depression should be routinely considered in all patients with heart failure, in addition to monitoring of these symptoms over time. It is important to be mindful too that certain symptoms in HF are likely to mimic those of depression such as fatigue and lassitude. Given that the safety of antidepressant drugs in patients with CHF has yet to be established, potential risks and benefits of antidepressant therapy need to be carefully considered by physicians, making the referral to a mental health professional in this context all the more important.
Anxiety in HF While depression has been extensively addressed and is an accepted concomitant of HF, fewer studies have investigated the impact of anxiety on health outcomes in patients with HF, despite the fact that it appears to be more prevalent in this patient group. Anxiety ultimately reflects a patient’s inability to predict or control personally salient outcomes (Konstam, Moser, & De Jong, 2005), and given that HF is a
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life-threatening chronic condition characterized by prognostic uncertainty – at least half of patients die suddenly due to arrhythmia or an infection – it would seem an understandable reaction to such circumstances. While the extant research is limited, the prevalence of anxiety in patients with HF can reportedly be as high as 63% (Haworth et al., 2005; Friedmann et al., 2006; De Jong et al., 2004). Pattenden, Roberts, and Lewin (2007) reported that some patients were anxious for several weeks after an acute episode, and as many as a third of patients with HF have elevated levels of anxiety 12 months after being diagnosed (Artinian, 2003). Furthermore, in the EuroHeart Failure survey, almost twothirds of patients reported difficulty falling asleep and lack of restorative sleep in the previous week, and a further third reported being woken by nocturnal dyspnea (Lainscak & Keber, 2003). Anticipating an exacerbating event during sleep such as nocturnal dyspnea, or indeed thoughts of not waking, may well contribute to persistent insomnia in this patient group. Anxiety has also been linked to higher mortality (Friedmann et al., 2006; Jiang et al., 2004), although a clear association between anxiety in HF patients and rehospitalization rates, similar to that seen in depression, has yet to be established (Konstam et al., 2005; Tsuchihashi-Makaya, Kato, Chishaki, Takeshita, & Tsutsui, 2009). In reality, anxiety and depression are frequently linked in heart failure, with anxious reactions to dyspnea, for example, found to be more common in depressed patients (Freedland & Carney, 2000). However, there is some evidence that both depression and anxiety, as well as their respective increases over time, independently predict the decline in physical health functioning among HF patients (Shen et al., 2011). Mixed results, however, have been observed with respect to the relationship between anxiety and adherence in patients with a chronic illness. A meta-analysis examining the relationship between anxiety and adherence found no correlation between these two factors, leading the authors to conclude that anxiety in some patients may actually enhance treatment adherence due to patient fears of worsening outcomes, while it may also decrease adherence given its established co-occurrence with depression in half of chronically ill patients (DiMatteo, Lepper, & Croghan, 2000). Additional prospective research would further enable the teasing apart of key interrelationships between anxiety and health outcomes in patients with HF. As issues of sudden death and managing uncertainty are salient for all patients with HF, ongoing support and the opportunity to discuss these and related issues should be available to patients with HF throughout the individual course of their illness. Other interventions that have been employed to good effect in managing anxiety in this patient group include breathing retraining, progressive muscular relaxation, and sleep hygiene with cognitive restructuring. Where phobic avoidance of individually recommended physical activity is an issue, liaising with a HF exercise rehabilitation program can be particularly effective. Symptoms of anxiety typically abate when the patient is helped to realize that their condition is very controllable, and that rather than facing a death sentence, they can help slow down its progression, avoid exacerbations, and maintain a good quality of life.
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Cognitive Functioning in HF While research in the area is not well developed, cognitive impairment, in part due to the effects of hypoxia (Dai et al., 2008), is relatively widespread in patients with HF (Almeida & Flicker, 2001), with up to 80% of people with severe heart failure displaying deficits in memory, attention, and learning abilities (Schall, Petrucci, Brozena, Cavarocchi, & Jessup, 1989; Cacciatore et al., 1998; Zuccalà et al., 2001; Riegel et al., 2002). These skills are deemed crucial for day-to-day functioning such as self-care and particularly in the management of a complex chronic illness such as heart failure. Cognitive deficits can represent a significant barrier to communication with health-care providers, and self-management of one’s condition is likely to be impeded if a patient’s memory is impaired, they have difficulty sustaining attention, or are unable to make decisions as quickly as before. All these skills are called into play when one is managing a condition such as HF, and even a mild cognitive impairment may affect a HF patient’s ability to remember to take their medication. In cases where depression is present in addition to HF itself, this can further compound the effect on cognitive functioning and adversely impact treatment adherence. Patients with HF displaying such cognitive deficits should be considered for referral for formal neuropsychological testing, as early identification of such difficulties will provide insight into the capacity of HF patients to implement treatment plans consistently and flexibly, as well as highlight areas in which they require support. A comprehensive neuropsychological profile of the patient may be necessary to develop individualized educational and self-management interventions (Wolfe, Worrall-Carter, Foister, Keks, & Howe, 2006). At the very least, one must be mindful of cognitive ability when sharing health-related information and tailor how this information is imparted accordingly. Frequently, intervention is targeted both to and through the primary caregiver or spouse, whether in relation to ongoing support for a partner, or advice with regard to behavioral aspects of treatment plan implementation. Again, referral to a tailored cardiac rehabilitation program as appropriate can be helpful with improvements in some cognitive domains reported in patients with HF completing an exercise training program (Tanne et al., 2005).
Mind–Body Pathways: Psychobiological Links in HF Pathophysiology Other than the established route between distress in HF patients and outcomes, recent research has focused on the impact of psychological distress in this patient population on the body at a cellular level. Several biological mechanisms have been proposed to link depression with disease progression in the patient with chronic heart disease. Two explanatory models which have gained particular attention are those concerning either neurohormonal imbalance or inflammatory activation changes observed common to both depressed individuals and patients with HF (Pelle et al., 2008).
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The Neurohormonal Activation Model Both HF and depression have been associated with abnormal nervous system activation in isolated cases (Joynt, Whellan, & O’connor, 2004). HF is frequently the result of an initial insult to the heart muscle setting in motion certain maladaptive processes (Francis, 2001), including the release of catecholamines via the sympathetic nervous system. This process is known to be a contributing biologic factor in the progression of HF, and levels of catecholamines such as norepinephrine are found to be elevated in patients with HF (Joynt et al., 2004). This catecholamine cardiotoxicity has been well established in the pathophysiology of HF by causing further ischemia of myocardium (Triposkiadis et al., 2009). Depression is also associated with sympathetic nervous system hyperactivity, and plasma norepinephrine levels have been found to be elevated in clinically depressed individuals (Joynt et al., 2004). These similar neurohormonal changes observed in both depressed patients and patients with HF suggest one possible biological explanation linking depression in HF patients to poorer outcomes.
The Inflammatory Activation Model In addition to abnormal neurohormonal activation, elevated inflammatory markers are also common to both patients with HF and those suffering with depression. In HF, destruction of myocardium results in localized upregulation of inflammatory markers involved in immune cell recruitment (Redwine et al., 2009). As the heart muscle becomes damaged, this immune cell recruitment forms part of the maladaptive process involved in the remodeling of the ventricles seen in the development of HF (Redwine et al., 2009), and similarly elevated inflammatory markers have also been identified in patients with major depression (Miller, Maletic, & Raison, 2009). With a view to investigating the relationship between depression and HF with respect to inflammation, one study with HF patients observed that those diagnosed with depression had increased inflammatory mediators such as tumor necrosis factor alpha (TNF-a) when compared to HF patients without diagnosed depression, suggesting that depression, via its impact on inflammatory markers, may play a role in advancing the pathophysiology of HF (Redwine et al., 2009). While many studies have observed an increase in inflammation in both depressed patients and HF patients, future research investigating this relationship specifically among depressed HF patients would allow the link to be elucidated further.
Depression as a Risk Factor for Development of HF? While the relationship between depression and poorer outcomes in patients with HF has been addressed to some extent, few studies have looked at depression as a risk factor for developing HF. Many researchers have proposed a causal link between
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depression and the subsequent development of HF, but few studies have actually tested this hypothesis. One large-scale study conducted with over 13,000 patients with coronary artery disease (CAD) but without diagnosed HF found that the incidence of developing HF in nondepressed CAD patients was 3.6 per 100 compared to 16.4 per 100 in depressed CAD patients (May et al., 2009). While CAD is known to progress to HF in its own right, the findings from this large-scale study suggest that depression may be a significant contributing factor to the development of HF. For now, risk factors such as CAD, smoking, hypertension, obesity, diabetes, and valvular heart disease remain the key conditions considered to be causative of HF (May et al., 2009). Further research into this phenomenon, however, may result in depression making this list of factors deemed to increase one’s chances for developing HF later in life.
Behavioral Pathways: Adherence in Patients with HF and Factors Influencing Self-Management Notwithstanding the many medical advances enabling the effective treatment of HF, a crucial requirement to living well with HF is for the patient to actively engage in the management of their illness. Dealing with the ongoing demands of a HF requires adjustments to daily lifestyle and the learning of new skills. Self-management in HF comprises not only of medication adherence and symptom monitoring but also extends to dietary and weight management, smoking cessation, alcohol reduction, and management of emotions. However, as with the general population, healthful behavior in patients with HF is not the norm. Complete adherence to medical and behavioral recommendations is a rarity, with most patients nonadherent to some degree. Nonadherence in patients with HF has been estimated to be as high as 60% for HF medications and up to 80% for lifestyle recommendations (Van der Wal & Jaarsma, 2008). Selective adherence is common, with the lowest levels of self-management observed in daily weighing (Holst et al., 2007; Ni et al., 1999) and fluid restriction (Holst et al., 2007; Stromberg et al., 2003). This is particularly serious given that nonadherence to disease management therapies is known to be a contributing factor to symptom exacerbations (Van der Wal et al., 2006), hospital readmissions (DiMatteo et al., 2000; Van der Wal, Jaarsma, & Van Veldhuisen, 2005; Annema et al., 2009; Ambardekar et al., 2009), and mortality (Granger et al., 2005) in patients with HF, with up to 64% of HF exacerbations attributable to nonadherence to medical and dietary recommendations (Michaelsen, Konig, & Thimme, 1998; Van der Wal et al., 2005). Adherence in patients with HF can also be complicated by other comorbidities, complexity of medication regime (Evangelista et al., 2003), and age-related factors such as cognitive status, hearing loss, and visual impairment. However, there does not appear to be a consistent relationship between demographic factors and self-management in HF. While there is some evidence that higher rates of nonadherence are observed in patients from lower socioeconomic groups (Van der Wal & Jaarsma, 2008), evidence on the effect of age on adherence in HF is more equivocal, with older age demonstrated to be both a risk factor
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(Molloy et al., 2009) and a protective factor (Evangelista, Berg, & Dracup, 2001; Artinian, Magnan, Sloan, & Lange, 2002; Chriss, Sheposh, Carlson, & Riegel, 2004) for nonadherence to HF medication. Furthermore, sleep difficulties and exhaustion are common in patients with HF, and this can be exacerbated by the impact of diuretics on frequent nocturnal urination, with one recent study identifying sleep disruption as the most commonly reported barrier to medication compliance (Bennett et al., 2005). Adherence has been shown to be related to knowledge, cardiac beliefs, and depressive symptoms (Van der Wal et al., 2006), and psychoeducation addressing both patients’ illness beliefs and their concerns about medications (O’Carroll et al., 2010) is likely to improve treatment adherence in patients with HF. Particular attention should be paid to those patients with depressive symptoms (Van der Wal et al., 2006), and the importance of adherence to lifestyle recommendations (e.g., smoking cessation, exercise) underlines the need for the multidisciplinary team in HF to have at least one member of staff familiar with behavioral change techniques such as motivational interviewing (Brodie, Inoue, & Shaw, 2008).
Living with HF: The Patient’s Perspective “Becoming” a Patient with Heart Failure Response to a diagnosis of HF will vary for each patient and depends largely on the personal significance of the event and the view held by the individual patient. An elderly patient with a history of multiple cardiac events and numerous comorbidities, who views dying as a natural event perhaps unrelated to their cardiac diagnosis, may, for example, respond very differently to a young parent diagnosed suddenly with HF due to viral infection, faced with retiring early to accommodate a new debilitating illness with a reduced life expectancy. Most research in this area has focused on the patient beyond the initial phases of HF following diagnosis, with few studies investigating the psychosocial experience of becoming a patient with HF from the acute phase of illness. This process is considered to be an evolving one necessarily taking time to adapt to. A qualitative study investigating the patient experience directly following diagnosis of HF indicated that the search for a “new identity” and meaning in life is a common theme (Stull et al., 1999). The initial stages require patients to integrate a new view of the self that incorporates HF and to commence a “new way of life.” The authors identified five distinct phases involved in becoming a patient with HF: (1) the crisis event, (2) the diagnosis itself, (3) the patient’s and family’s response to this diagnosis, (4) adjustment to life with the condition, and (5) acceptance of the disease in order to continue on with life (Stull et al., 1999). This distinctive pattern of becoming a HF patient unfolds similarly for most patients with HF, and a better understanding of this process – by both the patient and the medical team – may help reduce the impact of psychological symptoms such as depression and anxiety and hasten the patient’s ability to come to terms with this chronic condition.
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The Crisis Event and Diagnosis The diagnosis of heart failure is not always straightforward, and furthermore, predicting the prognosis of each individual patient is very difficult. This uncertainty frequently leaves HF patients with considerable frustration as they work with clinicians to attach some identity to their symptoms. Diagnosis is often made following a symptomatic crisis, and it is unclear how long patients with HF live undiagnosed with this syndrome (Westland, Carson, & Rutherford, 2009). For the patient, this failure to be diagnosed or meaningfully attribute their symptoms can often lead to further distress, and, once diagnosis is ultimately made, this does not necessarily make their life any easier. Even the term “heart failure” can be incredibly upsetting and typically conjures up terrifying images for both the patient and their family. Furthermore, many patients can become overwhelmed as they grapple with the inherent uncertainty in the course of their illness, the fluctuating symptoms, an extensive treatment regimen, and the impact of the disease on their daily functioning (Westland et al., 2009).
Understanding of HF A recent study found that two out of every five HF patients were dissatisfied with the explanation of their condition provided to them by their medical team (Lainscak & Keber, 2003). The ensuing lack of understanding by this subgroup of patients is likely to compound the distress and frustration they already experience. A reduced fund of knowledge is fertile ground for erroneous assumptions which may prevent patients from responding adaptively to their circumstances, and thus many will default to anxious or depressive reactions (Stull et al., 1999). While patients with HF unquestionably require some information about HF as a disease, they also benefit from input on the emotional and behavioral expectations in management of this condition. Patients typically describe an anxious reaction to their initial diagnosis of HF, and such anxiety is known to impede information processing. Accordingly, some patients have reported that they were unable to formulate a meaningful reaction at this time as they could not understand what their clinician was talking about (Stull et al., 1999). This finding illustrates the necessity of clear communication by the medical team at this juncture, along with sensitivity to the patient’s emerging understanding of their condition. Members of the medical team should be mindful of the likelihood of cognitive overload for the patient at this time, of their choice of language and its impact, and should appreciate that the patient’s sense of self can be greatly impacted as they are informed, typically abruptly, of an unfamiliar chronic and life-altering condition. Given the inherent unpredictability of disease progression for any one patient, cardiologists are understandably reticent about giving anything other than ambiguous information about survival rates to patients (Lynn et al., 1999). While patients with HF certainly cannot afford to be complacent about their condition, they are
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unlikely to benefit from being bludgeoned with their diagnosis. Thus, patients may or may not have the required knowledge to appreciate the gravity of their situation with respect to the importance of treatment adherence and lifestyle change.
Communication and the Doctor–Patient Relationship in HF The relationship with the medical team can have a tremendous impact on the health and well-being of the patient. Clear communication and an open and trusting relationship with the medical team are associated with better patient outcomes (Shaw, Ibrahim, Reid, Ussher, & Rowlands, 2009). While communication between patients with HF and health-care providers has not been well studied, it should at least be conducive to supporting the patient through this progressive and complicated syndrome. Similarly, there is onus on the patient to share responsibility for their health with their clinician. Notwithstanding the limitations of health-care settings with respect to time and resources, realistic guidelines for effective patient education include pitching language at the patient’s level of understanding, eliciting their individual preferences for treatment-related information, soliciting follow-up questions to information provision, and remaining emotionally sensitive and empathetic to the patient’s reaction to information (Goodlin, Quill, & Arnold, 2008). For example, in one study of doctor-patient communication in HF, those patients receiving a diagnosis of heart failure viewed their illness more negatively and were more likely to be anxious or depressed than those receiving the preferred euphemism employed by their physician (fluid on your lungs because your heart is not pumping hard enough) (Tayler & Ogden, 2005). A further study of 321 cardiac patients asked participant about their preferred format for receiving health-related information, and of the different formats available (e.g., leaflets, Internet use, media, and discussion with doctors), 79% of patients preferred verbal communication with their doctors. The patients also identified a good relationship with their doctor as a requisite for effective management of a chronic condition, acknowledged the importance of asking questions, but indicated that they would do so only when they felt comfortable and perceived their healthcare provider as not pressed for time (Shaw et al., 2009). The authors further concluded that despite obvious advantages the leaflet mode was ineffective for patient education given the difficulty cited by many patients in understanding them and increased feelings of anxiety around this (Shaw et al., 2009). As HF is a complex disease with diverse etiologies specific for each patient, it is prudent for the health-care provider to accommodate the health literacy level of patient, making effective health education more likely and ultimately attenuating potential adverse reactions such as stress, anxiety, or depression. The Rapid Estimate of Adult Literacy in Medicine (REALM) (Davis et al., 1993) is one tool that could be considered to facilitate tailoring of health-care information provision to each patient’s level of need and understanding, and has been associated with enhanced doctor-patient relationships (Shaw et al., 2009).
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While good communication is best practice for all members of the multidisciplinary team interacting with the patient with HF, having a mental health professional on staff such as a psychologist can be particularly helpful. In addition to assessing cognitive ability and tailoring information to patients as appropriate, an important role of these team members is to serve as a patient advocate and provide a safe environment for patients to raise concerns or even air grievances surrounding their medical care. Having access to such a resource can ultimately enhance communication and paradoxically bring about greater treatment satisfaction with the medical team. However, while poor knowledge of rationale and importance of treatment adherence is common (Ni et al., 1999; Riegel & Carlson, 2002; Pattenden et al., 2007), there is not a strong relationship between knowledge and self-management (Michaelsen et al., 1998; Ni et al., 1999) in patients with HF. It would appear that patients’ idiosyncratic beliefs may play a more prominent role in how they respond to their illness.
Illness Perceptions in HF The patient’s emerging beliefs and understanding of their chronic illness will shape how they cope with the considerable emotional and behavioral demands associated with it, and these views are inextricably linked to their treatment adherence and quality of life. Beliefs about HF often diverge widely from medical evidence, and greater store is put in information from lay sources than from medical professionals. Where discordant views exist between the medical team and the patient, however, adherence is unlikely. These misconceptions may greatly influence management of the disease by the patient, and ignoring the patient’s perspective typically only serves to reinforce nonadherence. Such beliefs can be firmly held and cannot be simply refuted. Specific misconceptions such as only 40% of my heart is working and most of my heart is dead were identified as typical beliefs held by patients with HF (Lewin, Pattenden, & Ferguson, 2008) and relate to anxiety and avoidant coping in HF patients. A recent innovative study targeted patients’ idiosyncratic views of their heart condition by asking them to draw their own hearts after diagnosis with HF. Patients depicting their hearts as bigger compared to before diagnosis experienced greater levels of cardiac anxiety, and those depicting damage in their hearts viewed their illness more pessimistically and were more depressed. Intriguingly, these drawings were also significantly associated with important clinical markers of illness severity such as B-type natriuretic peptide level and sodium level (Reynolds, Broadbent, Ellis, Gamble, & Petrie, 2007). In addition, Hallas and colleagues found that patients with HF who viewed their condition as less amenable to control and as having greater consequences were more likely to be elevated in both anxiety and depressive symptoms (Hallas, Wray, Andreou, & Banner, 2011). Patient beliefs about HF and its treatment may also be important determinants of adherence. Molloy et al. (2009) found that patients’ beliefs about HF, relating to its chronicity and impact on their lives, were associated with objective measure of adherence to
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angiotensin-converting-enzyme (ACE) inhibitor medication. Those patients with HF who believed that their illness was more long term and had greater consequences on their lives were less likely to adhere to ACE inhibitors. Similarly, Ekman et al. (2006) reported that patients who predicted little benefit from beta-blockers during a clinical trial were more likely to withdraw, whereas Van der Wal et al. (2006) observed that patients with HF who perceived their treatment as beneficial were more likely to adhere to recommended health behaviors. To date, only one study has investigated concordance of illness perceptions in couples coping with a chronic cardiac condition. The study examined discrepancies in illness perceptions between 73 patients with chronic heart disease and their spouses and found that spouses were more likely to view their partner’s heart condition as long term, controllable, and distressing than the patients themselves (Karademas et al., 2009). With respect to initial views of HF, adopting a chronic model of illness is alien to most people. Patients tend to think of illness as a short-term problem to endure or be “cured” of and then to resume their normal lives (Weinman & Petrie, 1997). Similarly, patients are not naturally predisposed to managing their health when they are symptom-free, and the illness course in HF is marked by periods of relative stability. Horowitz, Rein, and Leventhal (2004) noted that patients’ understanding of their HF was so limited that they often failed to connect their condition with their chronic symptoms, were at a loss to explain their HF or what caused it, and only acted on symptoms when they were severe enough to require emergency medical care. The authors also noted that patients’ typical model of HF is an acute condition with episodic exacerbations rather than a chronic condition requiring continuous monitoring and self-management (Horowitz et al., 2004). While illness beliefs may be important in the management of HF, research in this particular area is at an early stage and requires further investigation if interventions are to be designed to target such beliefs effectively. However, comprehensive treatment of HF should at the very least seek to elicit patients’ understanding of their HF and clarify any potential misconceptions, particularly those known to be associated with maladaptive coping.
The Effect of HF on Quality of Life HF subjects the patient to an array of unfamiliar demands such as adhering to a complex regimen of multiple medications, and constant vigilance to bodily signs of deterioration for the rest of their lives. Patients will also frequently find themselves instructed to begin and maintain multiple lifestyle changes at a time when they feel emotionally overwhelmed and physically exhausted. Symptoms such as dyspnea, fatigue, and lower-limb swelling can drastically curtail daily activities and thus greatly diminish quality of life (Barnes et al., 2006). While breathing difficulties are known to be inherently anxiogenic, patients have also reported feeling “shattered” by how their dyspnea has affected even the simplest of daily living tasks (Pattenden et al., 2007). As with depression, quality of life in patients with HF is directly correlated with disease severity, and studies have shown that patients with HF, particularly elderly patients, not only evidenced reduced quality of life compared to reference
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populations, but fared worse on these measures when compared to other chronic diseases illness populations (Luttik, Lesman-Leegte, & Jaarsma, 2009).
Adapting to a Life with HF Clearly, a diagnosis of HF brings with it considerable difficulties in adjustment which can severely compromise quality of life, as patients grapple with its attendant losses and the realistic belief that their lives have been irrevocably changed. Underlining the importance of effective communication, one study found that after their initial diagnosis, few patients with HF were informed on how to remain safely active, and the resulting misconceptions led to many patients self-imposing reductions of activity levels in order to avoid an acute exacerbating event leading to readmission (Pattenden et al., 2007). While patients must indeed accommodate some limits to their activities of daily living, avoidance of physical activity can paradoxically increase the likelihood of a hospitalization due to physical deconditioning, or indeed by compounding depressed mood due to becoming isolated and housebound. Furthermore, patients have to contend with being unable to continue working outside of the home, and financial stresses are often cited by patients among the sequelae of HF (Pattenden et al., 2007). While patients inevitably have to plan for limitations and interruptions to their previous routines, or alter their work practices, it is certainly possible for patients with HF recover well and maintain a satisfying quality of life. This success with which they implement their “new blueprint for living” (O’Hea, Houseman, Bedek, & Sposato, 2009) is greatly influenced by their coping style.
Coping in Patients with Heart Failure How well patients adjust to living with HF is largely influenced by their individual coping responses. Coping responses represent the mental, behavioral, and emotional strategies people adopt when confronted with stressful situations. HF is comprised of an array of different stressors, and thus patients may employ different coping responses from their repertoire to each of these illness-related problems (Cohen, Reese, Kaplan, & Jackson, 1986). Lazarus and Folkman (1984) proposed that patients’ coping responses are determined by both their perception of the threat posed by an illness, and the resources they feel they have to cope with it. This model proposes that coping strategies divide into emotion-focused or problem-focused strategies, with problem-focused coping aiming to somehow alter the stressor, whereas emotion-focused coping is directed at reducing the distress associated with the stressors. Depending on how well matched the coping strategy is to the situation, either emotion-focused or problem-focused coping can be adaptive in HF. Additionally, coping responses are deemed to be strongly informed by illness perceptions (Leventhal, Meyer, &
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Nerenz, 1980), particularly those relating to the beliefs about controllability of HF and the perception of its impact on one’s life (Hallas et al., 2011). A series of recent studies of coping in patients with HF has indicated that the coping style adopted by the patients may relate not only to psychological well-being outcomes but also to endpoints such as mortality (Murberg, Furze, & Bru, 2004). Avoidant coping and other passive strategies such as denial and behavioral disengagement are viewed as maladaptive in this context and are associated with depressed mood in particular (Doering et al., 2004; Klein, Turvey, & Pies, 2007; Vollman, LaMontagne, & Hepworth, 2007; Murberg, Bru, & Stephens, 2002; Trivedi et al., 2009; Hallas et al., 2011). Patients with HF who rely on active coping and other problem-focused strategies such as seeking social support and problem-solving have been demonstrated to experience better psychological well-being (Carels et al., 2004; Park, Fenster, Suresh, & Bliss, 2006; Vollman et al., 2007; Trivedi et al., 2009). Other emotion-focused coping strategies associated with lowered mood in patients with HF are venting and self-blame (Klein et al., 2007; Hallas et al., 2011), whereas acceptance has been associated with reduced distress in this population (Carels et al., 2004). People vary as to which coping strategy they gravitate toward, and the strategies themselves are not static but can be reviewed in the light of their effectiveness or in the case of new information refining their illness beliefs. Whatever the patient’s natural coping style however, the aim is to help them learn the “cognitive flexibility” to switch strategies based on whether the stressors encountered in HF are amenable to control or are better served by reducing the emotional discomfort attached to the situation. This is particularly in evidence when we consider the strategy of denial adopted by these patients. As indicated previously, when patients with HF appear to disregard the gravity of their diagnosis, it is possible that they may not have been informed of the risk of mortality by their medical team. Frequently, patients avoid prognostic information about their condition in an effort to preserve morale (Agard, Hermeren, & Herlitz, 2004), and in some cases, short-term denial may be seen as a natural and potentially adaptive response preventing the patient from getting too overwhelmed by the stressful nature of their new circumstances. There is little benefit in challenging denial in patients with HF unless it has been associated with treatment nonadherence (e.g., “smoking to reduce stress” or continued excessive alcohol intake). Similarly, confronting patients with their diagnosis can cause many patients to become depressed and hopeless about their condition. Apprising patients of the gravity of their situation should be done judiciously and with great sensitivity, and patients should also have access to opportunities to learn alternative healthier coping strategies as are taught in individual therapy or HF self-management programs.
Caregiver Burden in HF While it is established that high levels of social support are associated with improved outcomes in patients with HF, the bulk of studies in this area have looked at the psychosocial response in patients, rather than addressing the disease’s impact on the
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social support network itself (Chung et al., 2009). The psychosocial impact of HF is far-reaching, and maintaining personal and social relationships is an important adaptive task of living well with this condition. HF can put considerable strain on the patient’s family, and these effects can even ripple through their wider social support system. Spouses and primary caregivers bear the brunt of this strain and often find themselves in the position of being the patient’s “first line of defense” and yet the most likely to suffer from the distress and frustrations borne of their loved one’s struggle to adapt to chronic illness. In addition, family responsibilities, completed by the patient prior to illness but no longer manageable, must now be assumed by the spouse or other family member, and this can evoke not only feelings of guilt and inadequacy in the patient but increased feelings of pressure and resentment within the patient’s family. The roles of caregivers are manifold and can range from facilitating adherence to treatment regimens, symptom monitoring, support in daily physical activities, and emergency resuscitation to help in implementing lifestyle changes (Agren, Evangelista, & Strömberg, 2010). For example, caregivers are often more likely to notice important changes in the patient’s condition requiring attention and may help reduce treatment delay and ultimately arrest deterioration of the patient’s condition. Other practical aid such as assuming household responsibilities, shopping or financial duties are the most common areas of assistance, but psychosocial support is an additional crucial caregiving role, and this is typically provided by the spouse or adult children. Unfortunately, these demands placed on the caregiver can frequently have an adverse impact on their own quality of life and psychological well-being. Partners charged with primary responsibility for the patient with HF have reported that their lives were changed by their partner’s disease, that they experienced depression, and felt exhausted by the demands of rigorous treatment and monitoring involved in the care of a patient with HF (Martensson, Dracup, Canary, & Fridlund, 2003). Anxiety was found to be particularly pronounced during acute episodes (Pattenden et al., 2007; Martensson et al., 2003), and female partners of patients with HF presented with more symptoms of depression and poorer well-being compared to their male counterparts (Luttik et al., 2009). One study investigating the impact of HF on spouses and caregivers demonstrated that approximately one-third experience significant levels of caregiver burden, with limitations of daily life and reduced personal freedom – the most commonly cited difficulties. While feelings of injustice, financial burden, and loneliness are common consequences, the most difficult aspects of the caregiving role, however, were deemed to be coping with behavioral problems of the patient with HF and limited opportunities for socializing with friends (Agren et al., 2010). It must be noted however that not all consequences of caring for someone with HF are negative. Enhanced self-esteem and greater intimacy with the patient are just some of the benefits reported to have accrued from the caregiving role in HF (Agren et al., 2010). Just as with the patient, coping within the context of the patient-caregiver dyad can be adaptive or maladaptive. Families displaying healthy coping before the cardiac diagnosis typically withstand caregiver burden better than those with poorer coping
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abilities, and one study found that premorbid marital quality predicted mortality 4 years later as accurately as NYHA stage (Coyne et al., 2001). A further study of cardiac patients and spouses found that protectiveness – manifested as hiding concerns from either the spouse or patient – was associated with increased distress in both patients and spouses when this occurred (Suls, Green, Rose, Lounsbury, & Gordon, 1997). Caring for someone with HF clearly has a significant psychological impact on the patient’s social support network, and it behooves the health-care provider to be mindful of the mental health and needs of the carer as well as the patient. Partners are at less risk for distress when they themselves feel supported and come to view the patient’s condition as amenable to control. Both partner of the patients and/or the family as a whole should be considered for interventions or ongoing support.
Acceptance of a Chronic Condition in Patients with HF While a diagnosis of HF can be very challenging for the patient to successfully integrate into their lives, many are capable of working through the difficulties of their unique psychosocial experience and ultimately come to terms with their condition. This acceptance has been referred to as the final step of “becoming a patient with HF” (Stull et al., 1999). Patients need to appreciate that their condition not only exists but will accompany them for the rest of their lives, and they must also be helped to understand that they can resume living and maintain a good quality of life despite their challenging circumstances. Effective support will enable the patient to maintain a realistic and positive outlook of their situation; respond constructively to their condition rather than with fear, anxiety, or anger (Stull et al., 1999); and experience improved outcomes when compared to others with comorbidities such as depression (Jiang et al., 2008).
Interventions in Patients with HF Pharmacologic Interventions The use of antidepressant medications in HF patients has long been debated, but up to recently, studies have published equivocal findings pertaining to both the safety and efficacy of antidepressant medications. In the Cardiac Arrhythmia Suppression Trial (CAST), the use of tricyclic antidepressants (TCAs) in patients with cardiac disease was actually found to increase mortality rates (O’Connor et al., 2008). Furthermore, TCA overdose has been demonstrated to cause AV block, bundle branch block, and ventricular arrhythmias (Peacock & Henry, 1987), and studies have shown that TCA use may elevate the risk of myocardial infarction, an effect not
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observed in selective serotonin reuptake inhibitors (SSRIs) (Tousoulis et al., 2010). The safety of SSRIs has frequently been called into question by previous studies; however, many of these studies were limited by small sample sizes and thus precluded from drawing firm conclusions (O’Connor et al., 2008). In an attempt to clarify the debate on the safety of antidepressants with patients with HF, and drawing from a sample of 1,005 HF patients, O’Connor and colleagues demonstrated that the use of SSRIs was not associated with an increase risk of death in patients with HF. Disappointingly however, despite this claim on safety, they also found that the use of SSRIs did not help to reduce mortality in this patient population (O’Connor et al., 2008). Given the high incidence of depression in patients with HF, more data on the use of pharmacotherapy with this population is warranted, and SADHARTCHF is a randomized clinical trial currently investigating the safety and efficacy of sertraline (SSRI) versus placebo in a large sample of patients with HF (Jiang et al., 2008). Similarly, MOOD-HF is a large double-blind, placebo-controlled study currently examining the use of escitalopram (SSRI) in patients with HF. This trial is testing the hypothesis that use of escitalopram in patients with HF is not only safe but will also improve clinical outcome through reduction in deaths and unplanned hospitalizations (Angermann et al., 2007). The use of SSRIs in healthy participants and their effect on the sympathetic nervous system has been studied, with one study observing that sertraline suppressed sympathetic nervous system (SNS) activity in healthy subjects as indicated by decreased plasma norepinephrine (Shores, Pascualy, Lewis, Flatness, & Veith, 2001). Given that the SNS is involved in the progression of HF, this effect may represent a potential added benefit for the use of SSRIs in treatment of depression in patients with HF. However, due to the currently equivocal findings, this association will need to be examined in more detail before clinical recommendations can be made. It has further been suggested that antidepressants may lower inflammatory markers typically observed to be elevated in depressed patients, with one study observing a similar level of inflammatory markers in nondepressed HF patients as in depressed HF patients treated with an SSRI (Tousoulis et al., 2009). SSRIs as a sympathetic nervous system and inflammation modulator in patients with HF will also require further investigation however. Another class of antidepressants, the monoaminoxidase (MAO) inhibitors, have not been studied in patients with HF because this class of drug has established adverse effects on blood pressure postulated to be unsafe in this population (Tousoulis et al., 2010). Evidently, the data on the use of SSRIs in patients with HF is currently mixed. While it is clear that depression is associated with poorer outcomes in patients with HF, it is not yet clear whether the treatment of depression in these patients with SSRI therapy is both safe and effective.
Nonpharmacological Interventions There is currently no consensus as to what the optimal model of HF management is. What is clear, however, is that certain elements are necessary for HF interventions
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to be effective and that a one-size-fits-all approach is not appropriate. A stepped-care approach is indicated, allowing for simpler, low-intensity interventions first (e.g., education), but allowing for specialist mental health care available to those patients with HF requiring it (e.g., CBT). Similarly, it would appear too that certain subgroups within the HF population should be targeted differently, for example, in respect to their socioeconomic background, length of diagnosis, and presence of clinically significant depression.
Self-Management in HF Self-management has been described as “the individual’s ability to manage the symptoms, treatment, physical and psychosocial consequences and lifestyle changes inherent in living with a chronic condition” (Barlow, Hearnshaw, & Sturt, 2002). While it is reasonable to assume that adjusting to HF and coping with its emotional impact are issues encompassed by this definition, in practice, self-management interventions emphasize managing the medical aspects of the illness and have traditionally relied on the premise that informing patients about the recommended selfmanagement behaviors (e.g., self-monitoring, weighing) will be sufficient to improve clinical outcomes. Furthermore, while treatment adherence and behavioral change are accepted to be complex issues, very few studies have been informed by the extensive research on facilitating behavior change (Mulligan, 2009), and only recently have self-management programs been augmented to comprise of a wider, multicomponent approach incorporating elements such as the management of emotions associated with HF. While it is accepted that psychological support for patients with HF is important, few intervention studies for depression in this patient group have been carried out (Lane, Chong, & Lip, 2005). Exercise training is also encouraged in patients with stable heart failure and represents a key component of HF rehabilitation programs (Corra et al., 2005), and self-management interventions are often delivered in conjunction with exercise sessions in hospital-based programs. Many self-management trials to date (Harrison et al., 2002; Sethares & Elliott, 2004; Wright et al., 2003; Prasun, Kocheril, Klass, Dunlap, & Piano, 2005) have been criticized for methodological shortcomings such as small sample sizes, short durations, and brief follow-up periods (Powell et al., 2010); however, a recent systematic review of self-management programs in HF concluded that they were shown to be effective in reducing overall hospital and HF readmissions although they did not reduce mortality (Jovicic, Holroyd-Leduc, & Straus, 2006). The recent COACH (Coordinating study evaluating Outcomes of Advising and Counseling in Heart Failure) study similarly found that patients with HF were found to benefit in terms of reduced readmissions, but again, mortality rates were not improved. It was further noted that patients with depression did not have improved outcomes, and that the intervention in fact led to an increase in admissions (Jaarsma et al., 2010). The authors argued that as self-management programs require patients to be sufficiently motivated to actively engage with the intervention, standard programs
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may not be suitable for depressive patients, and that tailored interventions may be required for this patient group. Another recent and methodologically robust trial, the HART (Heart Failure Adherence and Retention Randomized Behavioral Trial) study, investigated the impact of a self-management intervention on 900 patients with HF. It was demonstrated that the addition of 1 year of self-management counseling to usual care did not reduce death or hospitalization in patients with moderate HF, although some benefit was observed for low-income HF patients (Powell et al., 2010). Accordingly, the authors concluded that their trial demonstrated that there was no benefit of self-management counseling on clinical endpoints in patients with HF, but qualified this by noting that their study was only powered to detect a large effect size, and that the education control group received more active treatment than expected which improved outcomes such as depression, salt intake, and confidence in self-management (Powell et al., 2010). As it stands, the efficacy of SM programs in improving outcomes in patients with HF is unproven, and interventions addressing the broader aspects of HF self-management need to be further developed and evaluated. While targeting the emotional aspects of living with HF has only recently begun to be incorporated in self-management interventions, this is improving. Recently, the remit of self-management programs in HF has been widened to include a much broader range of issues with an explicit focus on emotional and behavioral issues. These programs typically incorporate elements of cognitive behavioral therapy (CBT) to a greater or lesser degree and have addressed issues such as misconceptions in HF; managing fatigue and insomnia; dealing with difficult emotions such as anxiety, depression, anger; pacing and the overactivity-rest cycle; assertiveness and communication with the medical team; stress management, cognitive restructuring, and relaxation training; maximizing social support and coping with changing relationships; and countering barriers to adherence and lifestyle change (Lewin et al., 2008; Baird & Clarke, 2011). Encouragingly, trials are also currently underway investigating more wideranging interventions aimed to help patients with HF to cope more effectively with their condition. The COPE-HF (Coping Effectively with Heart Failure) study is an ongoing randomized trial of 200 patients with HF evaluating whether a coping skills training (CST) intervention improves cardiac biomarkers and quality of life in addition to reducing mortality and hospitalizations (Sherwood, Blumenthal, Trivedi et al., 2011). This intervention will comprise of motivational interviewing and individually tailored CBT. Similarly, Nezu and Nezu are leading the “Coping with Heart Failure Project,” another trial currently underway examining the efficacy of problem-solving training (PST) with depressed patients with HF. PST is a relatively brief structured intervention comprising of a subset of CBT techniques targeting an individual’s beliefs and attitudes about problem-solving (their “problem orientation”) in addition to improving one’s problem-solving style in order to deal with current and imminent problems, which consequently alleviate emotional distress such as depression. It is debatable as to whether the range of difficulties experienced by patients with HF may be readily construed as “problems to be solved”; however, this model is designed to be flexible and may also, for example, be incorporated into a broader CBT framework.
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CBT and Heart Failure Cognitive behavioral therapy (CBT) (Beck, Rush, Shaw, & Emery, 1979) has been researched more than any other form of psychotherapy, and there exists strong empirical support for its use in treating patients with depression (Robinson, Berman, & Neimeyer, 1990). However, despite the clearly established link between HF and depression, only a minority of depressed patients with HF receive treatment (Jacob, Sebastian, & Abraham, 2003), and until recently, few studies have investigated the efficacy of CBT with HF patients (Lane et al., 2005). While there is no standard recommended treatment for concomitant psychological problems in HF, CBT is typically the psychological treatment of choice for cardiac problems, particularly when they are found to co-occur with depression. CBT operates on the view that rather than being passively influenced by external and biological factors, we are actively involved in constructing our own reality (Clark, 1995). Adverse events can be greatly exacerbated by the unhelpful thoughts we may hold. Such beliefs can interfere with our ability to cope constructively, and learning to develop alternative viewpoints is considered crucial, as is the realization that there is always more than one viewpoint to choose from. Another tenet of CBT is that the various spheres of our lives (physical, mental, emotional, behavioral, and environmental) are interlinked so that changes in one area naturally affect the others (Greenberger & Padesky, 1995). When positive change is brought about in one of these areas, this quite naturally and simply has a knock-on effect for the other areas. During depressed mood, it is assumed that recurring negative automatic thoughts (NATs) bring about both lowered mood and cause people to behave in such a way to maintain depression. Key strategies used in CBT are behavioral activation, identifying and modifying negative thoughts (cognitive restructuring), and improving coping skills (O’Hea et al., 2009). Behavioral interventions such as activity scheduling aim to help patients with HF actively re-engage with their lives by resuming abandoned activities and ensuring that their daily life does not become bereft of stimulation. Such activities also help to preserve the patient’s independence and counter the idea that they can no longer experience enjoyment in their lives. In addition these activities also help to interrupt ruminative patterns of thinking which consequently reduce distress. Cognitive interventions help patients with HF to identify and challenge distressing thoughts such as those relating to perceived worthlessness, inability to cope, and the sense of being a burden on others. New ways of coping taught to patients with HF include problem-solving (e.g., pacing and brainstorming alternative modes of resuming valued activities), reframing, selectively attending to one’s assets rather than recent losses, and maximizing social support. The patient’s repertoire of coping skills can further be enhanced by skills training in relaxation techniques and mindfulness. In addition to helping implement a treatment plan for depression and decreasing feelings of isolation, families and caregivers can play a crucial role in conveying a sense of realistic hope to patients adjusting to HF. By modeling desired behavioral changes, reinforcing even modest successes, and helping the patient to selectively attend to their achievements, a more positive
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mindset is bolstered and perceptions of control are enhanced. The cognitive behavioral framework is particularly suited to modifying treatment-interfering illness beliefs and can easily be adapted for patients with HF to integrate interventions targeting improvements in sleep, diet, and smoking cessation (Sykes & Simpson, 2011). Although exercise on its own will not modify the cognitive distortions and illness perceptions associated with maladaptive coping, it plays a prominent role in any effective treatment plan for patients with HF experiencing depression. Furthermore, given the synergistic relationship between depression and functioning in HF, and the established beneficial effects of exercise training on both mood and HF outcomes, it would appear plausible that combination therapy of CBT and exercise training in patients with HF may represent an optimized intervention for this patient population. Gary and colleagues, in a study of 74 patients with comorbid depression and HF, tested just such an assumption. The performance of a combined 12-week homebased exercise training and CBT program was compared with CBT alone, exercise alone, and usual care in patients with stable HF. The greatest reduction in depression scores was indeed observed in the combined group compared to the other arms, but this change was not significant. However, only those patients in the combined group had sustained improvements in depression at 3- and 6-month follow-ups, and this group experienced the greatest improvement in health-related quality of life (Gary, Dunbar, Higgins, Musselman, & Smith, 2010). CBT reinforces the effects of exercise in the treatment of patients with HF, and these two parallel modes of intervention can be delivered together seamlessly in the context of HF rehabilitation programs. While the impact of CBT on cardiac endpoints is still unproven, its beneficial impact on both depression and quality of life has been demonstrated, which is reason enough for it to continue to be indicated for this patient group.
Conclusions HF is a chronic disease that is both progressive and complex in nature. From a psychosocial standpoint, patients are presented with myriad challenges ranging from the demands of managing the disease itself to adapting to its emotional consequences. Associated stressors and patients’ attempts to cope with them have been shown to impact their health outcomes. While psychological comorbidities are highly prevalent in this population, they are all too often overlooked, and it is the responsibility of the medical team to prioritize the patient’s mental health in addition to their physical status. While not all patients with HF will be amenable to intervention from a mental health professional, a selection of both proven and promising treatments are available to draw from on a stepped-care basis, enabling the individual needs of each patient with HF to be met. Although interventions for comorbid conditions such as depression have not yet proven to reduce mortality in patients with HF, health-related quality of life can clearly be enhanced. With or without formal intervention, patients with HF can be supported psychologically by
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both the medical team and their families by reinforcing the view that their condition is controllable and that a satisfying quality of life is still possible. Such support will typically foster acceptance of this chronic condition and facilitate successful management of its long-term course. Given the congruence of CBT and physical activity in HF, further research into enhanced cardiac rehabilitation and key factors (e.g., personality traits) associated with sustained physical activity will assist in optimizing future interventions with this patient group.
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Chapter 6
Psychiatric Symptoms, Personality Profile, and Takotsubo Syndrome: Clinical Considerations Ilan S. Wittstein, Riccardo Proietti, and Angelo Compare
Clinical Description of the Takotsubo Syndrome Takotsubo cardiomyopathy (TTC) is a recently described syndrome of heart failure and transient left ventricular dysfunction that is frequently precipitated by acute emotional or physical stress. Because patients with TTC typically present with chest pain, electrocardiographic abnormalities, elevated cardiac enzymes, and focal ventricular wall motion abnormalities, it is not surprising that they are often mistakenly diagnosed with acute myocardial infarction. As familiarity with TTC has increased, however, it has become clear that this syndrome not only has unique clinical features that can readily be distinguished from those of acute infarction, it also appears to have a distinct pathophysiology. In contrast to the irreversible myocardial injury seen with acute infarction, TTC is characterized by myocardial dysfunction that is transient and completely reversible and occurs in the absence of plaque rupture and coronary thrombosis. There is evidence that the myocardial stunning of TTC may be sympathetically mediated, but the precise pathogenesis of this disorder remains incompletely understood.
I.S. Wittstein, M.D. Department of Medicine, Division of Cardiology, The Johns Hopkins University School of Medicine, 568 Carnegie, 600 N. Wolfe Street, Baltimore, MD 21287, USA e-mail:
[email protected] R. Proietti, M.D. Cardiac Electrophysiology Laboratory, Luigi Sacco Hospital, Milano, Italy e-mail:
[email protected] A. Compare, Ph.D. (*) Department of Human Sciences, University of Bergamo, S. Agostino, Bergamo 2-24129, Bergamo, Italy e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_6, © Springer Science+Business Media, LLC 2012
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TTC was first described in Japan by Satoh and colleagues in 1990 (Satoh et al., 1990). They named the condition takotsubo cardiomyopathy after the octopus trapping pot with a wide base and narrow neck that resembled the unusual left ventricular shape seen in patients with this condition. While initial reports of TTC were exclusively from Japan, the syndrome has now been reported from countries all over the world and is referred to by many other names including stress cardiomyopathy (Wittstein et al., 2005), transient left ventricular apical ballooning syndrome (Tsuchihashi et al. 2001), and broken heart syndrome (Wittstein et al., 2005). TTC was initially felt to be a rare condition, but it is now clear from the rapidly expanding medical literature that the syndrome is far more prevalent than what was originally believed. Several retrospective series have demonstrated that TTC accounts for approximately 2% of patients with a suspected acute coronary syndrome (ACS) (Buja et al., 2008; Eshtehardi et al., 2009; Kurowski et al., 2007; Parodi et al., 2007). The prevalence is even higher in women presenting with suspected ACS, with rates ranging from 4.7% to 7.5% (Parodi et al., 2007; Previtali, Repetto, Panigada, Camporotondo, & Tavazzi, 2008; Strunk et al., 2006; Wedekind, Moller, & Scholz, 2006). All series to date have demonstrated a marked age and gender discrepancy, with older postmenopausal women being most commonly affected (Elesber et al., 2007; Hoyt, Lerman, Lennon, Rihal, & Prasad, 2010; Regnante et al., 2009; Sharkey et al., 2010; Singh, Rumman, Mikell, Nallamothu, & Rangaswamy, 2010; Tsuchihashi et al., 2001). Coronary risk factors are common in patients with TTC (Pilgrim & Wyss, 2008), and frequently observed comorbidities in these patients include thyroid disease, chronic obstructive pulmonary disease, and mood disorders such as anxiety and depression (Del Pace et al., 2011; Regnante et al., 2009). Patients with TTC typically present with symptoms indistinguishable from those of an acute myocardial infarction, with chest pain and shortness of breath being the most common. While the majority of patients with TTC are hemodynamically stable at the time of admission, heart failure and pulmonary edema have been described in 15.9% of the reported cases, with cardiogenic shock and life-threatening arrhythmias occurring in 10.3% and14.6% of the cases, respectively (Pilgrim & Wyss, 2008). In a large Japanese series, 20% of the patients required intra-aortic balloon counterpulsation or pressor support (Tsuchihashi et al., 2001). Cases of apical thrombus formation, cardioembolic stroke, left ventricular free wall rupture, and pericarditis have also been reported. There are no uniformly accepted diagnostic criteria for TTC, though guidelines have been proposed (Kawai, Kitabatake, & Tomoike, 2007; Novo et al., 2008). The most widely cited criteria were introduced by investigators from the Mayo Clinic in 2004 and were modified in 2008 (Table 6.1) (Prasad, Lerman, & Rihal, 2008). While not all of the criteria are uniformly agreed upon, it is our opinion that the following six criteria can assist in making the diagnosis of TTC and can help to distinguish the syndrome from acute myocardial infarction: 1. An acute trigger (see section on proposed mechanism of TTC) 2. Characteristic electrocardiographic changes: At the time of presentation, patients with TTC can have a normal ECG, nonspecific ST segment and T wave
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Table 6.1 Modified Mayo Clinic criteria for the diagnosis of takotsubo cardiomyopathy (Prasad et al., 2008) Transient hypokinesis, akinesis, or dyskinesis of the left ventricular midsegments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always, present Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture New electrocardiographic abnormalities (either ST segment elevation or T wave inversion) or modest elevation in cardiac troponin Absence of pheochromocytoma and myocarditis
changes, or ST segment elevation, typically seen in precordial leads. Compared to patients with anterior ST segment elevation myocardial infarction (STEMI), patients with TTC tend to have a smaller magnitude of ST segment elevation (Sharkey, 2008) and are less likely to have reciprocal inferior ST segment depression at the time of admission (Ogura et al., 2003). Within 24–48 h of the initial presentation, patients with TTC typically develop marked QT interval prolongation (Wittstein et al., 2005), and the majority of patients also develop deep diffuse T wave inversion in both precordial and limb leads. Patients with TTC can also present with pathologic Q waves that are usually seen in precordial leads, but unlike with acute myocardial infarction, these Q waves are transient in most cases and typically resolve within days to weeks of the initial presentation (Wittstein et al., 2005). 3. Mild cardiac enzyme elevation: Most patients with TTC have only mildly elevated cardiac enzymes at the time of admission. These enzyme levels can appear paradoxically low given the extensive ventricular wall motion abnormalities that are typical for these patients. Cardiac enzyme levels are much lower in patients with TTC than in patients with acute infarction (Ogura et al., 2003; Parodi et al., 2007). 4. Absence of coronary thrombosis or plaque rupture: TTC is characterized by the absence of obstructive coronary disease. While the majority of reported cases have described normal coronary arteries (Gianni et al., 2006; Pilgrim & Wyss, 2008), it is now well recognized that many patients with this condition have angiographic evidence of nonobstructive coronary atherosclerosis (Hoyt et al., 2010; Winchester, Ragosta, & Taylor, 2008). Because patients typically present with chest pain, dynamic ECG changes, elevated cardiac enzymes, and focal wall motion abnormalities, coronary angiography should be performed unless there is an obvious contraindication to definitively exclude evidence of acute plaque rupture and coronary thrombosis. 5. Ventricular “ballooning”: In contrast to patients with acute infarction, patients with TTC have left ventricular wall motion abnormalities that extend beyond a single coronary territory. The majority of patients have the well-described “apical ballooning” pattern in which there is akinesis or dense hypokinesis of the apical and midventricular segments with sparing of the base (Fig. 6.1). More recently, “midventricular” and “basal” variants of this syndrome have been reported in which the apex is not affected (Fig. 6.2) (Hurst et al., 2006; Reuss et al., 2007).
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Fig. 6.1 Left ventriculography and coronary angiography of a patient with takotsubo cardiomyopathy. The ventriculogram illustrates the apical ballooning pattern with akinesis of the apex and midventricular segments and hypercontractility of the base (left panel). Despite these focal ventricular wall motion abnormalities, the angiogram reveals that the left coronary arteries (middle panel) and right coronary artery (right panel) are normal and without obstructive disease
Fig. 6.2 Nonapical ballooning variants observed in some patients with takotsubo syndrome. Patients with the midventricular ballooning variant (left) have hypokinesis or akinesis of the midventricle with sparing of both the apex and basal segments. With the basal ballooning variant (right), there is hypokinesis or akinesis of the midventricular and basal segments with preserved contractility of the apex
While TTC is characterized primarily by left ventricular dysfunction, a third of the patients with left ventricular apical ballooning also have right ventricular dysfunction (Elesber et al., 2006). Patients with biventricular involvement are more likely to have severe heart failure and hemodynamic instability. 6. Recovery of left ventricular function: Complete recovery of ventricular systolic function is one of the hallmarks of TTC. Most patients demonstrate significant improvement in systolic function within a week of the initial presentation, and complete recovery is often observed by the end of the third week. Cases of very slow left ventricular recovery have been published (Kitaoka et al., 2006), and some authors have reported a recovery period of up to 1 year (Sharkey et al., 2010). This tends to be the exception, however, and as a general rule, if systolic function in a patient suspected of having TTC has not completely normalized within 12 weeks, alternative diagnoses should be considered.
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Patients with TTC appear to have a favorable prognosis and a relatively low risk of recurrence. As a group, these patients have a better long-term survival and fewer major adverse cardiac events than patients with myocardial infarction (Nunez-Gil et al., 2008). In a systematic review of 28 case series of TTC, the recurrence and in-hospital mortality rates were only 3.1% and 1.7%, respectively (Pilgrim & Wyss, 2008). In a large single center retrospective experience from the Mayo Clinic, the recurrence rate of TTC was 11.4% during the 4 years following the initial presentation. Four-year survival was no different than that observed in an age- and gendermatched population (Elesber et al., 2007). Sharkey and colleagues recently reported a 15% 5-year mortality rate and a 5% recurrence rate in a large series of patients with TTC (Sharkey et al., 2010). These patients had reduced survival compared to an age- and sex-matched population, but most of the deaths occurred within the first year and were due to noncardiac causes. The treatment of TTC is primarily supportive in the acute period. Hemodynamically stable patients are frequently treated with diuretics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers. Unless there is an obvious contraindication, patients with apical akinesis should be anticoagulated until apical contractility improves in order to reduce thromboembolic risk. For hemodynamically unstable patients, reported treatment has included inotropes, vasopressor support, and intraaortic balloon counterpulsation. There are also some limited reports that patients with hypotension and left ventricular cavity obstruction may derive hemodynamic and echocardiographic benefit from the administration of intravenous beta-blockade (Kyuma et al., 2002). Because catecholamines may be central to the pathogenesis of TTC and have been associated with ventricular outflow tract obstruction in some patients (Sharkey et al., 2005), we prefer to use intra-aortic balloon counterpulsation for hemodynamically unstable patients and to avoid the administration of exogenous catecholamines whenever possible. Fortunately, even the most unstable patients typically demonstrate rapid clinical improvement and rarely require hemodynamic support for more than a few days. There is no consensus regarding the long-term management of TTC. Patients are frequently treated with ACE inhibitors, beta-blockers, or calcium channel blockers, but there are currently no data to support that the use of these agents prevents recurrence or improves survival. It has therefore become our practice to stop these medications once left ventricular function has normalized. Similarly, though patients with TTC have a high prevalence of anxiety and depression (Mudd, Kapur, Champion, Schulman, & Wittstein, 2007), no studies have examined whether psychological or pharmacologic treatment of these mood disorders improves long-term outcomes in these patients.
Case Presentation A 58-year-old woman presented to the emergency department of Sant’Andrea Hospital of Vercelli with 4 h of chest pain radiating to the jaw and left upper extremity. Her past medical history included hypertension, depression, a 10-pack-year history of tobacco
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use, fibromyalgia, irritable bowel syndrome, and gastroesophageal reflux disease. She had no prior history of cardiac disease. Her medications at the time of presentation included a nonselective beta-blocker for hypertension and a selective norepinephrine reuptake inhibitor (SNRI) for the treatment of her depressive disorder. Physical examination on admission revealed a pulse of 105 beats/min and a blood pressure of 90/60 mmHg. Auscultation of the chest revealed rales in the lower lung fields bilaterally. She was tachycardic with a regular rhythm on cardiac examination, but there were no murmurs, rubs, or gallops. Laboratory tests revealed a troponin I of 9.26 ng/mL (normal range, 0–0.4 ng/mL). Electrocardiography showed normal sinus rhythm with 2 mm ST segment elevation in leads V2 through V5. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with anteroapical akinesis and an ejection fraction (EF) of 20%. The patient was admitted to the Coronary Intensive Care Unit (CICU) where she was treated with aspirin and intravenous heparin, nitrates, and glycoprotein IIb-IIIa inhibitors. In light of the ST segment elevation, she was taken for urgent coronary angiography which revealed normal arteries without focal stenosis or obstruction. Left ventriculography revealed apical akinesis with hypercontractile basal segments, and the diagnosis of takotsubo cardiomyopathy was made. An intra-aortic balloon pump (IABP) was placed for persistent hypotension and congestive heart failure. By the next day, the patient had stabilized hemodynamically and the IABP was removed. She continued to improve clinically, and a repeat echocardiogram performed 4 days later demonstrated recovery of left ventricular systolic function with resolution of all regional wall motion abnormalities. A more detailed history was obtained once the patient had stabilized and revealed that she had experienced a major life stressor 6 months prior to admission with the death of a loved one. Further, an acute emotional trigger was also identified using the Paykel Life Stress Event Scale (Paykel, 2003) and uncovered that the patient had been involved in a heated domestic argument just 4 h prior to the onset of symptoms. She was discharged from the hospital in stable condition and 2 weeks later underwent formal psychological testing. The patient had a high level of depressive symptoms with a Beck Depression Inventory score of 49. The high level of depressive symptoms exhibited by this patient is illustrative of the distress often encountered in this patient population. An exploration of the potential link between Type D (distressed) personality and TTC is provided in a later section of this chapter. While the above case presentation is fairly representative of many patients presenting with TTC, it raises some very interesting and still unanswered questions. For example, what is the prevalence of mood disorders in patients diagnosed with TTC? Do mood disorders increase susceptibility to TTC and are there certain personality types that make an individual particularly vulnerable to this condition? If TTC is sympathetically mediated, could antidepressants that affect catecholamine metabolism (e.g., SNRI) potentially increase myocardial sensitivity to acute stress? This chapter will present available data from both clinical observations and experimental research that are beginning to provide insight into some of these complex issues.
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A Proposed Paradigm for the Mechanism of Takotsubo Cardiomyopathy While the clinical features of takotsubo syndrome have become increasingly well recognized during the past several years, the precise pathogenic mechanism of this unique disorder remains unknown. Because patients frequently present following an acute emotional or physiologic trigger, it is now widely believed that TTC may be sympathetically mediated. The precise mechanism in which acute stress results in transient myocardial dysfunction and heart failure, however, remains incompletely understood. A proposed paradigm for the etiologic basis of TTC is illustrated in Fig. 6.3. In this model, an acute emotional or physical stressor results in a series of
Fig. 6.3 Possible mechanistic link between acute stress and takotsubo cardiomyopathy. Acute emotional or physical stress results in increased sympathetic stimulation and catecholamine production. Catecholamine excess may mediate myocardial stunning through a variety of possible pathophysiologic effects that include microvascular dysfunction and direct myocyte toxicity. Mood disorders may potentiate the physiologic response to stress, while sex hormones, endothelial dysfunction, certain antidepressants, and adrenoceptor polymorphisms may increase myocyte and microvascular sensitivity to sympathetic stimulation. These pathophysiologic effects result in the clinical features that characterize takotsubo syndrome (Modified from Bhattacharyya & Steptoe, 2007, Fig. 6.1. Copyright © 2007. With permission from Elsevier)
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Table 6.2 Frequency of identifiable triggers of takotsubo cardiomyopathy in some of the larger reported series Number Emotional Physical No trigger Reference in study Study design trigger (%) trigger (%) identified (%) Tsuchihashi et al. 88 Retrospective 20 53 27 (Tsuchihashi et al., 2001) Parodi et al. 68 Prospective 38 34 28 (Parodi et al., 2007) Elesber et al. 100 Retrospective 26 30 44 (Elesber et al., 2007) Singh et al. 114 Retrospective 33 50 17 (Singh et al., 2010) Nunez-Gil et al. 62 Prospective 39 8 53 (Nunez-Gil et al., 2008) Sharkey et al. 136 Prospective 47 42 11 (Sharkey et al., 2010) Previtali et al. 128 Prospective 36 23 41 (Previtali et al., 2011)
physiologic responses. These responses may be hemodynamic, neurohormonal, inflammatory, and prothrombotic, but there is growing evidence that the key physiologic response in the development of TTC is enhanced sympathetic stimulation. A hyperadrenergic response to acute stress causes specific pathophysiologic myocardial effects that ultimately result in the clinical features that characterize the syndrome of TTC. This chapter will review the available data that support each aspect of this proposed paradigm. Further, factors that may increase susceptibility to TTC by either enhancing the physiologic response to stress or the myocardial vulnerability to sympathetic stimulation will be presented. The acute trigger: One of the unique features of TTC is that the clinical syndrome is frequently precipitated by an acute emotional or physiologic stressor. It is for this reason that the syndrome is often referred to as “stress cardiomyopathy” (Wittstein et al., 2005). While early reports of this syndrome highlighted primarily the emotional triggers of TTC, it is now clear from the literature that physical triggers account for a large percentage of the reported cases (Table 6.2). It is important to remember, however, that the identification of an acute stressor is not required to make the diagnosis of TTC. In a systematic review of 14 case series, an acute trigger could not be identified in 34% of the cases (Gianni et al., 2006), possibly reflecting the retrospective nature in which many of these series were collected. In centers where TTC has been followed prospectively for many years, however, the frequency of identifiable triggers appears to be considerably higher. Sharkey and colleagues recently reported a large series of TTC in which an acute precipitant was identified in 89% of the cases (Sharkey et al., 2010). This is similar to what we have observed at our own institution where we have been following TTC prospectively for the past 11 years. At Johns Hopkins Hospital, 27% of the cases have been due to emotional triggers while 66% of the cases have resulted from a variety of physical stressors. The inability to identify an acute trigger has only occurred in 6% of our patients.
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Table 6.3 Spectrum of acute triggers precipitating takotsubo cardiomyopathy at Johns Hopkins Hospital (n = 201) % Total cohort Examples of trigger Emotional trigger (n = 55) 27 Grief (n = 24) 12 Death of a loved one; house burned down Fear (n = 10) 5 Motor vehicle accident; severe claustrophobia; victim of robbery Anger (n = 7) 3.5 Domestic argument; anger in court Anxiety (n = 12) 6 Panic attack; anxiety over public speaking; anxiety about surgery; anxiety about illness of a family member; severe marital stress Surprise (n = 2) 1 Surprise birthday party; unexpected reunion with family member Physical trigger (n = 133) 66 Neurologic injury (n = 43) 21 SAH; seizure; stroke; subdural hematoma; gunshot to the head; brain mass Surgery/procedure (n = 21) 10 Orthopedic surgery; exploratory laparotomy; AAA repair; adrenalectomy; cervical spine surgery; decortications of empyema; thyroidectomy Respiratory (n = 20) 10 Pneumonia; COPD exacerbation; pulmonary embolism; pneumothorax Drug related (n = 17) 8 Epinephrine administration; dobutamine administration; cocaine use; Ativan withdrawal; clonidine withdrawal; 5-FU infusion Syncope (n = 8) 4 Syncope; near syncope; severe vertigo Strenuous activity (n = 6) 3 Moving heavy furniture; triathlon; vigorous housework; sexual intercourse Gastrointestinal (n = 4) 2 Hematemesis from NSAID use; lower GI bleed from arteriovenous malformations; small-bowel obstruction; pancreatitis Metabolic (n = 4) 2 Diabetic ketoacidosis; acute hypoglycemia Severe pain (n = 3) 1.5 Kidney stones; severe muscle spasms Cardiac arrest (n = 3) 1.5 Ventricular tachycardia; ventricular fibrillation Allergic reaction (n = 2) 1 Transfusion reactions Sepsis (n = 2) 1 MRSA sepsis; gram-negative sepsis Unidentifiable trigger (n = 13) 6 AAA abdominal aortic aneurysm, COPD chronic obstructive pulmonary disease, GI gastrointestinal, MRSA methicillin-resistant Staphylococcus aureus, NSAID nonsteroidal anti-inflammatory drug, SAH subarachnoid hemorrhage, 5-FU 5-fluorouracil
The most common emotional triggers have included acute grief, anxiety, and fear, while the most common physical precipitants have been acute neurologic injury, surgical procedures, and respiratory emergencies (Table 6.3). The physiologic response: There is significant clinical evidence to suggest that enhanced sympathetic stimulation is central to the pathogenesis of TTC. Patients with TTC following emotional stress have markedly elevated plasma catecholamine
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levels compared to patients with Killip III myocardial infarction (Wittstein et al., 2005). An increase in local myocardial catecholamine release in patients with this syndrome has also been demonstrated with coronary sinus sampling (Kume et al., 2008). Looking at indices of heart rate variability, Ortak and colleagues have demonstrated sympathetic predominance and a marked depression of cardiac parasympathetic activity during the acute phase of TTC (Ortak et al., 2009), and parasympathetic blockade with atropine has been shown to exacerbate the signs and symptoms of TTC (Sandhu, Servetnyk, Croitor, & Herzog, 2010). Enhanced sympathetic activity has been suggested by the increased washout rate of the norepinephrine analogue 123I-metaiodobenzyl-guanidine (MIBG) using myocardial scintigraphy (Akashi et al., 2004). TTC has also been associated with catecholaminesecreting tumors such as pheochromocytoma and paraganglioma (Takizawa et al., 2007; Van Spall, Roberts, Sawka, Swallow, & Mak, 2007). Further, all of the clinical features of TTC have been precipitated by the intravenous administration of catecholamines and beta-agonists in patients undergoing routine diagnostic procedures (Abraham et al., 2009). Data from animal models also support the central role of adrenergic stimulation in the pathogenesis of TTC. Ueyama was able to precipitate left ventricular apical ballooning in rats subjected to immobilization stress, and this effect could be attenuated with alpha- and beta-blockade (Ueyama et al., 2002). Izumi and colleagues induced TTC in monkeys with the infusion of intravenous epinephrine and demonstrated increased myocytolysis in the apical portion of the ventricle (Izumi et al., 2009). Administration of the beta-blocker metoprolol decreased epinephrine-mediated myocytolysis and resulted in an improvement in left ventricular ejection fraction. Pathophysiologic effects: Several pathophysiologic mechanisms have been proposed to explain how enhanced sympathetic stimulation could result in the transient myocardial dysfunction seen with TTC. One of the earliest mechanisms suggested was catecholamine-mediated plaque rupture with rapid and complete lysis of the ensuing thrombus, thus providing a potential explanation for the elevated cardiac enzymes, electrocardiographic (ECG) changes, and focal myocardial wall motion abnormalities seen in this syndrome despite the absence of obstructive epicardial disease. Some authors initially reported eccentric atherosclerotic plaque in the midportion of the left anterior descending (LAD) coronary artery using intravascular ultrasound (Ibanez, Navarro, Cordoba, Alberca, & Farre, 2005), but these findings have not been uniformly supported. It was also proposed that plaque rupture and transient coronary thrombosis had to occur in a long wraparound LAD in order to explain the apical ballooning pattern typically seen in this syndrome (Ibanez et al., 2004). It has since been demonstrated, however, that apical ballooning can occur even in the absence of a wraparound LAD and that the prevalence of this coronary anatomy is no higher in patients with TTC than it is in a control population (Hoyt et al., 2010). Further, transient thrombosis in a large wraparound LAD would not explain the basal and midventricular ballooning patterns that have also been reported. Sympathetically mediated coronary spasm could result in ischemia and could potentially account for the myocardial stunning that characterizes TTC, but most of
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the available data do not support this hypothesis. First, while epicardial spasm has been reported in cases of TTC, it is rarely observed during angiography, even when provocative agents such as ergonovine and acetylcholine are administered (Pilgrim & Wyss, 2008). Second, most patients have only mild cardiac enzyme elevation, and many have no evidence of ST segment elevation on ECG, findings that are inconsistent with diffuse epicardial spasm. Finally, it is difficult to explain the different “ballooning” patterns based on an epicardial vascular distribution, and even multivessel spasm would not account for the unusual patterns of akinesis that have been reported. An intraventricular pressure gradient can be measured in some patients with TTC during the acute presentation (Kyuma et al., 2002; Sharkey et al., 2005; Tsuchihashi et al., 2001; Yoshioka et al., 2008). It has been suggested that patients with smaller ventricles and localized midventricular septal thickening may be predisposed to severe midcavity obstruction during periods of excessive sympathetic stimulation. This obstruction could cause a large pressure gradient between the apex and base, resulting in apical subendocardial ischemia and transient dysfunction. It is likely, however, that the intraventricular gradient observed in some patients with TTC is a consequence rather than the underlying cause of the myocardial dysfunction. Only a small minority of cases of TTC reported in the literature have described an intraventricular gradient (Pilgrim & Wyss, 2008). In addition, while a large gradient between left ventricular apex and base could theoretically result in apical ischemia and ballooning, it does not provide a very plausible explanation for the basal and midventricular variants or for the right ventricular dysfunction seen in about a third of patients with this syndrome. Sympathetically mediated microvascular dysfunction is another potential mechanism of the myocardial stunning seen with TTC. A significant reduction in coronary flow reserve during the acute phase of the syndrome has been demonstrated with both a Doppler flow wire at the time of coronary angiography (Kume et al., 2005) and Doppler transthoracic echocardiography following the infusion of adenosine (Meimoun et al., 2008) or dipyridamole (Rigo et al., 2009). Despite the absence of obstructive coronary disease, patients with TTC have elevated Thrombolysis in Myocardial Infarction (TIMI) frame counts (Bybee et al., 2004), a well-validated angiographic index of coronary blood flow, and abnormal TIMI myocardial perfusion grades (Elesber, Lerman et al., 2006). In the majority of these patients, TIMI frame counts are elevated in multiple vessels, and perfusion abnormalities involve multiple coronary territories, suggesting that catecholamine-mediated microvascular dysfunction may account for the unusual patterns of left ventricular dysfunction seen with this syndrome. This idea is supported by a recent study in which patients with TTC were found to have elevated plasma catecholamine levels and endomyocardial biopsy evidence of microvascular endothelial cell apoptosis (Uchida et al., 2010). Myocardial stunning in TTC may alternatively result from the direct effects of catecholamines on cardiac myocytes through adrenergic receptor signaling. Catecholamines can decrease myocyte viability through cyclic adenosine monophosphate–mediated calcium overload. This results in contraction band necrosis, a
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histologic finding known to occur in states of catecholamine excess that has also been observed in the endomyocardial biopsy samples of patients with TTC (Nef et al., 2007; Wittstein et al., 2005). Using tissue from endomyocardial biopsies, Nef and colleagues recently demonstrated evidence of abnormal calcium regulation in patients with TTC (Nef et al., 2009). At the time of presentation, there was significant downregulation of sarcoplasmic Ca2+ ATPase (SERCA2a) gene expression, increased ventricular expression of sarcolipin, and dephosphorylation of phospholamban (PLN), potentially resulting in decreased calcium affinity and subsequent myocardial contractile dysfunction. The PLN/SERCA2a ratio returned to normal when endomyocardial biopsies were repeated following ventricular recovery. Abnormal calcium handling in TTC is also supported by data from animal models. In a rat model of TTC, acute beta-adrenergic stimulation resulted in left ventricular dysfunction and myocyte injury through calcium leakage due to hyperphosphorylation of the ryanodine receptor 2 (RyR2) (Ellison et al., 2007).
Factors That May Increase Susceptibility to Takotsubo Cardiomyopathy While most individuals are subjected to repeated emotional and physiologic stressors throughout their lives, the fact that only a relatively small number develop TTC suggests that there are likely risk factors that increase individual susceptibility to this disorder. These risk factors may influence a person’s physiologic response to stress and increase their vulnerability to the pathophysiologic mechanisms that result in myocardial stunning (Fig. 6.3). While it is likely that numerous such risk factors exist, only a few that are supported by clinical observations and research will be discussed here. Hormonal influence: A consistent observation in all series reported to date is the striking preponderance of postmenopausal women. Female hormones exert important influences on the sympathetic neurohormonal axis as well as on coronary vasoreactivity and myocyte calcium handling. As women age, cardiac vagal tone and baroreflex sensitivity decrease significantly (Lavi et al., 2007), potentially making postmenopausal women more susceptible to the deleterious cardiovascular effects of sympathetic stimulation following an acute stressor. There is clinical evidence that estrogen attenuates catecholamine-mediated vasoconstriction (Sung, Ching, Izzo, Dandona, & Wilson, 1999) and the catecholamine response to mental stress (Komesaroff, Esler, & Sudhir, 1999) in postmenopausal women. In a rat model of TTC, left ventricular dysfunction due to immobilization stress could be attenuated with estrogen supplementation (Ueyama et al., 2007). These observations suggest that sex hormones likely have an important influence on stress-related myocardial stunning, but there are currently no clinical data to suggest that estrogen replacement can prevent the occurrence or recurrence of TTC.
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Endothelial dysfunction: Recent data have suggested that patients with TTC may be individuals with inherent endothelial dysfunction and chronic impairment of coronary vasodilatory reserve. Barletta and colleagues performed cold pressor testing (CPT) on subjects who had fully recovered from an episode of TTC (median 688 days from the acute presentation) (Barletta et al., 2009). Peripheral venous catecholamines were measured, and left ventricular function and perfusion were assessed using real-time three-dimensional echocardiography and myocardial contrast 2D echocardiography, respectively. Compared to an age-, sex-, and risk factor–matched control group, CPT in patients with TTC resulted in significant catecholamine elevation and transient apical and midventricular wall motion abnormalities, and there was no detectable increase in coronary blood flow. Martin and colleagues used peripheral arterial tonometry (PAT) to assess endothelial function in subjects with a prior episode of TTC (Martin, Prasad, Rihal, Lerman, & Lerman, 2010). In contrast to a postmenopausal control group, subjects with prior TTC demonstrated increased catecholamine production, impaired vascular vasodilation, and increased vasoconstriction when subjected to mental stress testing. These studies suggest that patients with TTC may be individuals who are particularly susceptible to myocardial stunning during periods of acute stress and catecholamine excess due to inherent abnormalities of endothelial function and coronary flow reserve. Genetic factors: TTC has been reported in siblings (Pison, De Vusser, & Mullens, 2004), but the genetic determinants of this syndrome have yet to be defined. Zaroff and colleagues studied the impact of adrenergic receptor polymorphisms on cardiac dysfunction in patients with neurogenic stunned myocardium, a condition seen commonly after central neurologic injury that is believed to be catecholamine mediated and that likely shares an overlapping pathophysiology with TTC (Zaroff et al., 2006). They found that the incidence of cardiac dysfunction and troponin elevation following subarachnoid hemorrhage was greatly increased in individuals with specific a- and b-adrenergic receptor polymorphisms. An increased frequency of these same polymorphisms has not been found in patients with TTC (Sharkey et al., 2009), but Spinelli and colleagues have demonstrated that patients with TTC have an increased frequency of the L41Q polymorphism of the G protein–coupled receptor kinase 5 (GRK5) (Spinelli et al., 2010). The L41 variant of GRK5 enhances b-adrenergic receptor desensitization and attenuates the receptor’s response to catecholamine stimulation. The negative inotropic effect of b-receptor uncoupling may make individuals with this polymorphism more susceptible to TTC in the setting of enhanced sympathetic stimulation. Alternatively, myocardial stunning could result from ischemia due to an imbalance between a1-adrenergic coronary vasoconstriction and b-adrenergic vasodilation. While larger genetic studies are needed, these initial reports suggest the possibility that individual susceptibility to TTC may in part be genetically determined. Mood disorders and antidepressant use: Several reports have suggested that patients with depression and anxiety may be particularly susceptible to TTC (Table 6.4). We previously reported a high prevalence of mood disorders and antidepressant use in patients with TTC (Mudd et al., 2007), and this prevalence was just as high in
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Table 6.4 Prevalence of mood disorders and antidepressant use in patients with takotsubo cardiomyopathy Prevalence Prevalence Number Mood of mood of antidepressant Reference of patients disorder disorder (%) use (%) Mudd et al. 110 Depression/ 40 21 (Mudd et al., 2007) anxiety Regnante et al. 70 Depression/ 37 NR (Regnante et al., 2009) anxiety Vidi et al. 34 Depression/ 21 24 (SSRI) (Vidi et al., 2009) anxiety 29 (Benzo) Sobnosky et al. 53 Depression/ 36 (D); 30 (A) 40 (Sobnosky et al., 2010b) anxiety Summers et al. 2010 25 Depression/ 48 (D); 56 (A) NR anxiety Del Pace et al. 50 Anxiety 60 NR (Del Pace et al., 2011) A anxiety, Benzo benzodiazepine, D depression, NR not reported, SSRI selective serotonin reuptake inhibitor
patients with physical triggers of TTC as it was in those with emotional precipitants. In a recent study of 50 patients with TTC, high-anxiety trait was identified in 60% of the subjects using the Spielberger Trait Anxiety Inventory (STAI) (Del Pace et al., 2011). It is possible that mood disorders may have pathogenic importance in TTC since individuals with depression have decreased vagal tone and an increased adrenomedullary hormonal response to stressful events (Cevik & Nugent, 2008), and some patients with depressive disorders appear to have very high noradrenaline spillover (Barton et al., 2007). Further, the increased use of antidepressants such as selective norepinephrine reuptake inhibitors may facilitate myocardial stunning in this population by increasing local catecholamine levels.
Personality Traits and Vulnerability to TTC with Emotional Triggers Although the onset of TTC is typically precipitated by an acute trigger (Connelly, MacIsaac, & Jelinek, 2004; Nef et al., 2008; Sharkey et al., 2008; Wittstein et al., 2005; Yaghoubi et al., 2009), the precise pathogenic mechanisms linking acute stress to myocardial stunning remain poorly understood (Abraham et al., 2009; Wittstein, 2008). While the specific determinants of cardiovascular vulnerability to acute stress remain in large part unknown, Table 6.4 suggests that mood disorders such as anxiety and depression may increase individual susceptibility to TTC. At our institution in Italy, we carried out an exploratory study to test the hypothesis that patients with TTC would be differentiated from patients with acute myocardial infarction by specific personality traits (Fig. 6.4) (Compare et al., 2009). In an
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Fig. 6.4 Possible link between personality type and takotsubo cardiomyopathy. There is an increased incidence of mood disorders in individuals with Type D personality who have increased social inhibition and negative affectivity. Patients with depressive disorders may have decreased vagal tone and an increased adrenomedullary hormonal response to stressful stimuli, thus making them more susceptible to the development of takotsubo cardiomyopathy
age- and gender-matched case–control study, we compared the psychological profiles of TTC versus acute myocardial infarction (TTC vs AMI) in patients admitted to Niguarda Hospital of Milan and Sant’Andrea Hospital of Vercelli (Italy). Seventy-five patients were diagnosed with TTC using the Mayo Clinic criteria (Prasad et al., 2008). Emotional stressors preceding the presentation (within approximately 12 h) were identified in 37 patients through careful history taking, while a physical stressor such as a medical/surgical procedure or diagnostic test was identified in 38 patients. Patients with emotional precipitants of TTC and patients with AMI underwent psychological evaluation. The Paykel Life Stress Event Scale (Paykel, 2003) was used to quantify the frequency of emotional triggers in each group occurring prior to presentation. The Paykel Stress Index score was significantly higher in TTC (14.5, interquartile range 13.4–15.5) than it was in
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AMI (1.25, interquartile range 0.5–2; p < 0.001), suggesting a closer association with the trigger event. An emotional trigger occurring within 12 h of admission was identified in 100% of the TTC patients and in only 24% of the AMI patients. The mean time from the acute trigger to hospital admission was 4.2 h (interquartile range 3.7–4.8) in TTC and 9.3 h (interquartile range 6.4–12) in AMI (p < 0.001). The sudden loss of an emotionally significant person was the most frequent (35%) emotional trigger of TTC. Personality traits (Type D personality, cynical hostility, and trait anger) that have been previously associated with increased cardiovascular risk were compared between the two groups. Type D personality has been described as a “distressed” personality, characterized by the tendency to experience negative emotions and social inhibition, and this construct has been shown to be associated with poorer prognosis in cardiac patients (Denollet & Kupper, 2007; Spindler, Kruse, Zwisler, & Pedersen, 2009; Tully, Baker, Winefield, & Turnbull, 2010). Patients with TTC compared to AMI had higher scores on both the negative affect and social inhibition scales of the Type D personality measure. Multivariate analysis revealed that the odds ratio of Type D personality in TTC compared with AMI was 10.85 (C.I. 2.63–44.78). Preliminary findings from this study show that the social inhibition component of Type D personality is more likely to be observed in patients with TTC compared to age- and sex-matched AMI patients. In previous studies, inhibition of emotions has been associated with higher cardiovascular reactivity (Gross & Levenson, 1997), lower cardiovascular recovery and heart rate variability (Brosschot & Thayer, 1998), and overactivity of the sympathetic nervous system (Roberts, Levenson, & Gross, 2008). Type D personality is associated with mood disorders (Denollet & Kupper, 2007; Spindler, Pedersen, Serruys, Erdman, & van Domburg, 2007). Individuals who develop TTC have been shown to have a high prevalence of depression (Mudd et al., 2007; Summers, Lennon, & Prasad, 2010) and anxiety (Del Pace et al., 2011). Based on these observations and considering evidence that supports the central role of enhanced sympathetic stimulation in the pathogenesis of TTC, it is reasonable to infer that the origin of sympathetic hyperactivity may be located in the cognitive-emotional subcortical regions of the brain (Critchley et al., 2005) and may be associated with specific personality traits. Thus, personality traits may contribute to individual differences in cardiovascular reactivity to emotional stress through variability in cardiac sympathetic outflow, with cardiac noradrenaline spillover potentially achieving very high levels in certain individuals (Baumert et al., 2009). There is a great deal of variation in how well people adjust emotional responses to meet current situational demands (Gross & Thompson, 2007; Mayer, DiPaolo, & Salovey, 1990). Inappropriate or ineffective expression of emotions is emerging as a critical component in the development and maintenance of depression and anxiety disorders (Barlow, Allen, & Choate, 2004; Campbell-Sills, Barlow, Brown, & Hofmann, 2006a, b; Kashdan, Barrios, Forsyth, & Steger, 2006; Kashdan & Steger, 2006; Mennin, 2006). The following discussion will focus on the components of Type D personality. Emphasis will be placed on social inhibition which, as previously discussed, appears to be particularly prevalent in individuals with TTC.
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Type D personality: The distressed personality (Type D) was developed by Denollet in 1996 (Denollet et al., 1996) in his investigation of coping styles in men with coronary heart disease. The “distressed” personality subtype is characterized by the joint tendency to experience negative emotions and to inhibit these emotions while avoiding social contact with others (Habra, Linden, Anderson, & Weinberg, 2003). The taxonomy is based on two broad and stable traits: negative affectivity and social inhibition (Denollet & De Potter, 1992). Negative affectivity denotes the tendency to experience increased negative distress across time and situations. Individuals scoring highly on negative affectivity are not only dysphoric but have a negative view of self, report more somatic symptoms, have an attention bias toward adverse stimuli (Denollet, 2000; Denollet & Van Heck, 2001), and seem to scan the world for signs of impending trouble. Social inhibition refers to the tendency to inhibit the expression of negative emotions/behaviors in social interactions to avoid disapproval by others. Individuals scoring highly on social inhibition frequently feel inhibited, tense, uncomfortable, and insecure when encountering other people (Sher, 2005). Type D personality has been associated with a variety of emotional and social difficulties, including depressive and anxiety symptoms, chronic tension, anger, pessimism, lack of perceived social support, a low level of subjective well-being, and posttraumatic stress disorder (Compare, Manzoni, & Molinari, 2006; Pedersen & Denollet, 2003, 2004; Pedersen, van Domburg, Theuns, Jordaens, & Erdman, 2004). Emotional regulation: The mental elaboration of emotions is a complex process that involves initiating, inhibiting, or modulating (Siegler, 2006) the subjective experience of emotion, emotion-related cognitions, emotion-related physiological processes, and emotion-related behaviors. A process model of emotion regulation (Gross & Thompson, 2007) suggests that people also regulate emotions by altering the effect of emotion-generating cues (antecedent-focused regulation) (Moore, Zoellner, & Mollenholt, 2008) or by altering emotional output (response-focused regulation). Antecedent-focused regulation modulates emotional response tendencies early on, before they give rise to full-fledged responses. An individual can regulate the precursors of emotion such as the situation or the appraisal (Grandey, 2000). Response-focused regulation, which acts late in the process, modulates the emotional responses once they have arisen by modifying the physiological or observable signs of emotion (Grandey, 2000). The social inhibition subscale of Type D might be viewed as a response-focused regulation strategy, which acts late in the process of emotional regulation. People scoring high on social inhibition may inhibit emotion-expressive behavior, typically with little or no change in subjective emotion experience, and increased sympathetic activation of the cardiovascular system (Demaree et al., 2006; Gross, 2002; Gross & Levenson, 1993). Consistent with previous research (Gross & Levenson, 1993, 1997), Roberts and colleagues (Roberts et al., 2008) recently found that emotion suppression is associated with decreases in facial behavior and body movement and an increase in sympathetic activation of the cardiovascular system. They found that suppression also is associated with increases in systolic and diastolic blood pressure. Other research has shown that facial modulation of disgust is associated with increased cardiac sympathetic control but not with respiratory activation,
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electrodermal activation, or cardiac vagal control (Demaree et al., 2006). Inhibition is not helpful in reducing the experience of negative emotion, which is not directly targeted by suppression, and which continues to linger and accumulate. It requires the individual to make effort to manage emotion response tendencies as they continually arise. Moreover, inhibition creates in the individual a sense of incongruence, between inner experience and outer expression. This sense of not being true to oneself, of being inauthentic rather than honest with others, may well lead to negative feelings about the self and alienate the individual not only from the self but also from others. Investigations of inhibitory control in human and nonhuman primates, however, suggest that the right ventrolateral prefrontal cortex is associated with volitional response inhibition (Brass, Derrfuss, & von Cramon, 2005; Buchsbaum, Greer, Chang, & Berman, 2005; Elliott & Deakin, 2005; Garavan, Hester, Murphy, Fassbender, & Kelly, 2006; Kelly et al., 2004; Li, Huang, Constable, & Sinha, 2006; Rubia, Smith, Brammer, & Taylor, 2003; Vollm et al., 2006). Over the long term, frequent use of suppression results in diminished control of emotion, interpersonal functioning, memory, and well-being and greater depressive symptomatology (Gross & John, 2003).
Clinical Implications Patients with a history of depressive symptoms may be more prone to TTC (Mudd et al., 2007; Regnante et al., 2009; Sobnosky et al., 2010a; Summers et al., 2010; Vidi et al., 2009). It is plausible that chronic emotional dysregulation that renders some individuals more vulnerable to depressive symptoms (Bradley et al., 2011) may also increase susceptibility to TTC. Genetic vulnerability may be a common denominator underlying both emotional dysregulation and propensity to TTC (Uhart, McCaul, Oswald, Choi, & Wand, 2004; Wittstein, 2007). Type D personality is associated not only with depression but also with hyperarousal reactions in response to stress (Denollet & Kupper, 2007; Spindler et al., 2009; Tully et al., 2010) (Molloy, Perkins-Porras, Strike, & Steptoe, 2008). Our preliminary data (Compare et al., 2009) are consistent with the findings of others (Quartana & Burns, 2010) and imply that the risk of an event may depend not only on the individual’s cardiovascular vulnerability following stress exposure but also on his or her emotional coping mechanisms. This paradigm is in keeping with findings from experimental studies showing that the cardiovascular effects of acute stress may be amplified by the presence of chronic psychosocial stress (Chida & Hamer, 2008). Given the apparently different underlying pathophysiologies of TTC and AMI, it is logical that conceptual constructs that serve as a basis for diagnostic testing and treatment of patients with chronic coronary artery disease may not be appropriate for TTC. Pathophysiological constructs need to be established, and associated diagnostic and treatment models need to be developed and tested, so that these patients can be identified and appropriately treated. Future research examining the psychological correlates of TTC could help to solve the pathophysiological puzzle of stress-mediated cardiomyopathy.
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Chapter 7
Psychological Aspects of Cardiac Transplantation Brigitta Bunzel
Evaluation The Transplant Team For the transplant team, the process begins with an evaluation of the patient through a doctor’s medical finding and evaluation: is the given patient suitable as a candidate for a donor organ, according to medical and psychosocial criteria? The medical criteria, indications, and counterindications for heart transplantation are precisely defined (e.g., Cimato & Jessup, 2002). More difficult is clarification in the psychosocial area (Levenson & Olbrisch, 1993; Favaloro et al., 1999). In the early years of heart transplantation, it was determined that only patients with a clarified brain-organic disturbance or patients with florid psychosis were excluded for nonmedical reasons from being organ recipients, and that a patient was only rejected for psychosocial reasons when it could not be avoided (Christopherson & Lunde, 1971). In the course of time, through observing long-term successes in various areas, the following factors could be identified, which allow the success of transplantation to be predicted with a high probability: support of the (family) environment, strong will to survive, and, above all, the cooperation of the patient in their own recovery process (compliance, above all, with regard to taking medications, follow-ups, and reporting of physical symptoms). Indications for a poor transplantation result and therefore possible counterindications of the heart transplantation are: noncompliance with regard to medicines, dependencies (alcohol, drugs, nicotine, medications), the (partial or complete) lack of or negative support of family, personality disorders (above all with narcissistic and antisocial components), long-term history of (above all untreated) psychiatric illness, brain disorders, or mental retardation without a B. Bunzel, Ph.D. (*) Department of Cardiac Surgery, Medical University of Vienna, Waehringer Guertel 18-20, A 1090 Vienna, Austria e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_7, © Springer Science+Business Media, LLC 2012
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best-case social environment (Dew & Dimartini, 2006; Rivard et al., 2005). Ultimately, the success of heart transplantation remains dependent upon the recipient’s ability to cope psychologically and comply with the medical regimen. As clear as the above criteria may seem, they are still very unclear in their practical application. Christopherson’s regret in 1971 that “no set of definitive criteria for the selection of suitable candidates has yet been formulated” (Christopherson, 1987) is still true today. Although test instruments and recommendations for patient selection have been developed in the area of psychiatry (e.g., Bernazzali et al., 2005), it can thus be expected to be more of a reference than a complete, precise prediction of the suitability of the patient as an organ recipient. Herrick et al. (1987) warn of the rejection of a patient: “Denial of transplantation for nonmedical reason is filled with potential for bias and prejudice because of the inherently nonobjective nature of the criteria and also carries the possibility for grievous misjudgement and even legal ramifications.” And Shapiro summarizes the difficult problematic of all involved in the selection process when he writes, “it is difficult to refuse to give the patient a chance” (Shapiro, 1990). Yet, we cannot make problems disappear by ignoring them. Evaluation of concrete selection criteria according to the state of the scientific findings and practical experience must make their primary goal in the decision process the participation of psychologists, psychosomatics, and psychiatrists. When accepting or denying a patient as a candidate to receive an organ, it should, however, be mentioned that a moderate degree of fear and depression in the preoperative phase does not pose a counterindication; rather, it only presents added difficulties in the transplantation process. It is considered a logical consequence of the process of illness and according to many studies has no negative effect on transplantation. It is even reported that a certain degree of fear and depression is connected with greater operation success: it reflects the circumstance that the patient has understood the reality, without being overcome by it.
The Patients For patients, the process of “heart transplantation” begins much earlier, with the report that conventional therapy is no longer capable of halting the progressive course of their terminal heart failure. Patients experience that their life expectancy is in all probability limited, and that a replacement of the irreparably damaged heart through a healthy one by a brain-dead donor is the only possibility of avoiding a high probability of death in the near future. The patient further learns that the transplantation could help them toward a better quality of life and improved longevity, that for the individual, however, it constitutes a final decision: they do not have the possibility to go back to the “original condition” (such as, for a patient receiving a kidney transplant, returning to dialysis). When the patient realizes the necessity of heart transplantation, it presents a new chapter in the course of the illness, to which they must react. This requires a confrontation with the illness and adaptation to the changed situation, and is thus a problem of the patient’s coping with the illness. It is
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precisely during this time spent waiting for a donor heart that the transplant team can also observe the patient’s actual endurance and tolerance for frustration, which are often seen as indicators for the success of an operation. Despite encouraging long-term results in a medical as well as psychological sense (Bunzel et al., 2002), heart transplantation for those affected is not simply a chance for survival; it also poses a vital and psychological threat. Patients must live with the fact that transplantation is a massive surgical intervention that can also ultimately be fatal. They must reliably take medication, which often has considerable side effects; they must undergo endomyocardial biopsies at regular intervals in order to monitor organ rejection. But the threat does not stop with physical aspects; psychologically, too, the surgery presents a threat: losing one’s own heart and receiving one from a person who has died (mostly as a result of an accident, tragic illness, or suicide), constitutes more than an operation, more than the mere “exchange” of an organ that no longer works (Bunzel et al., 1992a, b). The heart is largely considered the site of our emotions, even of personality, and its “exchange” often causes the patient to fear losing their identity along with the congenital organ. From the above, it becomes clear that the diagnosis of terminal heart failure with transplantation as the only long-term chance for survival must be difficult for the patient to understand and also must be difficult for the doctor to impart. In a study with over 50 consecutive patients at the heart transplantation department of the Medical University of Vienna (Bunzel et al., 1991), the following result was observed: in reaction to being told of the necessity of a heart transplantation, the patients that we interviewed could be classified into two groups. For somewhat more than a third of the patients, the indication for heart transplantation presented a logical consequence – predictable after a certain point in their medical history – and a chance and hope for survival in the absence of any real alternative. This group comprised all of those persons who had been ill for a long period, who had already taken on the identity of a chronically ill person and who had had enough time to adjust their lives to the illness, who had become painfully familiar with the limitations that illness imposes, and who, already years before the acute necessity for transplantation, had been informed about this operation in case their illness should continue to worsen. These patients generally reacted thankfully for the possibility to prolong their lives. The most prominent emotions are the hope for survival and the fear of sudden death before undergoing the operation. The mechanisms or styles of coping among these patients are above all acting intentionally (“for all cases” writing a last will and testament), acceptance, as well as compliance-related strategies, i.e., trusting the doctors, following medical advice, etc. Patients with (longterm) heart murmurs and those who had had multiple heart attacks are distinctly represented in this group. These patients are aware of the life-threatening aspects of their illness (“I was in the ICU for 9 weeks; I could have died at any moment”); they have confronted the possibility of death. For them, the possibility of transplantation therefore often constitutes the only hope of surviving in an otherwise hopeless situation. For the other 62% of the patients, the notification of the necessity for transplantation came completely unexpectedly and constituted a shock. They explained quite emotionally that they were entirely unprepared for the notification, that they
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denied the truth of it and that the notification “hit them in the head,” “as if they were in the wrong film.” Defensiveness and denial were initially the only possible means of dealing with the physical and psychological threat. Above all, cardiomyopathic patients, whose extensive heart damage had developed rapidly, often within weeks, had mostly had too little time to confront their illness at all. If transplantation is then mentioned in such an acute situation, the reaction to it is a disbelieving astonishment, fear, denial, and retreat. The decision for transplantation must therefore be met by the patient; fear and ambivalence must be sustained and expressed. Heart transplantation, however, requires two decisions: one from a medical team and one from the patient. It is possible that the transplantation team refuses an organ recipient candidate. Common reactions to this refusal are expressions of fear, anger, frustration, hopelessness, sadness, but also release and relief. It also happens, however, that a patient whom the doctors have accepted refuses the operation. Frierson and Tabler (Frierson et al., 1990) report a share of 15% of patients who refuse transplantation surgery. Factors influencing the decision to refuse surgery included: • • • • • •
Ambivalence about surgery and/or survival Persistent depression Past negative experiences with surgery Acceptance of the inevitability of death Concerns about postoperative quality of life Fear of transplant exceeded fear of dying (wish “to die with the original equipment intact”) • Organicity • Denial of the severity of their cardiac disease, and thus, the need for transplantation The authors emphatically warn against pressuring patients to make the decision for transplantation and stress the fatal result of surgery for patients who have been under any kind of pressure for transplantation by either a social group or family. The decision of a potential organ recipient to refuse an operation is difficult to understand, both for the patient’s social circle as well as for the transplantation team, when there is anger, frustration, or concern for someone who “does not want to be saved.” Nevertheless, for every patient, the possibility to refuse the surgery should remain open without losing the operation team’s good will.
The Waiting Period Patients If the patient is determined a suitable candidate for receiving an organ and also agrees to the transplantation, the actual waiting period for a heart donation begins, which is a time of physical and psychological instability.
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Positive feelings about acceptance as an organ recipient candidate are clouded by the justifiable fear of dying before the arrival of a donor heart. In the weeks to months of waiting, the progression of the condition is usually not a steady decline, but is instead interrupted by phases of relative physical stability. During the “good times,” the patient is plagued with the question of whether the decision for surgery was the right one, whether surgery is even necessary. Some patients during such periods wish to be taken off the waiting list. Should the unavoidable phase of physical decline be characterized by a further decline in abilities, these patients are eager to undergo the transplantation as quickly as possible. The loss of strength, each limitation of activity, is accompanied by irritability, frustration, and depression. This ambivalence toward the decision for transplantation, being torn between fear and fulfillment of a wish, the oscillation between postponement and wanting it immediately creates extreme psychological stress for the affected and is accompanied by social withdrawal, weak decision making in everyday affairs, and feelings of extreme dependency. Contact with other transplantation patients who have completed surgery and who could serve as role models is often crucial and clearly reduces fear and tension (“if they’ve done it I can too”). Patients suffer during this waiting period from a laming certainty that they can do nothing at all to influence the arrival of a donor heart. It could come at any time of the day, or also not arrive before death. The patient during this time must come to terms with the fact that their irreparably damaged heart will be replaced by one from a brain-dead donor, the tragic victim of a traffic accident, a fateful illness, or one who has taken one’s own life. Taking the heart of another for one’s own survival and thus to have “wanted the death of another, unknown person,” often presents an almost unbearable burden on the patient. Many heart patients waiting for a donor heart are burdened by uncontrolled thoughts: they wish for ice storms, so that more accidents will occur, they hope there is a severe injury in their blood type as soon as they hear the ambulance sirens, and they search through newspapers for the reports of devastating traffic accidents. How typical this reaction is during the waiting period is evident in the term for this extremely psychological burden: “rainy day syndrome” (Freeman et al., 1984) and “donor weather” (Kuhn et al., 1988). These obsessive thoughts in patients lead to feelings of guilt and shame and are often so compulsive that in many cases they cannot be suppressed but instead – often coming as a huge shock to relatives and hospital staff – are voiced repeatedly. The collusion of guilt, fear, shame, ambivalence, and their survival instinct presents a borderline situation par excellence for the affected and involved. For the patient’s caretaker, it is very important during this phase to address these thoughts, to accept without sanctioning them, and above all to point out that they are the logical consequence of the will to survive and thus something that all other waiting patients hold in common. Precisely during this phase, patients show their actual endurance to the transplant team. The waiting period should therefore, from the viewpoint of the patient’s condition, be seen as an extension of the selection process, in which above all frustration tolerance and compliance are shown as predictors of a successful operation.
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From the patient’s point of view, primarily, one question dominates: “Will I even survive the transplantation?” The symbolic meaning of a heart is during this phase usually not as important; any projected ideas about the personality of the donor are repressed in order to keep fear and tension from escalating. “Who” is therefore less important than “when.”
Partners and Spouses During the waiting period for a donor heart, patients’ spouses feel fully responsible for the well-being of the patient; parallel to the doctors’ efforts, they also strive to keep the patient alive and to keep any harmful influences away. The patient stands at the center of attention; any activities, emotions, or information are measured by how good or bad they might be for the patient. Relatives place their own concerns, burdens, and feelings at a distance. Even illnesses in the family circle (e.g., of children) are perceived not as a personal catastrophe, but as a threat to the physical and psychological stability of the transplantation candidate. Indeed, wives filter all incoming information in the sense of preventing any exciting or troubling information from reaching the partner: newspapers are read to the patient and censored, and family difficulties are kept silent (“I think of every answer before I talk”). At the same time, above all, wives feel responsible for the physical well-being. In many cases, they take control over what the husband hears or says, and they observe his behavior, his wake-sleep rhythm, and his breathing at night. Despite this enormous burden, they think that they should not show any signs of exhaustion or being overwhelmed; instead, they feel responsible for giving their partner strength, energy, and attention. Many wives confirm after the waiting period is over that they could not have endured the weeks and months had they not been conscious of the fact that it was a temporary condition and that, after a successful transplantation, everything could return to normal. Mishel and Murdaugh (1987) observe succinctly concerning the waiting period: “Patients benefit, partners suffer.” Patients also benefit from the partners’ symbiosis and from being completely cared for, while partners suffer from losing connection with themselves. Any form of private life appears unjustifiable. This ambivalence consisting of dependency, irritability, and anger often results in feelings ranging from tension to animosity on the side of the patient. Wives often complain that they could not please their husbands: if they cared for them, they were seen as overbearing and mothering; if they were less caring, they were seen as cold and unable to sympathize. The longer the patient waits for a heart transplant, the more negative the impact is on the spouse’s life (Collins et al., 1996). According to Haugh and Salyer (2007), tolerating uncertainty was the main theme describing perceptions of the time spent waiting. Partners of organ recipient candidates often want the waiting period to be a time of closeness, one that could perhaps be the last, while the patients tend to withdraw. Merely surviving requires the greater part of their physical and psychological energy, and the necessary emotions are detracted from the partner. Contact with the clinic and the transplant team is often attended to by many spouses, becoming more
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important than the private partnership. During this time, which seems predisposed for the greatest possible closeness, women experience their husbands “like a wall that they come up against again and again.” They experience a time of loneliness, feeling pushed away, misused as a nurse; they suffer from the mood swings of their husbands, who seem to find the closeness unbearable, without being able to show anything resembling aggression (“we can’t afford to have an argument”). During this time of acute heart failure, many partnerships experience a reversal of roles and tasks in which women take on traditionally male roles, above all with regard to earning a living and “men’s agendas” such as carrying suitcases, shoveling snow, or managing household contractors. For many women, this change means, after the initial orientation phase, a boost to their personalities, an affirmation, increased trust in one’s own hitherto unrecognized abilities, and more contacts outside of the family. For the patient, this phase brings with it a decrease in feelings of worthiness, a threat to male identity, a diminished social status, as well as fewer contacts outside of the family. The patient’s depression, fear, and distancing from the partner are therefore understandable.
The Postoperative Period Patients When patients, “winners of the organ donor lottery,” have received a new heart and withstood the surgery well and without complications, there begins, despite all postoperative discomfort, a phase of absolute well-being and relief: the donor heart came just in time; the worrisome physical symptoms of angina pectoris and shortness of breath are now gone; gone are the torturous feeling of helplessness, inability to react, and dependency on fate. In this euphoria, any kind of setback seems unthinkable; victory over death is wonderful; the possibility of the transplant being rejected is repressed; unrealistic feelings of invulnerability, of absolute feasibility of all things are all pushed into the forefront of thought, feeling, and behavior. Feelings of being “reborn,” of “the chance for a second life” fully overshadow all circumstantial conditions. This phase of high hopes, which lasts a few days, mostly until leaving the ICU, should be seen merely as a circumstance of the operation, which goes away on its own and makes room for a realistic assessment of the situation. However, this favorable mood breaks up the minute complications in the recovery process occur, if the routine biopsy indicates a rejection of the donor heart. Patients are thus mercilessly shown that the success of the operation is in no way guaranteed, that the fight for life is not over yet, that death continues to be a reality. The fear, uncertainty, dependency, and despair of the preoperative phase returns, accompanied by depression. One must suddenly acknowledge one’s own mortality. The presentation of rejection crises now finally eradicates the idea that everything will be wonderful and uncomplicated from now on. The uncertainty of the future must now be slowly and painfully accepted as a reality.
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It presents enormous mortification to the patient when the body rejects the new, healthy heart that is so very necessary for survival. The patient experiences their “self” and their body as separate, divided, as disparate beings with opposing desires, and the patient is angry with the body. This splitting of the body from the person presents a great threat to identity and massive stress precisely for those patients who were able to use or abuse their bodies as they wished up until the illness emerged. They are mostly shocked to experience for the first time that: it is not I that has a body, but a body that has ME; my needs and desires have no influence on it. Some patients imagine in their reaction to the heart rejection that the heart does not want them (“the heart is rejecting me”). Not only the confrontation with one’s own reaction to rejection presents a jolt to the patient’s self-confidence; it is also experiencing others’ crises of rejection and the death of another heart transplantation patient. This is, for the group of transplant patients, not only a tragic personal loss, but it also represents a “surrogate death” for the survivor (“I could be next”). The optimism of the group disappears, and often, this effectuates the patients’ retreat from the family and from group activities with other patients. If another patient’s heart rejection comes soon after a successful transplantation, usually selective coping mechanisms are adopted, above all denial (“he died because he didn’t have a good match, but I have a good match and so will I live”). These mechanisms become weaker if the patient’s own rejection or that of a co-patient comes first after a long period, often manifesting itself years after the operation. Questions of life expectancy are the primary topic of conversation among the group of survivors. Psychological support on the part of the family as well as the transplant team is of great importance during this crisis period. If the rejection crisis is brought under control using medication and if the new biopsy confirms the standstill of the process, patients learn that any further complications that may arise or difficulties in the recovery process can be treated and are not a pronouncement of death. In many cases, a rejection crisis that has been overcome strengthens the patient’s compliance to a significant degree. During this time, the patient is grateful for any positive attention, be it from a nurse or through conversations with others; patients experience emotional security and support which is needed in this state of fragile balance. In a course of recovery without complications, in these first days, the emotional climate of the transplantation unit can be described as cheerfully relaxed and could correspond with the atmosphere of a maternity ward.
Spouses After successful transplantation, patients stand clearly at the midpoint; naturally, all possible care available from the hospital staff is directed at them. After a good operational result, the patient is in a state of euphoria, feels a return of energy, and is happy to have lived until the operation and survived the operation. In contrast to
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the patient, the spouse is aware of the threat of a health setback, which can happen at any time, and it is difficult to speak with someone who appears to confront objective reality in an entirely uncritical way. Spouses feel that it is now more difficult to communicate their feelings and fears with the patient, and they look for other ways to alleviate their fears, above all in the wish for detailed conversations with the members of the transplant team, the doctors, nurses, and psychologists. While the patient thus requires full attention, the spouse feels liberated from the burden of symbiosis and the ambivalence that results from it. However, it is also a time of mixed feelings for spouses and partners. The energy-draining balancing act between the fear of the partner’s death and the hope for a continued life together has ceased for the moment. And yet, the healthy partner is both physically and psychologically exhausted and depleted from the event of the last weeks or months. In an ideal case, as often suggested by the psychologists of the team, spouses talk together about the hardship surrounding the waiting period, in which it is liberating above all for the healthy partners, in the sense of a catharsis, to be able to speak for the first time about their own difficulties, desires, and fears during the waiting period, which the partner would not have dared to express before. The period of the patient’s hospital treatment is in general a time of closeness for the couple. The burdensome waiting period is now in the past; plans for the future are made—for a future that should bring only good things, making up for the hardship of the past months.
Discharge from Hospital As usual, when a phase is completed, so is the discharge from medical treatment into the home environment felt ambivalently. Expectation, excitement, and curiosity are present as are guilt, fear of what is to come, and a feeling of a changed physical existence. Above all the dependent, regressive patients show a fear of exchanging the security of the hospital with the demands of everyday life. Back home in the family, it is expected that the patient returns to them happy and satisfied. The individual patient usually does not feel that way. It is disturbing that the approaching release should be a cause for celebration, which is expected by everyone, yet, it is not the case. On the contrary, the strong ambivalence regarding hospital discharge often results in a depressive phase, which is often very confusing for the relatives and dependents of the patient. The protected environment of the hospital, which makes no great demands of the patient, is often equally desirable as life in the family after giving up all of the advantages of the ill patient’s role. Clearly, more anxious are those patients for whom complications suddenly arise in the course of their hospital stay, which can be overcome through the rapid help of a doctor (i.e., blood pressure crises, fever, infections). During this time of ambivalence, it is especially the contact with former transplantation patients that is very helpful. They can serve as “models” and direct the ambivalence in the direction of positive anticipation and therefore weaken the ambivalence.
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Finally, one must not forget that the separation from the hospital goes both ways. Not only does the patient have to part and again assume a large degree of independence, but also the patient’s caretakers must let him or her go. It is often not easy for the hospital personnel to release the thankful, dependent patient and with this the influence that they have had in the life of the transplant patient. In fact, the patient’s self-confidence is very dependent on the trust and confidence that the caretakers place in the patient and his or her abilities, particularly at this time.
The First Postoperative Year The first postoperative year is a time of reorientation with all of the positive and negative circumstances that occur. Many patients enjoy the very special interest that is taken in them through their transplantation history. Their self-confidence rises to the degree that they realize they have something to offer that immediately commands the attention of all those surrounding them. The identity of the patient consists in the self-definition as, first, a heart transplant survivor, and then, much further down the line, all other things, for example, father, teacher, and husband. Commonly, in the majority of the patient’s conversations, a description arises of the operational procedure with dramatically embellished details. The patient’s crisis begins after a few weeks or months when the initial curiosity in their circle has worn off, when there are fewer visits, and when relatives and friends do not want to hear any more stories of the operation and the fact of the heart transplantation is no longer a sensation. Christopherson and Lunde (1971) report in this context about a patient, who telephoned in round-robin fashion the deans of his children’s schools, announcing “This is Jack Doe, heart transplant—Jane’s father. I just wanted to catch up on how she is doing.” The other side of the coin shows patients who would rather keep the fact of their transplantation a secret from everyone who may view this condition not as a merit to an individual, but as a stigma. “My boss gets dramatic when he talks about the transplant. I’d rather talk about football,” quotes Christopherson (1987) from one of these patients. During these first few months at home, the patient realizes those things that had perhaps been acknowledged in the weeks and months prior, however, which could not be appreciated in their extent, their degree of difficulty, and in their meaning. Typically, patients experience at this time, during which they want to enjoy their newly won endurance capacity, the first unsettling or at least irritating side effects of the medication therapy: women complain of heavy growth of hair on their faces, arms, and legs, and they begin the battle against it with creams and razors; patients are often called into the clinic for a necessary control of their hemogram and must wait for long periods; they suffer from the distortion of facial features and their hands shake. Christopherson and Lunde (1971) quotes pointedly in this reference to a patient: “I know they said I’d develop acne, but are you sure they meant this acne?” Mainly, the severe forms of side effects from medication or the increase thereof shows patients bitterly that, through transplantation, they have only temporarily exchanged one kind
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of problem for another. Disappointment, fear, and regret with regard to the quality of life become noticeable; a lifelong dependency on the clinic team now first becomes clear. At this stage, interventions to improve medication adherence should be established (Dew & Dimartini 2005, 2007; De Bleser et al., 2009). A further demand on the patient is the rethinking of the roles and the distribution of chores within the family, whereby giving up the role of the sick person means the withdrawal of attention, care, and privileges. Furthermore, patients must rejoin those groups in which they had been members before their illness or the worsening of their health condition: this applies to, for example, schools, workplace, sports clubs, and social groups. Especially, the reintegration into working life is a test of the patient’s strength since the majority of all heart patients have an important source of self-confidence precisely in their professional life. Some employers are not unhappy about the separation from an employee about whose abilities they have only a vague or even a negative impression. “Employers are terrified,” reports Rodgers (1984), “that a heart transplant will suddenly be rejected in the middle of the factory floor and explode out of the chest.” This cleft between that which the patient would like to achieve and that which they are estimated to be capable of is often crucial and leads to phases of hopelessness, depression, and withdrawal the more the patient senses disapproval and rejection. Along with these and other difficulties, patients experience a quite positively esteemed transformation in the world of values: they are more conscious of their experiences, which are more intense than before; they have learned to enjoy themselves; they set new priorities and change their measure of values. The striving for achievements, prestige, and status is given up; life itself becomes the highest value. Although all patients hope for it, a long life is not of foremost importance, but rather, having the best possible existence, a good quality of life. After rehabilitation, successful transplant patients have feelings of gratitude toward their donor and the doctors, and they want to give back the goodness that they have been shown by staying in contact at all times with those waiting for an organ donation. Thus, for example, in every province of Austria, there are former patients who, immediately after being contacted, get in touch with another patient and usually visit them during and after their operation and offer support.
Spouses The first preoperative year is usually a time of reorientation. Mishel and Murdaugh (1987) call their work on the cardiac transplantation’s effect on the family “redesigning the dream.” When former patients, after completion of rehabilitation, are actively and positively brought back into the domestic environment, they experience that the ideal of a future without problems is unreal. Wives are usually not willing to quickly give up the roles and tasks that they had to take on during the period of their spouse’s severe illness, from which they have also drawn a number of personal advantages – much to the irritation of the patient, who “left a housewife
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and returned to find a family manager,” as one patient described. Roles must be redefined, tasks newly distributed; a difficult path for the partnership begins just when the expectation from both sides is for nothing but happiness and contentment. This happiness – which can indeed also be a chance for the partners – in fact exists along with the other factors. Women report that they can now watch their partners for hours as they work in the garden, and they are simply happy that they are there: nothing is taken for granted anymore. Men say that they now enjoy time together as never before. Even something they would never have been caught doing before, such as window shopping, becomes something fun to do. Hand in hand with the pleasure of having had a successful operation, there is, however, also the recognition that the patient in many cases is no longer the same as before cardiac failure. Above all, women speak of their husbands as coming undone, having a limited tolerance for frustration, being irritable, and having bouts of aggressiveness, egocentric behavior, and demanding loyalty. The problems of the waiting period again emerge: the men wish to be cared for, yet they cannot bear their wives’ care. With the recognition of the changes in the partner’s personality, the spouse again beings close observation and control (“because she knows that that drives me crazy, she does it behind my back. She spies on me, knows if I take my medication, etc. That really drives me crazy,” one patient reports). Life with a completely unpredictable future must be recognized and assumed as such. Thus, it is typically the healthy partner who looks for security in order to be prepared for the uncertain future. Of decisive importance for women during this phase are children, their own professional employment, and finances. Patients on the other hand tend to look for challenge. They see primarily the possibilities of a “second chance” and dive fully into activities they had hardly done before. It appears as if the patients were trying to convince both themselves and all others of their total health. Mood swings and discord are only too willingly attributed completely to the partner’s behavior. This new discrepancy in the desires for the future – security versus challenge – brings new problems for the partnership. Thus, the success of the heart transplantation should be seen, with regard to the participation of the family of the transplant, not only from the narrow view of the patient and his/her convalescence but also with regard to the postoperative family situation. Shapiro (1990) describes in particular the effect on the family that such an intrusive event as a heart transplantation has: “You cannot overemphasize the toll the transplant process takes on even the most committed and recourceful family.” The end of the first postoperative year is for most of the patients and their families a caesura; they celebrate on the anniversary of the transplantation their “first birthday.” The probability of a rejection reaction becomes ever more minimal; the radius of activity continually expands and mobility increases (Bunzel et al., 2002). After the 1-year examination, checkups can continue at the clinic in ever greater time segments; there are no longer routine biopsies. The battle for life seems to have been won for now, but the fight to live a full and fulfilled life continues. Every phase of a transplantation story has its specific problems and presents the patients with different tasks. The following table (Table 7.1) shows the phases of the transplantation process and its emotional correlates, summarized in review.
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Table 7.1 Phases of the transplantation process and its emotional correlates Phases of the transplantation process Emotional correlates Announcement of the transplantation Shock, denial, disbelief, fear, withdrawal; fear of death vs. hope of longer life with a good quality of life Selection as organ recipient Anxiousness, relief, and hope after being selected Depression, frustration, and hopelessness if not selected Waiting period Ambivalence regarding the decision, fear of dying before the donor heart arrives, guilt and shame (recipient – donor problematic), impatience, frustration, tension, reactive depression Early postoperative time Euphoria, relaxation, relief, fragile psychological balance; disappointment with postoperative complications (“nonevents”) Rejection crises Fear, uncertainty, feelings of dependency and disappointment, aggression, discouragement Postoperative stationary period Self-confidence, pride, fear of setbacks, intensive self-observation (hypervigilance) Release from the hospital Ambivalence – anticipation/fear First postoperative year Reorientation, adaptation (difficulty with adaptation!), change or shift of values, crisis in the partnership
Living with a Ventricular Assist Device (VAD) Ventricular assist devices (VAD) are used as invasive treatment options for patients with terminal heart failure, who are at impending risk of death before donor heart availability. If patients’ physical status deteriorates dramatically during the waiting period, or the surgeons could not accept the current risk of transplantation, clinicians implant an “artificial heart.” This device supports the failing circulation in either a pulsatile or a nonpulsatile way and bridges the patients to transplantation while fully or at least partially mobilized. Left ventricular assist devices (LVAD) are blood pumps that are connected to an external controller and rechargeable battery packs. Patients on these devices can be fully mobilized and are discharged to their homes while waiting for cardiac transplantation. These systems provide the benefit of freedom to move and maintain a good quality of life. Due to its size, the pump can be implanted intra-abdominally, and a cable is led through the skin. Next generation continuous flow axial pumps produce a low-pulsatile blood flow pattern. These pumps are completely noiseless and do not produce a palpable pulse. Biventricular assist devices (BiVAD) are pulsatile assist devices. Transparent inflow and outflow cannulae are connected to paracorporeal (external) pneumatically driven ventricles with a portable driving console about the same size as a small suitcase. Patients can see their own blood being pumped by these artificial ventricles, which might lead to some discomfort. In our hospital, patients on BiVAD were usually not discharged; only short out-of-hospital excursions under supervision were possible. Major severe complications of such support systems are right heart failure (LVAD), bleeding, renal failure, infection, and cerebrovascular accidents (Rose et al., 2001).
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It has been clinically proven that these devices substantially reduce short-term mortality and morbidity, and provide suffering patients with quite a good quality of life during the waiting time (Grady et al., 2003, 2004; Dew et al., 2001). However, the same technical environment with its range of restrictions that serves as a lifesaving intervention can lead, on the other hand, to physical and emotional stress. Many VAD recipients had no other choice to survive but to accept a mechanical device that apparently replaced their heart and dramatically changed their body schema. Furthermore, the fact that physicians and technicians manipulate control buttons that affect the patients’ blood pressure, heart frequency, and nonautonomous body sensations is experienced by patients and spouses alike as fear inducing. Studies to pinpoint psychosocial implications and psychiatric morbidity associated with these devices are important yet scarce. Dew et al. (2000) state that despite the positive perceptions held by the majority of the patients, up to 55% indicated that they had concerns and worries about specific aspects of living with this device. The prevalence of most concerns rose with the duration of VAD support. Shapiro et al. (1996) report a variety of burdens following implantation and identified major depression, organic mental syndromes, and serious adjustment disorders as the most commonly required psychiatric interventions. With increased VAD duration, neuropsychiatric factors can be expected to play a large role in determining quality of life and outcome both before and after heart transplantation. Accordingly, Petrucci et al. (1999) describe VAD patients in their study on psychiatric morbidity as a “vulnerable cardiac end-of-life group” and a “fragile patient population.” However, severe, life-threatening illness followed by high technology support and heart transplantation affects not only the lives of patients but also their whole family, especially spouses, and could represent a traumatic event also their lives. Authors reported a variety of family crises and a high degree of family caregiver burden following implantation of a mechanical circulatory support system as a bridge to transplantation (Dew et al., 2000; Shapiro et al., 1996; Savage & Canody, 1999). The prime objective of our study (Bunzel et al., 2007) was to investigate the psychosocial consequences of the implantation of a ventricular assist device followed by heart transplantation in patients and their spouses. As there is evidence that VAD implantation meets all the criteria for posttraumatic stress disorder (PTSD), we might assume that symptoms of PTSD are present in this group, even many years after operation. Furthermore, as PTSD is defined not only as “experiencing” but also as “witnessing an event that involves threat to physical integrity of another person, or learning about such events experienced by a family member,” we could assume that not only the patients but also the spouses may later show symptoms of PTSD. Finally, we want to learn more about the fears and concerns of patients and spouses when the patient is connected to the device: are they uniform in both groups? Our study cohort comprised 38 patients (36 male) and 27 spouses (26 female) 6 to 136 months posttransplant. The results of our study were striking: none of the patients met the criteria for PTSD. There might be some reasons for the absence of PTSD in (male) patients, including that experiencing that one’s own heart is to a large extent replaced by a machine does not necessarily constitute a traumatic event, or that it was not of such a disastrous nature to lead to PTSD, or, if there were PTSD
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symptoms in patients, they did not remain in the long run. Furthermore, having a psychotherapist provide daily psychological support to our patients might mean that completely normal stress reactions are given immediate treatment and consequently do not turn into full-blown psychiatric disorders like PTSD. Quite the contrary was true for the spouses. In contrast to patients who did not suffer from a stress-related disorder (at least not in the long term), 26% of spouses – a very heterogeneous group regarding age, marital status, and place of residence – definitely show symptoms of PTSD, even many years after their partner’s terminal illness, VAD implantation, and transplantation. The amount of time elapsed does not seem to have any impact. We also could suppose that the existence of PTSD symptoms in spouses may also be ascribed to communication deficits. Only 40% of the spouses of VAD patients agreed with the statement: “I was adequately prepared for what to expect.” Overall, we must conclude that spouses of patients with terminal illness and life-saving operations can suffer psychological trauma even if they are not physically injured themselves. This fits well in the concept of learned helplessness which is believed to trigger depression and anxiety and can become manifest in PTSD. It is not the event itself that is traumatizing, but one’s own helplessness. With respect to fears and concerns relating to VAD implantation, our findings correspond perfectly to the PTSD results: again, partners of patients did worry considerably more than patients themselves. They worried more about device malfunction or failure and were more afraid of infection and pain than the patients afflicted by these problems. They worried twice as much as the patients themselves about the danger of stroke, perhaps because they knew the burden of caring for a patient suffering from the consequences of a stroke. These results show that patients considered the most adverse effects of VAD implantation to be inconveniences, for example, noise and sleep disturbances. On the other hand, their spouses were far more concerned about life- and death-related problems such as device malfunction or failure, stroke, and infection. Dew et al. (2000) also investigate the concerns of patients who had had a VAD system and their primary family caregivers retrospectively in semistructured interviews. The main worries were worries about the danger of getting an infection, about difficulty sleeping due to the position of the driveline, and about device malfunction. Interestingly, and in contrast to our findings, only about 20% of their patients worried about having a stroke (in our study, 52%) – a substantial risk and realistic danger in this population with poorer prognosis due to anticoagulation-induced cerebral bleeding. In conclusion, both studies revealed that spouses had turned out to be most afflicted with psychological stress and needed at least the same amount of emotional support as the patients themselves, including counseling and treatment offers. We may close this chapter about psychological aspects of heart transplantation with a quotation by the psychiatrist Peter Shapiro who wrote “Although cardiac surgeons may emphasize the operative procedure, it is what precedes and follows surgery that is, for patients and for others involved, the enduring focus of attention” (Shapiro, 1990). During this transplant process, we ask a lot from the patients, indeed. But we should not overlook that we ask the same, probably even more, from their spouses and caregivers.
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Acknowledgement This chapter was translated from German by Charlotte Eckler.
References Bernazzali, S., Basile, A., et al. (2005). Standardized psychological evaluation pre- and posttransplantation: A new option. Transplantation Proceedings, 37(2), 669–671. Bunzel, B., Laederach-Hofmann, K., et al. (2002). Survival, clinical data and quality of life 10 years after heart transplantation: A prospective study. Zeitschrift für Kardiologie, 91(4), 319–327. Bunzel, B., Laederach-Hofmann, K., et al. (2007). Mechanical circulatory support as a bridge to heart transplantation: What remains? Long-term emotional sequelae in patients and spouses. The Journal of Heart and Lung Transplantation, 26(4), 384–389. Bunzel, B., Titscher, G., et al. (1991). “You need a new heart”. The problem of diagnostic disclosure from the viewpoint of the affected cardiologic patient. Psychotherapie Psychosomatik Medizinische Psychologie, 41(11), 419–428. Bunzel, B., Wollenek, G., et al. (1992a). Living with a donor heart: Feelings and attitudes of patients toward the donor and the donor organ. The Journal of Heart and Lung Transplantation, 11(6), 1151–1155. Bunzel, B., Wollenek, G., et al. (1992b). Psychosocial problems of donor heart recipients adversely affecting quality of life. Quality of Life Research, 1(5), 307–313. Christopherson, L. K. (1987). Cardiac transplantation: A psychological perspective. Circulation, 75(1), 57–62. Christopherson, L. K., & Lunde, D. T. (1971). Selection of cardiac transplant recipients and their subsequent psychosocial adjustment. Seminars in Psychiatry, 3(1), 36–45. Cimato, T. R., & Jessup, M. (2002). Recipient selection in cardiac transplantation: Contraindications and risk factors for mortality. The Journal of Heart and Lung Transplantation, 21(11), 1161–1173. Collins, E. G., White-Williams, C., et al. (1996). Impact of the heart transplant waiting process on spouses. The Journal of Heart and Lung Transplantation, 15(6), 623–630. De Bleser, L., Matteson, M., et al. (2009). Interventions to improve medication-adherence after transplantation: A systematic review. Transplant International, 22(8), 780–797. Dew, M. A., & DiMartini, A. F. (2005). Psychological disorders and distress after adult cardiothoracic transplantation. Journal of Cardiovascular Nursing, 20(5 Suppl), S51–66. Dew, M. A., & Dimartini, A. F. (2006). The incidence of nonadherence after organ transplant: Ensuring that our efforts at counting really count. Liver Transplantation, 12(12), 1736–1740. Dew, M. A., DiMartini, A. F., et al. (2007). Rates and risk factors for nonadherence to the medical regimen after adult solid organ transplantation. Transplantation, 83(7), 858–873. Dew, M. A., Kormos, R. L., et al. (2000). Human factors issues in ventricular assist device recipients and their family caregivers. ASAIO Journal, 46(3), 367–373. Dew, M. A., Kormos, R. L., et al. (2001). Quality of life outcomes after heart transplantation in individuals bridged to transplant with ventricular assist devices. The Journal of Heart and Lung Transplantation, 20(11), 1199–1212. Favaloro, R. R., Perrone, S. V., et al. (1999). Value of pre-heart-transplant psychological evaluation: Long-term follow-up. Transplantation Proceedings, 31(7), 3000–3001. Freeman, A. M., III & Watts, D., et al. (1984). Evaluation of cardiac transplant candidates: Preliminary observations. Psychosomatics, 25(3), 197–199, 202–203, 207. Frierson, R. L., Tabler, J. B., et al. (1990). Patients who refuse heart transplantation. The Journal of Heart Transplantation, 9(4), 385–391. Grady, K. L., Meyer, P. M., et al. (2003). Change in quality of life from after left ventricular assist device implantation to after heart transplantation. The Journal of Heart and Lung Transplantation, 22(11), 1254–1267. Grady, K. L., Meyer, P. M., et al. (2004). Longitudinal change in quality of life and impact on survival after left ventricular assist device implantation. The Annals of Thoracic Surgery, 77(4), 1321–1327.
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Haugh, K. H., & Salyer, J. (2007). Needs of patients and families during the wait for a donor heart. Heart & Lung, 36(5), 319–329. Herrick, C. M., Mealey, P. C., et al. (1987). Combined heart failure transplant program: Advantages in assessing medical compliance. The Journal of Heart Transplantation, 6(3), 141–146. Kuhn, W. F., Davis, M. H., et al. (1988). Emotional adjustment to cardiac transplantation. General Hospital Psychiatry, 10(2), 108–113. Levenson, J. L., & Olbrisch, M. E. (1993). Psychosocial evaluation of organ transplant candidates. A comparative survey of process, criteria, and outcomes in heart, liver, and kidney transplantation. Psychosomatics, 34(4), 314–323. Mishel, M. H., & Murdaugh, C. L. (1987). Family adjustment to heart transplantation: Redesigning the dream. Nursing Research, 36(6), 332–338. Petrucci, R., Kushon, D., et al. (1999). Cardiac ventricular support. Considerations for psychiatry. Psychosomatics, 40(4), 298–303. Rivard, A. L., Hellmich, C., et al. (2005). Preoperative predictors for postoperative problems in heart transplantation: Psychiatric and psychosocial considerations. Progress in Transplantation, 15(3), 276–282. Rodgers, J. (1984). Life on the cutting edge. Psychology Today, 18(10), 58–67. Rose, E. A., Gelijns, A. C., et al. (2001). Long-term mechanical left ventricular assistance for end-stage heart failure. The New England Journal of Medicine, 345(20), 1435–1443. Savage, L. S., & Canody, C. (1999). Life with a left ventricular assist device: The patient’s perspective. American Journal of Critical Care, 8(5), 340–343. Shapiro, P. A. (1990). Life after heart transplantation. Progress in Cardiovascular Diseases, 32(6), 405–418. Shapiro, P. A., Levin, H. R., et al. (1996). Left ventricular assist devices. Psychosocial burden and implications for heart transplant programs. General Hospital Psychiatry, 18(6 Suppl), 30S–35S.
Part II
Psychological Interventions for Cardiac Patients
Chapter 8
Anxiety and Depression: Risk Factors for Cardiovascular Disease Angelo Compare, Riccardo Proietti, Elena Germani, and David Janeway
Introduction Coronary heart disease (CHD) is the leading cause of death worldwide, accounting for around 16.7 million deaths each year, mainly from heart attacks and strokes. Furthermore, this number is predicted to increase to approximately 25 million deaths by 2020 if current trends continue. Yet fatalities represent only the tip of the iceberg; the greater burden of cardiovascular disease, affecting an estimated 128 million people, is attributable to nonfatal cardiovascular events and their long-term consequences. Though there are well-accepted national guidelines for the primary and secondary prevention of cardiac illness, far less attention has been paid to the impact of psychological risk factors on cardiovascular disease. Nonetheless, there is compelling evidence that psychological risk factors confer equal and, in some cases, greater risk than other traditional clinical risk factors (Kubzansky & Kawachi, 2000; Rozanski, Blumenthal, & Kaplan, 1999). In patients with ischemic heart disease, anxiety and depression are predictive of adverse short- and long-term outcomes (Barefoot et al., 1996; Jiang et al., 2001). Patients who have anxiety or depression during hospital admission are at increased risk for higher rates of in-hospital complications such as recurrent ischemia, reinfarction, and malignant arrhythmias (Janszky, Ahnve, Lundberg, & Hemmingsson, 2010; Zuidersma, Thombs, & de Jonge, 2011). They also suffer higher mortality A. Compare, Ph.D. (*) Department of Human Sciences, University of Bergamo, Bergamo, Italy e-mail:
[email protected] R. Proietti, M.D. Cardiac Electrophysiology Laboratory, Luigi Sacco Hospital, Milano, Italy E. Germani, Psy.D. Centro Diagnostico Italiano, Milano, Italy D. Janeway, M.D. Department of Psychiatry, New York Medical College, Valhalla, NY, USA E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_8, © Springer Science+Business Media, LLC 2012
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and reinfarction rates months to years after their initial cardiac event (Janszky et al., 2010; Nabi et al., 2010; Watkins et al., 2010; Whang et al., 2010). Failure to understand and address psychological risk factors for CHD events may be one reason that CHD morbidity and mortality remain so high. Anxiety disorders and depression are among the most prevalent psychiatric disorders (Kubzansky, Kawachi, Weiss, & Sparrow, 1998). Given the prevalence of anxiety and depression in the general population and in patients with CHD, the potential public-health impact for preventing the development and progression of CHD by appreciating the nature of the relationship between anxiety, depression, and CHD is enormous (Moser & Dracup, 1996). Thus, it is clinically relevant in patient with cardiovascular disease to assess the patient’s psychological profile and treat the emotional conditions that confer an increased risk for major adverse cardiovascular events.
Anxiety Anxiety is a negative affective state resulting from an individual’s perception of threat and characterized by a perceived inability to predict, control, or gain the preferred results in given situations (Barlow, 1988). Anxiety is a distinct emotional experience that has cognitive, neurobiological, and behavioral components and that arises out of the interaction of an individual with the environment (Kubzansky et al., 1998) and involves a wide range of emotional and physical symptoms. Anxiety is considered an adaptive process until its magnitude or persistence renders it a dysfunctional response that can have negative consequences. Anxiety includes both emotional and physical symptoms (see Table 8.1). Physical symptoms of anxiety are often indistinguishable from cardiac symptoms (e.g., increased heart rate, muscle tension, sweating), and so, it is not surprising that many people admitted to the emergency room with chest pain are often diagnosed with panic disorder Table 8.1 DSM-IV conditions that include anxiety Anxiety disorders DSM-IVa Other DSM-IV conditions with anxiety Generalized anxiety disorder Somatization disorder Panic disorder w/or w/o agoraphobia Hypochondriasis Specific phobia Pain disorder Social phobia Sleep disorder Obsessive-compulsive disorder Eating disorder Substance-induced anxiety disorder Sexual disorder Posttraumatic stress disorder Adjustment disorders Acute stress disorder ADDb and ADHD Anxiety due to a general medical condition Mood disorders/bipolar disorder Agoraphobia w/o history of panic disorder Factitious disorders Anxiety disorder NOS (anxiety disorder not Personality disorders otherwise specified) a Diagnostic and Statistical Manual of Mental Disorders, 4th edition, American Psychiatric Association, Washington, D.C., 1994 b Attention-deficit disorder and attention-deficit/hyperactivity disorder
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(see Table 8.2). The prevalence of anxiety has been estimated to be as high as 70–80% among patients suffering an acute cardiac event and chronically persists in about 20–25% of individuals with CHD (Moser, Mckinley, Riegel, Doering, & Garvin, 2002). Phobic anxiety refers to fears about things such as enclosed spaces, traveling in crowds, or contracting an incurable illness; it has been found associated with an almost fourfold increase in the relative risk for fatal myocardial infarction (Haines, Imeson, & Meade, 1987) (see Table 8.3). This observation has received confirmation in a much larger study, on subjects with no prior history of CHD, where a doseresponse relationship was found between phobic anxiety and coronary heart disease mortality (relative risk, 2.5, 95%; confidence interval, 1.00–5.96) (Kawachi, Sparrow, Table 8.2 Symptoms of anxiety Emotional symptoms of anxiety • Anticipating the worst • Feeling like your mind has gone blank • • • • • •
Feeling tense and jumpy Feelings of apprehension or dread Irritability Restlessness Trouble concentrating Watching for signs of danger
Physical symptoms of anxiety • Fatigue • Frequent urination or diarrhea • Headaches • Insomnia • Muscle tension • Pounding heart • Shortness of breath • Stomach upset or dizziness • Sweating • Tremors and twitches
Table 8.3 Anxiety disorders Panic disorder Panic disorder is an anxiety disorder and is characterized by unexpected and repeated episodes of intense fear accompanied by physical symptoms. People with panic disorder have feelings of terror that strike suddenly and repeatedly with no warning According to the DSM-IV-TR, a panic attack is a period of intense fear or discomfort, developing abruptly and peaking within 10 min, and requiring at least four of the following: • • • • • • • • • • • • •
Chest pain or discomfort Chills or hot flushes Fear of losing control or going crazy Feeling dizzy, unsteady, light-headed, or faint Feeling of choking Derealization (feelings of unreality) or depersonalization (being detached from oneself) Nausea or abdominal distress Palpitations or tachycardia Numbness or tingling sensations (paresthesia) Sensations of shortness of breath or smothering Sweating Trembling or shaking Sense of impending doom (continued)
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Table 8.3 (continued) Phobic anxiety DSM-IV-TR delineates seven diagnostic criteria for specific phobia: •
•
• • •
• •
Significant and enduring fear of phobic stimulus: Patients with specific phobia display marked and enduring fear when they encounter a defined situation or object, the phobic stimulus Anxiety response to phobic stimulus: Patients with specific phobia display anxiety as soon as they confront the phobic stimulus. When they confront the phobic stimulus, a defined situation or object, patients with specific phobia may experience a panic attack related to the specific situation. Children may cry, cling, freeze, or display tantrums when they express their anxiety in the face of the phobic stimulus Recognition: Although adolescents and adults realize that their fear is unreasonable and disproportionate to the situation, children may not recognize that their fear is excessive Avoidance: Individuals with specific phobia avoid the phobic stimulus or endure it with deep distress and anxiety Impairment and distress: Individuals with specific phobia display avoidance, distress, and anxious anticipation when they encounter the phobic stimulus. Their avoidance reactions interfere with their daily functioning, or they express significant distress about having a phobia Duration: To diagnose specific phobia in a patient who is under 18 years of age, the duration of the disorder needs to be at least 6 months Not accounted for by another disorder: A diagnosis of specific phobia is assigned if the phobic avoidance, panic attacks, or anxiety related to the defined situation or object are not better accounted for by other disorders
Generalized anxiety disorder (GAD) According to the DSM-IV-TR, the criteria for GAD are as follows: •
•
•
•
•
Excessive anxiety and worry about a number of events or activities (such as work, school, family, health), occurring more days than not, for at least 6 months. Generally, “excessive” can be interpreted as more than would be expected for a particular situation or event. Most people become anxious over certain things, but the intensity of the anxiety typically corresponds to the situation The person finds it difficult to control the worry and often experience other related symptoms including restlessness, irritability, and muscle tension. If someone has a very difficult struggle to regain control, relax, or cope with the anxiety and worry, then this requirement is met The anxiety and worry are associated with at least three of the following six symptoms (with at least some symptoms present for more days than not, for the past 6 months): restlessness or feeling keyed up or on edge, being easily fatigued, difficulty concentrating or mind going blank, irritability, muscle tension, and sleep disturbance The symptoms are not part of another mental disorder. The focus of the anxiety and worry is not confined to features of an Axis I disorder, being embarrassed in public (as in social phobia), being contaminated (as in obsessive-compulsive disorder), being away from home or close relatives (as in separation anxiety disorder), gaining weight (as in anorexia nervosa), having multiple physical complaints (as in somatization disorder), or having a serious illness (as in hypochondriasis), and the anxiety and worry do not occur exclusively during posttraumatic stress disorder The symptoms cause clinically significant distress or impairment in daily life, in social, or in occupa-tional functioning. The disturbance does not occur exclusively during a mood disorder, a psychotic disorder, pervasive developmental disorder, substance use, or general medical condition
Anxiety reaction It is an anxiety disorder characterized by chronic free-floating anxiety and such symptoms as tension or sweating or trembling or light-headedness or irritability, etc., that have lasted for more than 6 months. Diagnostic and Statistical Manual of Mental Disorders, 4th edition, American Psychiatric Association, Washington, D.C., 1994
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Vokonas, & Weiss, 1994). However, after adjusting for other cardiovascular risk factors, the multivariate odds ratio for fatal coronary heart disease became nonsignificant (Kawachi, Colditz, et al., 1994). Anxiety can hinder psychosocial adaptation to CHD and physical recovery after an acute event and predicts poorer quality of life for CHD patients in the short and long term (Lane, Carroll, Ring, Beevers, & Lip, 2000, 2001). Patients who are too anxious frequently are unable to learn or act upon new information about necessary lifestyle changes (Rose, Conn, & Rodeman, 1994). Furthermore, anxious patients experience problems coping with challenges and anxiety adversely affects adherence and rehabilitation efforts. Persistent anxiety predicts worse disability, more physical symptoms, and poorer functional status in CHD patients (Sullivan, LaCroix, Spertus, & Hecht, 2000). Anxious CHD patients return to work slower or less often than nonanxious patients and have more problems resuming sexual activity after an acute event (Rosal, Downing, Littman, & Ahern, 1994). Patients with higher anxiety soon after acute myocardial infarction have a longer stay in the cardiac care unit and hospital (Lane et al., 2001), report sustained anxiety and long-term distress, suffer more symptoms regardless of the severity of their physical condition, consume more health-care resources (Mayou et al., 2000), and report a lower quality of life (Brown et al., 1999) than patients with lower anxiety. Perceived control may moderate the association between anxiety and medical complications that occur in the hospital (Moser et al., 2002). Though anxiety predicts risk for complications in acute myocardial infarction patients, the relationship is attenuated in patients with “high perceived control.” These findings imply that interventions that increase patient perception of control may help diminish the link between anxiety and poorer outcomes. Anxiety seems to be an independent risk factor for incident CHD and cardiac mortality. The most recent meta-analysis (Roest, Martens, de Jonge, & Denollet, 2010) of references (1980–2009) on prospective studies of nonpsychiatric cohorts of initially healthy persons, in which anxiety was assessed at baseline, has shown that anxious persons were at risk of CHD (hazard ratio, 1.26) and cardiac death (hazard ratio, 1.48), independent of demographic variables, biological risk factors, and health behaviors. This result shows an association between anxiety and incident CHD with a 26% increase in risk; moreover, anxiety is also specifically associated with cardiac mortality, with anxious persons having a 48% increased risk of cardiac death. These findings line up with those which demonstrate a significant association between anxiety and myocardial infarction (Jakobsen, Foldager, Parker, & Munk-Jorgensen, 2008) and panic disorder and CHD (Gomez-Caminero, Blumentals, Russo, Brown, & Castilla-Puentes, 2005; Walters, Rait, Petersen, Williams, & Nazareth, 2008). A recent Swedish 37-year longitudinal study (Janszky et al., 2010) which has investigated the long-term cardiac effects of depression and anxiety assessed at young age (18–20 years), according to International Classification of Diseases-8th Revision (ICD-8) criteria, has shown that anxiety is an independent predictor of subsequent CHD events. Hazard ratios associated with anxiety were 2.17 and 2.51 for CHD and acute myocardial infarction, respectively, against corresponding hazard ratios associated with depression of 1.04 and 1.03.
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Depression Major depressive disorder is an episodic clinical syndrome defined by symptoms such as depressed mood, anhedonia, sleep disturbance, psychomotor agitation or retardation, loss of energy, as well as other emotional and physical symptoms. Symptoms of depression usually develop over days to weeks, and an untreated episode of major depression can last up to 6 months. However, less severe clinical presentation is also often seen in the cardiac population, and while these less severe clinical presentations do not meet diagnostic criteria for depression, they have been linked to poorer prognosis after acute coronary syndrome. Prevalence estimates of depressive disorders in coronary artery disease patients range from 15% to 40% (Kop, 1999; Lesperance & Frasure-Smith, 2000). Despite the high prevalence, depression is underdiagnosed and, hence, frequently untreated in coronary artery disease patients (Hirschfeld et al., 1997). Untreated depression is of particular concern because depression is associated with a two- to sevenfold elevated risk of subsequent cardiac events, which is comparable to that of traditional cardiovascular risk factors such as hypercholesterolemia and hypertension (Lesperance & Frasure-Smith, 2000). The atypical clinical presentation of depression is an important factor in the underdiagnosis of depression among cardiac patients. Patients with medical disorders may be reluctant to disclose depressive mood symptoms because they believe their symptoms are normal reactions to a cardiac event. Some somatic symptoms of depression such as fatigue are in fact part of normal recovery from a cardiac event and should be treated accordingly (Kop & Ader, 2001). Considerable epidemiological evidence now shows a fairly reliable association between depression and CHD. The most serious consequence of depression in cardiac patients is cardiac mortality. Major depression following myocardial infarction is associated with a fourfold increased risk of cardiac mortality during the first year, and there is risk with minor forms of depression as well (Frasure-Smith, Lesperance, & Talajic, 1995a). The prognostic impact of depression is as large as, and independent of, other major prognostic factors, including ventricular dysfunction and the severity of coronary atherosclerosis. Additionally, Frasure-Smith and Lesperance (2003) reported that depressive symptoms predicted 5-year cardiac mortality in a large post–myocardial infarction sample, and, previously, Barefoot and colleagues (Barefoot et al., 1996) found that even after 10 years of a cardiac event, depressed patients have a greater risk of cardiac death than nondepressed patients. A more recent meta-analysis showed that depression was associated with a 46% increased risk of cardiovascular disease (Van der Kooy et al., 2007), with an impact of depression on cardiac death (55% increased risk) comparable to the impact of anxiety found in the following meta-analysis (Roest et al., 2010). From a clinical perspective, depressive and anxious symptoms frequently co-occur in the same patient. This suggests that depression and anxiety might also interact synergistically to affect CHD. Indeed, in a study by Phillips et al. (2009), subjects with both generalized anxiety disorder and major depressive disorder were at greatest risk of subsequent cardiac death.
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Depressive symptom dimensions after myocardial infarction (MI) may be differently related to prognosis. Somatic/affective (e.g., fatigue, sleep problems, and poor appetite) dimensions appear to be associated with a worse cardiac outcome than cognitive/affective dimensions (e.g., shame, guilt, and negative self-image). Specifically, somatic/affective symptoms of depression have been observed to be related to a higher Killip class and mortality during a 12-month follow-up period (Roest et al., 2011). These findings, which are in concordance with earlier studies (de Jonge et al., 2006; Martens, Hoen, Mittelhaeuser, de Jonge, & Denollet, 2010; Smolderen et al., 2009), put further light on possible behavioral pathways which could explain the relationship between depressive symptoms and prognosis in ACS patients via unhealthy behavior, like smoking, less compliance, unhealthy diet (van Melle et al., 2004), and lack of physical activity (Whooley et al., 2008). Negative mood may be a transient phenomenon for some patients after acute coronary syndrome, with studies reporting improvements in self-report measures of positive and negative mood after 3 months of cardiac rehabilitation (Denollet, 1993). It is notable, however, that almost one-third of patients have been found to develop clinically meaningful levels of depressive symptoms within a year following myocardial infarction (Lesperance, Frasure-Smith, & Talajic, 1996). In addition to developing depression in the months following MI, patients who are initially distressed may show limited improvement. Taken as a whole, these findings suggest that depression among myocardial infarction patients is a reactive, transient phenomenon for some, whereas for others, depression is more persistent (Mayou et al., 2000). Studies have generally found the prevalence of major depression among CHD patients to range between 16% and 23% (Musselman, Evans, & Nemeroff, 1998), with several investigations demonstrating higher rates of clinically meaningful depressive symptoms (Lane et al., 2001). Depression is substantially more prevalent among coronary artery disease patients than in the general population (estimates ranging from 2.3% to 9.3%) (Statistics, 2000). Among patients with coronary artery disease, higher rates of depression and subthreshold depressive symptoms are observed in patients with unstable anginal complaints, severe heart failure (Freedland et al., 2002), and those awaiting coronary artery bypass graft (CABG) surgery (Blumenthal et al., 2003). Case studies of myocardial infarction patients suggest that some degree of depressive symptoms may be expected, given that patients often report feeling guilty over potential lifestyle contributions to their disease and given that they experience difficulty adjusting to acute physical limitations (Ziegelstein, 2001). A growing body of research indicates that depression may be prospectively related to the development of CHD, rather than merely a consequence of an acute coronary syndrome event. A recent meta-analysis (Rugulies, 2002) of 11 prospective studies of initially healthy samples reported a dose-response relationship between depression severity and risk for CHD, with a lifetime clinical diagnosis of depression associated with greater risk (RR = 2.69) than depressive mood measured by self-report (RR = 1.49). In 2008, the American Heart Association recommended (and the American Psychiatric Association endorsed) that “screening tests for depressive symptoms should
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be applied to identify patients who may require further assessment and treatment” if appropriate referral for further depression assessment and treatment is available. Partly, in response to this advisory, Thombs and colleagues (Thombs, de Jonge et al., 2008) conducted a systematic review of the evidence that screening or treatment improves outcomes of depression or CHD in patients with CHD. They found no trial that tested if depression screening was beneficial in patients with CHD, and the randomized controlled trials of depression treatment provided evidence of only mild improvement of depression symptoms and no improvement in CHD outcome. Therefore, they questioned whether routine depression screening was appropriate. Depression has multifactorial causes, including genetic predisposition, history of distressing environmental challenges, and current psychological and biological precipitants. In coronary artery disease patients, both psychological and biological factors specifically related to the disease process may further contribute to the onset and maintenance of depression.
Hypothesized Pathways Linking Depression and Anxiety with Heart Disease The mechanism by which depression and anxiety increase cardiac morbidity and mortality is not well understood; however, the evidence suggests that behavioral and physiological mechanisms work together to mediate the relationship between anxious and depressive symptoms and CHD. Depressed and anxious individuals may take poorer care of themselves, pay less attention to diet, drink more alcohol, smoke more, have less motivation and energy to exercise regularly, be less likely to seek medical care, and have poorer adherence to a medical regimen, cardiac risk factor modification, and rehabilitation and exercise programs (Bonnet et al., 2005; Carney, Freedland, Rich, & Jaffe, 1995; Gehi, Haas, Pipkin, & Whooley, 2005; Lesperance & Frasure-Smith, 1996; Rieckmann et al., 2006). Individuals with depression have enhanced cortisol secretion, increased sympathetic activation, elevated plasma catecholamine levels, endothelial dysfunction, and elevated levels of inflammatory cytokines (Strike & Steptoe, 2004). Studies of ventricular ectopic activity, heart rate variability (HRV), and depression provide evidence that sympathetic activation is a mechanism for worse clinical outcomes in depressed cardiac patients. Ventricular ectopic activity has a stronger association with death in patients who were depressed (Frasure-Smith et al., 1995a; FrasureSmith, Lesperance, & Talajic, 1995b). Moreover, it has been observed that depressed patients have more activation of the hypothalamic-pituitary-adrenocortical and sympathetic adrenal medullary systems (Musselman et al., 1998). Other studies have found that in patients with depression, there is evidence of a low HRV (Miyawaki & Salzman, 1991; Miyawaki, Kawamura, Komatsu, & Yasugi, 1991). Patients suffering from depression have higher sympathetic tone and blunted inhibitory reflexes (Rechlin, Weis, & Claus, 1994). Sympathetic activation in turn
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can lead to higher levels of catecholamines, predisposing to vasoconstriction, a rapid heart rate, and platelet activation. Regarding anxiety, the additive effect of mental stress contributes to excessive sympathetic nervous system (SNS) activation and catecholamine release (Sirois & Burg, 2003). Moreover, symptoms of anxiety have been associated with reduced baroreflex sensitivity in cardiac patients: Baroreflex control for patients with acute myocardial infarction and high anxiety has been shown to be about 20% lower than for patients with lower anxiety (Watkins, Blumenthal, & Carney, 2002). Anxiety has been associated with progression of atherosclerosis (Paterniti et al., 2001), decreased heart rate variability (Martens, Nyklicek, Szabo, & Kupper, 2008), and risk of ventricular arrhythmias (van den Broek et al., 2009; Watkins et al., 2006). Research supports the risk of arrhythmias particularly in the case of phobic anxiety, with studies showing an association between phobic anxiety and sudden cardiac death but not with nonfatal MI (Albert, Chae, Rexrode, Manson, & Kawachi, 2005; Kawachi, Colditz, et al., 1994). The growth of the evidences supporting biochemical similarities between platelets and central nervous system neuronal monoamine systems, particularly in the uptake, storage, and metabolism of serotonin, has given rise to studies investigating the influence of depression on platelet reactivity in patients with CHD (Brydon, Magid, & Steptoe, 2006). Moreover, it has been demonstrated that patients with depression have higher levels of platelet factor 4, b-thrombomodulin, P-selectin, and increased activation of platelet glycoprotein IIb/IIIa receptors and increased serotonin-mediated platelet reactivity (Brydon et al., 2006). Though platelet function in patients with depression has been studied extensively, contrary to anxiety, it has been hypothesized that the pathogenic link between depression and CHD is based on serotonin-mediated platelet activation; however, the overall results are inconsistent (Parakh, Sakhuja, Bhat, & Ziegelstein, 2008). More recently, a study by Zafar et al. (2010) has examined, by a cross-sectional method, the effects of both depression and anxiety on platelet reactivity in a patient population with stable coronary artery disease. Findings show subjects who were both depressed and anxious had significantly higher serotonin-mediated platelet aggregation compared with depressed-only subjects and subjects without affective symptoms. Moreover, contrary to depression, anxiety symptom severity correlated significantly with serotonin-mediated platelet aggregation and activation and remained a significant predictor of serotonin-mediated platelet reactivity. Despite the limitations due to sample size and self-report inventories, an important point of strength of this study concerns the sample characteristics that reflects the clinical reality that depression and anxiety frequently coexist. The primary finding of this study shows the potential additive effects of these disorders on platelet reactivity, probably due to activation of both serotonergic and adrenergic signaling pathways. This additive effect is supported by other studies (Aschbacher et al., 2008; Barton et al., 2007). On the basis of this data, Wittstein (2010) hypothesizes potential mechanisms of biological pathways between anxiety and serotonin to enhanced platelet activation. Anxiety perception by cerebral cortex induces, via the hypothalamus to sympathetic preganglionic neurons, release of catecholamines, primarily epinephrine, into circulation. Epinephrine
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stimulates platelet agonists and increasing intracellular calcium that release a variety of prothrombotic and inflammatory factors.
Ethnic and Cultural Variations for Anxiety and Depression Transcultural issues play an important role in the proper diagnosis and treatment of depression and anxiety. These include factors such as the biological/physiological differences in response to psychotropic medications, the role that complementary and alternative treatments play, cultural differences with respect to stigma, and epidemiological concerns. Individuals from different ethnic and cultural backgrounds may vary in their biological response to anxiety and depression. Ethnic and cultural backgrounds have been shown to influence electroencephalographic (EEG) sleep patterns and also neuroendocrine changes, more specifically, hypothalamic-pituitary-adrenal (HPA) axis activity and cortisol secretion (Lin, 2001). Compared with controls, depressed patients showed sleep-continuity disturbances such as increased sleep-onset latency and decrease in total sleep time and in sleep efficiency. Studies that have evaluated the effect on race, on EEG sleep, and on clinical symptom profile in people with unipolar major depression have shown that African American patients with depression had less total sleep, less slow-wave sleep, more stage 2 sleep, longer REM sleep latency, less REM sleep, and lower REM density than white patients (Giles, Perlis, Reynolds, & Kupfer, 1998). Moreover, comparison between four ethnic groups with unipolar major depression has shown that African American and Asian subjects had less total REM sleep and shorter REM duration during the first 3 REM episodes but longer REM duration during the fourth REM episode, compared with white and Hispanic groups (Poland et al., 1999; Rao et al., 1999). Prolonged HPA overactivity occurs at all levels of the axis in depressed patients. A commonly used marker for HPA axis function is the dexamethasone suppression test (DST), which measures suppression of cortisol, and a nonsuppression rate of 50% has been reported for depressed patients. Depressed African American patients had a relatively low rate of DST nonsuppression compared with depressed white patients (25% and 58% nonsuppression, respectively) (Poland, Rubin, Lesser, Lane, & Hart, 1987). African Americans have tended to have higher baseline urinary cortisol levels but lower free cortisol levels than individuals from Asian, white, and Hispanic groups (Lin, 2001). The combinations of genetic differences are quite specific across ethnic groups. Polymorphism in those genes encoding drug-metabolizing enzymes and genes controlling the function of therapeutic targets (e.g., transporters, receptors) is thought to be related to the pathogenesis of psychiatric disorders as depression and anxiety. These findings pose serious questions regarding whether genetic polymorphisms might lead to differential vulnerability of ethnic differences in psychopathology of depression and anxiety across ethnic groups. Observations showed that the rate of polymorphism in serotonin transported gene (SLC6A4) ranges from approximately
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20% in Eastern Asian, Japanese, and Chinese subjects to approximately 70% in African American subjects. Moreover, catechol-O-methyltransferase (COMT), a functional polymorphism that may be clinically important in terms of the pathophysiology of mood disorders, has been shown to be less prevalent in Asians compared to whites (18% and 50%, respectively) (Palmatier, Kang, & Kidd, 1999). Culture influences the perception of a stress-producing situation, symptoms of stress, and the expression of emotions (Kirmayer, 2001). Medical anthropology has shown how many aspects of psychiatric theory and practice are based on specific cultural concept of the person. Cultural variation has been shown to influence the regulation and expression of emotion and somatization. The clinical implications of ethnic and cultural differences in anxiety and depression have been summarized in a consensus statement made by an international consensus group on depression and anxiety (Ballenger et al., 2001). A novel approach to psychotherapy – based on strategies such as the use of trained interpreters, raising awareness, improved communication, a culturally sensitive approach to clinical practice, standardized diagnostic instruments based on establishing content, and semantic equivalence method – is indicated for the diagnosis and management of depression and anxiety across cultures.
Gender Differences for Anxiety and Depression and CHD Risk There is growing evidence that psychological stress can influence the onset and clinical course of heart disease, especially for women (Rozanski, Blumenthal, Davidson, Saab, & Kubzansky, 2005). In the INTERHEART study (Yusuf et al., 2004), the combined exposure to psychosocial risk factors including depression and anxiety was significantly associated with AMI with an adjusted odds ratio (OR) of 2.6 in men and 3.5 in women. Depression is about twofold more prevalent in women than in men; it is especially common, up to 40%, in younger women with AMI (Mallik et al., 2006). Depression is an important risk factor for adverse cardiac events in women, increasing a woman’s risk by at least 50% (Whang et al., 2009). In addition to cardiac outcomes, depression is related to worse quality of life in cardiac patients (Ruo et al., 2003) and worse health status benefits after bypass surgery, particularly in women (Mallik et al., 2005). A series of studies of Scandinavian women with acute coronary syndromes have demonstrated robust associations of marital stress, with anxious symptoms in wives, with subsequent cardiac events (Orth-Gomer et al., 2000) as well as with progression of coronary artery disease measured with quantitative coronary angiography (Wang et al., 2007). Psychological trauma, particularly if occurring early in life, such as childhood maltreatment, is an emerging risk factor for ischemic heart disease which is particularly common among women (Dong et al., 2004). Early trauma is also a risk factor for depression (Batten, Aslan, Maciejewski, & Mazure, 2004), which may contribute to cardiac risk in women exposed to childhood trauma.
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Moreover, acute psychological factors such as stressful events, acute anger, sudden mood disturbances, and extreme excitement can trigger AMI provoking a stressinduced condition known as “takotsubo cardiomyopathy”(Wittstein et al., 2005). Although it is unknown whether there are sex differences in these effects, this syndrome is almost exclusively seen among women (see Chap. 6 in this book). Regarding the gender differences in psychological interventions for cardiac patients, when results are reported separately by sex, men show a borderline statistically significant benefit (odd ratios, 0.73), whereas in women, the estimate is null (odd ratios, 1.01) (Linden, Phillips, & Leclerc, 2007). It may be that traditional psychosocial interventions do not work well for women and that strategies that address more specifically women’s needs and stressors should be developed. Indeed, this is suggested by a recent study by Orth-Gomer et al. (2009), documenting a remarkable decrease in mortality (about 70% lower) in women with ischemic heart disease randomized to a stress reduction intervention specifically tailored to women, compared with usual care. Although promising, the efficacy of such intervention needs to be confirmed in other studies.
Assessment of Depression and Anxiety Recently, the American Heart Association (AHA), the American College of Cardiology, and the American College of Physicians highlighted the need to adopt validated and easily performed screening tests for depressions and anxiety in patients with cardiovascular disease (Janeway, 2009). In clinical practice, anxiety and depressive disorders can be assessed with questionnaires and structured clinical interviews (Kop & Ader, 2006). Hospital personnel have difficulty in detecting depression in hospitalized CHD patients without a screening tool, indicating the need to use formal screening for symptoms of depression in acute MI patients (Pozuelo et al., 2009; Ziegelstein et al., 2005). Clinicians and researchers also frequently assess the presence of depressive symptoms through the use of self-report questionnaires. The advantage of questionnaires is their sensitivity for detecting depression and efficiency of administration. Perhaps, the most widely used questionnaire for this purpose has been the Beck Depression Inventory (Beck & Beamesderfer, 1974). This self-report measure has 21 items grouped by diagnostic symptom (e.g., feelings of guilt, sadness, self-confidence and discouragement, loss of interest, crying, changes in appetite, sleep difficulties, suicidal ideation), and the patient is asked to choose a response that indicates the level of severity for each item. Questionnaire scores, while not directly tied to diagnostic depression, have accepted anchors for depression severity. Investigations of depression and CHD commonly interpret results using a BDI score of 10 or greater to identify the presence of depression. Research has also found that scores at or above 10 are associated with poorer prognosis, whether for CHD progression (Carney et al., 1988) or “hard” medical endpoints such as death or myocardial infarction (Frasure-Smith et al., 1995a). The predictive nature of BDI scores is independent of important medical prognostic indicators, such as left ventricular
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function or CHD severity, and the predictive power of BDI scores extends over 5 years (Carney, Freedland, Miller, & Jaffe, 2002). Other symptom-based measures of depression commonly used in cardiac patients are the Center for Epidemiological Studies Depression (CES-D) Scale (Radloff, 1977; Schulz et al., 2000) and the Hospital Anxiety and Depression Scale (Herrmann, 1997). Most questionnaires assess mood and cognitive components (e.g., sadness, low self-esteem, and guilt feelings) as well as the “vegetative” components (e.g., sleep problems, appetite changes, and lack of energy) of depression. To specifically assess exhaustion, the Maastricht Questionnaire can be used (Appels, 1989). Questionnaires are sensitive screening tools for depression but tend to reveal “false positives.” Thus, questionnaire scores positive for depression require further evaluation using structured interviews. The Patient Health Questionnaire (PHQ-9) is a nine-item tool, easy to administer and score, and available in the public domain. It has been well studied in both screening for and follow-up of depression in primary care (Kroenke, Spitzer, & Williams, 2001; Lowe, Unutzer, Callahan, Perkins, & Kroenke, 2004). It was used in the Heart and Soul study and the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study (Freedland et al., 2003). It has also been used to identify and document depressive symptoms in patients with acute coronary syndrome (Amin, Jones, Nugent, Rumsfeld, & Spertus, 2006). A cutoff score of 10 or higher on the PHQ-9 is diagnostic of depression (McManus, Pipkin, & Whooley, 2005). The PHQ-2 consists of the two first questions of the PHQ-9, which deal with mood and lack of pleasure. A cutoff score of 3 or higher has a sensitivity of 83% and a specificity of 92% (Kroenke, Spitzer, & Williams, 2003), fulfilling the need for a quick and reliable depression screening tool. The clinician can also ask for a yes-orno answer to the two questions of the PHQ-2. A yes to either of the two questions is up to 90% sensitive and 75% specific (Lowe et al., 2004; Spitzer et al., 1994). Based on the DSM criteria, structured interviews have been developed to assess depression and other psychological disorders. Among the commonly used interviews are the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I), the Composite International Diagnostic Interview (CIDI), the Schedules for Clinical Assessment in Neuropsychiatry (SCAN), and the Diagnostic Interview Schedule (DIS) (Robins, Helzer, Croughan, & Ratcliff, 1981) (for a review, see Freedland et al., 2002). A combined self-report and clinical interview technique has been designed to assess depression in patients with medical conditions (Spitzer et al., 1994). Structured interviews are superior to questionnaires in differentiating dysthymia from minor depression. One of the limitations of structured interviews is that they are time consuming and tend to be resistant to change over time. The Hamilton Depression Scale is useful for evaluation severity as well as change (Freedland et al., 2002). For practical purposes, it is generally important that structured interviews allow sufficient flexibility to be amended to the patient’s clinical condition, the hospital setting, and the potential of interview administration by individuals without extensive psychological training (Kop & Ader, 2006). Patients with elevated questionnaire scores, but who do not fully qualify for all DSM Major or Minor Depression criteria based on structured interview, may still
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suffer from atypical or subclinical depression and may also be at risk for adverse cardiovascular events (Kop, 1999). A strong focus on the mood components of depression in the early phases of the diagnostic assessment may result in underdetection of depression because of the atypical nature of depression in patients with cardiac disease. Patients with medical disorders may be reluctant disclosing depressive mood symptoms because atypical features appear salient to them. Some somatic symptoms of depression such as fatigue may reflect angina equivalents and should be treated accordingly. Nonetheless, these complaints should also be counted in the assessment of depression in CAD patients, because it is generally not possible to validly differentiate the underlying causes of these symptoms. Thus, to adequately assess depression in cardiac patients, it is important to ask all items related to depression, starting with the vegetative symptoms (Kop & Ader, 2001). Assessment of diagnostic depression in CHD populations presents special challenges, in part, because most ACS patients are too ill to tolerate lengthy interviews and they have little unencumbered time during brief hospital stays. Many are also unaccustomed to discussing their emotional problems and have symptoms that are hard to assess in the hospital setting. Lastly, it is often difficult to ascertain whether a physical symptom associated with depression is due instead to some aspect of the patient’s CHD. Clinical interviews must therefore be flexible and conducted in a sensitive manner that fosters trust, rapport, and disclosure, rather than in the neutral, tightly structured manner of an epidemiologically based interview (Maier, Chatkoff, & Burg, 2006). Toward this end, the ENRICHD Study researchers utilized the Diagnostic Interview and Structured Hamilton (DISH). The DISH incorporates elements of other diagnostic and severity measures of depression and is well suited for use with this population. It provides for the initial establishment of rapport by allowing the patient to first discuss his or her experiences related to the ACS. It then provides the interviewer with a flexible structure (i.e., using the patient’s own way of describing his or her experiences) from which to probe for the presence of symptoms consistent with depression. The scoring takes into account symptom severity and duration in order to facilitate clinical determinations. Lastly, the DISH provides for a brief assessment of lifetime history of depression. The DISH is relatively easy to administer, and it provides a useful diagnostic tool for both clinical and research purposes (Freedland et al., 2002). The American Heart Association (AHA) (Lichtman et al., 2008) released a consensus document recommending that health-care providers screen for and treat depression and anxiety in patients with coronary heart disease. Also, Pozuelo and colleagues (Pozuelo et al., 2009) recommend that clinicians systematically screen it in their cardiac patients in view of the benefits of antidepressant therapy. These authors propose an algorithm for use in depressed cardiac patients, which is similar to the algorithm proposed by the AHA committee (Lichtman et al., 2008). Pozuelo and colleagues think that clinicians should routinely screen for depression in cardiac patients and should not hesitate to treat it and eligible patients should routinely be referred to cardiac rehabilitation programs (Pozuelo et al., 2009).
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To evaluate anxiety, simple screening questionnaires that have high reliability and validity are available. The Beck Anxiety Inventory (Beck & Steer, 1990), the Zung Self-Rating Anxiety Scale (Zung, 1971), or Hamilton Anxiety Scale (Hamilton, 1959) can be used as part of the routine workup of every patient. The Hamilton Anxiety Scale has the advantage of diagnosing depression as well as anxiety (Hamilton, 1959). The major disadvantages in using the above scales are the time required for administration (15–25 min as part of a full battery), the need for scoring, and significant cost to purchase (Janeway, 2009). The Beck Anxiety Inventory (BAI) is increasingly being used in studies that assess the impact of anxiety and depression on heart disease (Frasure-Smith & Lesperance, 2008; Huffman, Smith, Blais, Januzzi, & Fricchione, 2008). BAI consists of 21 questions about how the subject has been feeling in the last week, expressed as common symptoms of anxiety (such as numbness, hot and cold sweats, or feelings of dread). The respondent is asked to rate how much he or she has been bothered by each symptom over the past week on a 4-point scale ranging from 0 to 3. The scale obtained high internal consistency and item-total correlations ranging from .30 to .71. For a first screening by clinicians, assessment tools like the Prime-MD (Spitzer et al., 1994) are readily available, with their easy-to-ask questions such as “have you been bothered a lot by ‘nerves’ or feeling anxious or on edge?” Such questions allow to “open the door” of psychological symptoms that can be subsequently deepened with specific assessment tools by psychologist and or psychiatrist. A newly created instrument, which is in progress of empirical validation, is the Screening Tool for Psychologic Distress (STOP-D) designed specifically for the outpatient cardiology setting (Young, Ignaszewski, Fofonoff, & Kaan, 2007). This is a brief 5-item self-report which assesses the preceding 2-week period and asks questions such as how much the individual has been bothered by feeling sad, down, or uninterested in life or how often they have been bothered by feeling anxious or nervous. It points out when the cardiologist should treat and/or refer to a mental health professional. If further screening is desired to help make a diagnosis, then the Beck Anxiety Inventory (BAI), PHQ-9, and DSM-IV can be used. Allowing a patient to talk openly about their lives, feelings, relationships, and stress sets the tone toward reducing stigma and anxiety, which strengthens the therapeutic alliance and can improve compliance with treatment. In general, there is a need for more medical school training in behavioral medicine and in doctor–patient relationship issues (Guise, 2000; Olshansky, 2007).
Psychological Interventions for Anxiety and Depression Depression Atypical depression, subclinical depression, and exhaustion often require intervention as well, particularly if the patient has had prior depressive episodes or a family history of depression. Major behavioral and drug trials conducted in the last 15 years
Sertraline versus placebo
Mirtazapine versus placebo
Citalopram ± IPT
SADHART (Glassman et al., 2002)
MIND-IT
CREATE (Lesperance et al., 2007)
Table 8.4 Clinical trials of depression therapy in patients with cardiac diseases Trial Therapies M-HART (Frasure-Smith et al., 1997) Home nursing intervention (vs usual care) for psychological distress Roose and colleagues and Nelson and Nortriptyline versus paroxetine colleagues ENRICHD CBT versus usual medical care
12 weeks
24 weeks
11 sessions over 6 months 24 weeks
6 weeks
Treatment period 1 year
Results Prognosis: no improvement compared with usual care Depression: both effective Drug safety: nortriptyline toxic Depression: CBT modestly effective Prognosis: no difference versus usual care Depression: effective versus placebo Safety: safe Depression: no difference versus placebo Prognosis: no difference versus placebo Depression: citalopram effective IPT not effective
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have focused on how to best treat depression in cardiac patients (Lesperance et al., 2007) (see Table 8.4). The management of depression typically has three phases: (1) the acute phase to reduce symptoms (6–12 weeks), (2) the continuation phase to prevent relapse (4–9 months), and (3) the maintenance phase for individuals with known recurrent depression (long-term treatment) (Lesperance & Frasure-Smith, 2000). Many depressive episodes that emerge in the setting of an acute coronary syndrome (e.g., myocardial infarction) resemble that of adjustment disorders with high spontaneous recovery rates (Glassman et al., 2002). Treatment of depression generally requires careful coordination between internal medicine and cardiology with mental health professionals in the cardiac rehabilitation program. Psychotherapy has long been recommended for patients after acute coronary syndrome, both for those with depression and for those experiencing adjustment difficulties. Psychological interventions can be given on an individual basis or in groups and may range from providing social support to more intensive cognitivebehavioral therapy (Linden, 2000). Cognitive-behavioral therapy is often successfully used in the treatment of depressive disorders. The main goal of this approach is to modify dysfunctional thoughts and emotions by structured and empathic questioning of patients’ perceptions and thought processes. The Enhancing Recovery in Coronary Heart Disease (ENRICHD) trial examined the effects of cognitive-behavioral therapy in a large sample (N = 2,481) of post–myocardial infarction patients with major depression and/or social isolation (Berkman et al., 2003). The intervention was successful in reducing depression, but no beneficial effects in 2-year cardiac events were found between patients receiving the intervention (24.2%) versus a usual treatment control group (24.1%). Because dysfunctional cognitions play a relatively minor role in atypical depression, treatments other than cognitive-behavioral interventions may be more beneficial to CAD patients with atypical depression or exhaustion. Among the psychotherapies, cognitive-behavior therapy (CBT) and interpersonal psychotherapy (IPT) are the most effective, in both acute and maintenance treatments (Hollon et al., 2002). One treatment that may be particularly suited for depressed cardiac patients is IPT. This is a time-limited (12–16 weekly 1-h sessions), manualized psychotherapy that was developed in the early 1970s by Gerald Klerman and colleagues as a research intervention for outpatients with unipolar major depression (Klerman, Weissman, Rounsaville, & Chevron, 1984). IPT is based on the presumption that interpersonal issues affect mood and mood impairs interpersonal functioning. IPT conceptualizes clinical depression as having three component processes: symptom formation caused by biological and/or psychological mechanisms, social functioning (involving, obviously, social interactions with others), and enduring personality traits (Koszycki, 2006). IPT intervenes in symptom formation and social dysfunction but does not address enduring personality traits in view of the time limits of treatment, the relatively low level of psychotherapeutic intensity, the emphasis of treatment on the current depressive episode, and the difficulty in accurately evaluating personality in the midst of an Axis I disorder (Weissman, Markowitz, & Klerman, 2000). The brevity of the treatment imposes a structure that pressures the patient and therapist to work quickly to
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alleviate depressive symptoms and resolve the current interpersonal crisis linked with the depression, thus discouraging the patient’s becoming dependent on the therapist (Koszycki, 2006). For each patient, therapy focuses on one or, at most, two interpersonal problem areas that are identified as precursors of the current depressive episode. These problem areas were derived from extensive research on the role of environmental influences on mood and are characterized as unresolved grief following the death of a loved one, role transitions (difficulty adjusting to changed life circumstances), interpersonal role disputes (conflicts with a significant other), and interpersonal deficits (impoverished social networks). Maintaining the focus of treatment on a problematic interpersonal issue prevents the therapy from becoming too diffuse and forces the therapist and patient to discuss material that is relevant to the focal area and treatment objectives (Koszycki, 2006). IPT also focuses on the “here and now,” that is, on current problematic interpersonal issues that are amenable to change, rather than on reconciling unresolved interpersonal problems having to do with the past. The focus on resolving current interpersonal problems and developing strategies for warding off future problems helps reduce the depressed patient’s tendency to ruminate about past events and experiences that cannot be changed and which only serve to reinforce the patient’s already low sense of self-esteem and dysphoria (Koszycki, 2006). The primary goal of IPT is to obtain the remission of depressive symptoms by facilitating resolution of a current interpersonal crisis. Nevertheless, as treatment progresses, many patients acquire new interpersonal skills that may help compensate for characterological problems. The IPT therapist has an active stance and guides the patient in the discussion of relevant material during the therapeutic session, explores options that exist for change, provides clarification, promotes problem solving, and helps the patient feel more competent in managing life (Koszycki, 2006). The therapist actively works with the patient to relieve depression by conveying a hopeful attitude that treatment goals can be achieved, by being supportive and by reassuring the patient and providing direct advice when appropriate. The therapeutic strategies and techniques of IPT are designed to help the patient master the interpersonal problem area associated with depression. These techniques are similar to those used in other psychotherapies and include exploratory techniques, encouragement of affect, clarification, communication analysis, and the use of the therapeutic relationship and various behavioral change techniques (Koszycki, 2006). IPT has been extensively researched and shown to be effective as both an acute and preventive treatment for major depressive disorder (Weissman et al., 1979). At 1-year follow-up, patients who received IPT had better psychosocial functioning than those who did not receive this treatment (Weissman, Klerman, Prusoff, Sholomskas, & Padian, 1981). The National Institute of Mental Health Treatment of Depression Collaborative Research Program (NIMH TDCRP) found that, in general, IPT is an effective monotherapy for patients with mild to moderate depression, but that antidepressant medication should be used as a first-line treatment for severely ill patients. The Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) studied the efficacy of citalopram administered in conjunction with weekly clinical management for major depression among patients with CAD and
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have found no evidence of added value of IPT over clinical management (Lesperance et al., 2007). Citalopram was superior to placebo in reducing 12-week HAM-D scores (mean difference, 3.3 points), remission rates (35.9% vs 22.5%), and BDI-II scores (difference, 3.6 points). There was no evidence of a benefit of IPT over clinical management, with the mean HAM-D difference favoring clinical management (−2.26 points). The difference on the BDI-II did not favor clinical management (1.13 points).
Anxiety Evidence suggests that relaxation and breathing therapy are effective in alleviating anxiety and reducing exhaustion in CAD patients. Importantly, these interventions may also successfully prevent recurrent MI and clinical restenosis following coronary angioplasty (Appels, Bar, Lasker, Flamm, & Kop, 1997). At present, the efficacy of relaxation in CAD patients with depression has not been established. Patient support groups can provide social support, reduce anxiety, and help teach patients how to effectively report symptoms and communicate with their physicians. Social isolation is a risk factor for CAD and is often a concomitant of depression (Berkman et al., 2003). Social support from family and friends may promote treatment efficacy and patients’ recovery from depression. Although patients’ social networks generally respond in a supportive manner at early stages of depression, these resources can be drained as a result of the relentless demands of depressed individuals. Cognitive-behavioral therapy (CBT) is a well-documented evidence-based treatment appropriate for the treatment of anxiety that should be instituted at the beginning of cardiac treatment to ensure that patients understand their condition (Barlow, Gorman, Shear, & Woods, 2000). Using CBT, patients are taught to restructure anxiety-provoking thoughts leading to panic attacks, are taught relaxation techniques to counteract stress and anxiety, and are given exposure therapy to desensitize themselves to stressful stimuli. Other forms of psychotherapy, such as psychoanalytic, interpersonal, and supportive therapies, can be effective as adjunctive therapies, but do not carry the wealth of evidence-based research demonstrating their effectiveness in the treatment of anxiety disorders.
Conclusions The prevalence of depression and anxiety among patients with CHD and after acute coronary syndrome is higher than in the general population. Depression is far more common in coronary artery disease patients than in the general population, but often remains undiagnosed and untreated. In CAD patients, depression frequently presents as complaints of fatigue and other vegetative symptoms, rather than its typical mel-
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ancholic form. Initial screening of depression can be efficiently conducted in most medical settings using questionnaires; effective treatment requires involvement of a multidisciplinary team. Underdiagnosis has interfered with adequate treatment of depression in coronary artery disease patients. The currently available questionnaires are well suited as initial screening tools, but the subsequent clinical interviews for depression remain time consuming (approximately 60 min) (Freedland et al., 2002) and require improvements to be generally applicable in general medical practice. Although depression may at times be viewed as a response to the trauma of myocardial infarction, there is substantial prospective evidence that depression and anxiety predates and may play a causal role in CHD onset. Investigations suggest direct biological processes involved in both depression and coronary artery disease, and indirect pathways related to health behaviors. Behaviorally, nonadherence to medical regimens and poor health behaviors (such as smoking, atherogenic diets, and sedentary lifestyle) are important factors that may also contribute to the observed relationship between depression, anxiety, and CHD. Despite these plausible mechanisms, effective interventions to improve CHD outcomes by targeting depression remain elusive (Frasure-Smith & Lesperance, 2003). Treatment of depression among CHD patients therefore continues to be an area of active investigation. Findings from the ENRICHD study suggest the need for future research to better identify the degree of change in depression needed to impact CHD outcomes. In addition, differentiating patients with adjustment difficulties from those with depressive disorders may further clarify the benefit of cognitive therapy on depression and CHD outcomes. Understanding the many hypothesized behavioral and biological pathways linking depression to CHD outcome will likely facilitate the development of effective interventions. More basic research is therefore needed to elucidate the mechanisms by which depression and CHD are related. Depression can be treated effectively with a combination of psychological and pharmacological interventions. However, whether treatment of depression results in improved cardiovascular health outcomes remains to be determined. The type of treatment needs to be matched with the nature of depression and may explain why some interventions revealed unsuccessful results (Frasure-Smith et al., 1997). Depression adversely affects cardiovascular health by both biological processes and adverse health behaviors. Thus, treatment of depressive disorders in coronary artery disease will be most effective when symptom management is combined with strategies targeting both the causes as well as the biological and behavioral concomitants of depression. Also, anxiety is common among cardiac patients and should be treated to enhance recovery and decrease patients’ risk of subsequent cardiac events. One of the most important areas for future research is elucidating the mechanisms whereby anxiety causes poorer outcomes in acute myocardial infarction patients. The mechanisms (either physiological or behavioral) whereby anxiety is related to poorer short- and long-term outcomes in acute myocardial infarction patients have yet to be elucidated. Research in this area is important to help clinicians determine the best ways to manage acute myocardial infarction patients to decrease the negative impact of anxiety. Without understanding the basic underlying mechanisms, it is difficult to know whether treatment should concentrate on pharmacological strategies such as beta-blocker therapy to
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decrease sympathetic nervous system responses to anxiety or more directly on antianxiety drug therapy. The role of nonpharmacologic strategies that decrease psychophysiologic arousal also should be investigated (Moser & De Jong, 2006). Further research is warranted to determine factors that may moderate anxiety in order to better understand the phenomenon among acute myocardial infarction patients and develop effective interventions. It appears that anxiety after acute myocardial infarction is a universal phenomenon. Given the potentially negative impact of anxiety on mortality and quality of life after acute myocardial infarction, clinicians and researchers should continue to explore interventions to treat anxiety and minimize its untoward effects (Moser & De Jong, 2006). Future studies need to disentangle the cause-effect relationships between depression, anxiety, and adverse health behaviors in patients with coronary artery disease (Kop & Ader, 2006). As commented on by Dimsdale (2010), the recent findings regarding anxiety come at a time when psychiatry is once again redrawing diagnostic guidelines in the Diagnostic and Statistical Manual. For decades, the Diagnostic and Statistical Manual has differentiated between anxiety disorders and depressive disorders, but in clinical practice, these disorders rarely occur in isolation, and the distress associated with them increases synergistically when both sets of symptoms coexist. Future researches should analyze together the two symptoms and their synergic action in heart disease. It would be useful for clinical practice to develop treatments that combine strategies for anxiety and depression and evaluate whether such treatments would reduce cardiovascular risk. Finally, despite the large amount of evidence supporting significant and independent associations between anxiety and depression and the pathogenesis of cardiovascular disease, the 2010 American College of Cardiology Foundation/American Heart Association Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults (Greenland et al., 2010a, b) does not consider yet any of them.
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Wang, H. X., Leineweber, C., Kirkeeide, R., Svane, B., Schenck-Gustafsson, K., Theorell, T., & Orth-Gomer, K. (2007). Psychosocial stress and atherosclerosis: Family and work stress accelerate progression of coronary disease in women. The Stockholm Female Coronary Angiography Study. Journal of Internal Medicine, 261(3), 245–254. Watkins, L. L., Blumenthal, J. A., Babyak, M. A., Davidson, J. R., McCants, C. B., Jr., O’Connor, C., & Sketch, M. H., Jr. (2010). Phobic anxiety and increased risk of mortality in coronary heart disease. Psychosomatic Medicine, 72(7), 664–671. Watkins, L. L., Blumenthal, J. A., & Carney, R. M. (2002). Association of anxiety with reduced baroreflex cardiac control in patients after acute myocardial infarction. American Heart Journal, 143(3), 460–466. Watkins, L. L., Blumenthal, J. A., Davidson, J. R., Babyak, M. A., McCants, C. B., Jr., & Sketch, M. H., Jr. (2006). Phobic anxiety, depression, and risk of ventricular arrhythmias in patients with coronary heart disease. Psychosomatic Medicine, 68(5), 651–656. Weissman, M. M., Klerman, G. L., Prusoff, B. A., Sholomskas, D., & Padian, N. (1981). Depressed outpatients. Results one year after treatment with drugs and/or interpersonal psychotherapy. Archives of General Psychiatry, 38(1), 51–55. Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books. Weissman, M. M., Prusoff, B. A., Dimascio, A., Neu, C., Goklaney, M., & Klerman, G. L. (1979). The efficacy of drugs and psychotherapy in the treatment of acute depressive episodes. American Journal of Psychiatry, 136(4B), 555–558. Whang, W., Kubzansky, L. D., Kawachi, I., Rexrode, K. M., Kroenke, C. H., Glynn, R. J., et al. (2009). Depression and risk of sudden cardiac death and coronary heart disease in women: Results from the Nurses’ Health Study. Journal of the American College of Cardiology, 53(11), 950–958. Whang, W., Shimbo, D., Kronish, I. M., Duvall, W. L., Julien, H., Iyer, P., et al. (2010). Depressive symptoms and all-cause mortality in unstable angina pectoris (from the Coronary Psychosocial Evaluation Studies [COPES]). American Journal of Cardiology, 106(8), 1104–1107. Whooley, M. A., de Jonge, P., Vittinghoff, E., Otte, C., Moos, R., Carney, R. M., et al. (2008). Depressive symptoms, health behaviors, and risk of cardiovascular events in patients with coronary heart disease. JAMA, 300(20), 2379–2388. Wittstein, I. S. (2010). Depression, anxiety, and platelet reactivity in patients with coronary heart disease. European Heart Journal, 31(13), 1548–1550. Wittstein, I. S., Thiemann, D. R., Lima, J. A., Baughman, K. L., Schulman, S. P., Gerstenblith, G., et al. (2005). Neurohumoral features of myocardial stunning due to sudden emotional stress. New England Journal of Medicine, 352(6), 539–548. Young, Q. R., Ignaszewski, A., Fofonoff, D., & Kaan, A. (2007). Brief screen to identify 5 of the most common forms of psychosocial distress in cardiac patients: Validation of the screening tool for psychological distress. Journal of Cardiovascular Nursing, 22(6), 525–534. Yusuf, S., Hawken, S., Ounpuu, S., Dans, T., Avezum, A., Lanas, F., et al. (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet, 364(9438), 937–952. Zafar, M. U., Paz-Yepes, M., Shimbo, D., Vilahur, G., Burg, M. M., Chaplin, W., et al. (2010). Anxiety is a better predictor of platelet reactivity in coronary artery disease patients than depression. European Heart Journal, 31(13), 1573–1582. Ziegelstein, R. C. (2001). Depression in patients recovering from a myocardial infarction. JAMA, 286(13), 1621–1627. Ziegelstein, R. C., Kim, S. Y., Kao, D., Fauerbach, J. A., Thombs, B. D., McCann, U., et al. (2005). Can doctors and nurses recognize depression in patients hospitalized with an acute myocardial infarction in the absence of formal screening? Psychosomatic Medicine, 67(3), 393–397. Zuidersma, M., Thombs, B. D., & de Jonge, P. (2011). Onset and recurrence of depression as predictors of cardiovascular prognosis in depressed acute coronary syndrome patients: A systematic review. Psychotherapy and Psychosomatics, 80(4), 227–237. Zung, W. W. (1971). A rating instrument for anxiety disorders. Psychosomatics, 12(6), 371–379.
Chapter 9
Interventions in the Context of the Distressed (Type D) Personality Aline J. Pelle, Krista C. van den Broek, and Johan Denollet
Abbreviations CABG CAD CBT CHF CREATE DS14 ENRICHD EPC EXIT HPA ICD IPT MBCT MI NIH PAD PCI RCT SEARCH SPIRR-CAD
Coronary artery bypass grafting Coronary artery disease Cognitive behavioral therapy Chronic heart failure Canadian cardiac randomized evaluation of antidepressant and psychotherapy efficacy Type D questionnaire ENhancing recovery in coronary heart disease Endothelial progenitor cells EXhaustion Intervention Trial Hypothalamic-pituitary-adrenal Implantable cardioverter defibrillator Interpersonal therapy Mindfulness-based cognitive therapy Myocardial infarction National Institutes of Health Peripheral arterial disease Percutaneous coronary intervention Randomized controlled trial Support, Education, and Research in Chronic Heart Failure Study Stepwise psychotherapy intervention for reducing risk in coronary artery disease
A.J. Pelle, Ph.D. (*) • K.C. van den Broek, Ph.D. • J. Denollet, Ph.D. Center of Research on Psychology in Somatic diseases, Tilburg University, P.O. Box 90153, 5000 LE, Tilburg, The Netherlands e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_9, © Springer Science+Business Media, LLC 2012
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Selective serotonin receptor inhibitor Short-term psychotherapy in acute myocardial infarction Tumor necrosis factor WEB-based distress management program for implantable CARdioverter dEfibrillator patients
Clinical Vignette The distressed (Type D) personality is characterized by a general propensity to psychological distress, defined by the combination of high negative affectivity and social inhibition. Across cardiac conditions, Type D patients are at increased risk for impaired health outcomes, including increased morbidity and mortality, and impaired mood and health status. Further, Type Ds are likely to display poor healthrelated behaviors and are characterized by impaired social functioning. In this chapter, a general introduction on the background, assessment, and clinical relevance of Type D personality is provided. Building on existing evidence, interventions for improving mood and health status, health-related behaviors, and interpersonal functioning in the context of Type D personality are discussed. Finally, practical guidelines for clinicians in the context of Type D personality are provided and suggestions for future work are presented.
The Type D Personality Construct Background and Definition In the field of cardiology, state-of-the-art treatments are rapidly improving. In general, cardiac patients receive excellent therapies for their medical condition, which substantially improve quality of life and prevent clinical deterioration (Epstein et al., 2008; Krumholz et al., 2008). A substantial number of patients, however, experience impaired quality of life, despite successful treatment. Because impaired quality of life is associated with an increased risk for mortality (Koch et al., 2007; Mommersteeg, Denollet, Spertus, & Pedersen, 2009), it is important to timely identify high-risk patients. Personality factors may play an important role in this identification process of high-risk individuals. In the 1950s, the Type A behavior pattern was introduced as a risk factor for cardiovascular disease (Friedman & Rosenman, 1959, 1971). This behavior pattern is characterized by competitiveness, hard-driving behavior, hostility, and impatience (Friedman & Rosenman, 1959). Although initial results seemed promising, later studies reported that the Type A behavior pattern was not a risk factor for cardiovascular disease (Razzini et al., 2008). Due to these conflicting results, attention faded for the role of behavior or personality patterns during several decades. In the early 1990s, Denollet introduced the distressed personality, or Type D personality, as a vulnerability factor for adverse health outcomes in cardiac patients
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(Denollet, Sys, & Brutsaert, 1995). In the setting of outpatient cardiac rehabilitation, he observed that some patients were not inclined to express their negative emotions, but at the same time experienced high levels of distress and did not improve as much as other patients. Denollet conceptualized the distressed personality based on clinical observations, established personality theories, and empirical evidence (Denollet et al., 1995). The Type D personality is characterized by two normal and broad personality traits: negative affectivity and social inhibition. Negative affectivity refers to the tendency to experience negative emotions, such as dysphoria, anxiety, and irritability, across time and situations (Watson & Pennebaker, 1989). Individuals high on negative affectivity have a negative view of the self and continuously scan the world for signs of impeding trouble (Watson & Pennebaker, 1989). Social inhibition refers to the tendency to consciously inhibit the expression of emotions and behaviors in social interactions to avoid disapproval by others, because of fear of rejection (Asendorpf, 1993). Individuals with high levels of social inhibition tend to feel insecure, tense, and inhibited in social interactions (Asendorpf, 1993; Friedman & Booth-Kewley, 1987). Some argue that Type D personality does not distinguish itself from depression. However, both constructs differ in several ways (Pelle, Denollet, Zwisler, & Pedersen, 2009). Type D individuals may experience depressive symptoms, but also a wide range of other negative emotions, such as anxiety and irritability (Denollet, 2005). Likewise, although Type D individuals are at increased risk for depression (Pedersen, Ong, et al., 2006; Schiffer et al., 2005), not all Type Ds are depressed, and not all depressed patients can be classified as Type D (Denollet, de Jonge, et al., 2009). One study elaborated on this study and based on the diagnosis of either depression or Type D, and concluded that one out of four distressed patients displayed both depression and Type D, whereas 74% of patients displayed one form of distress – i.e., clinical depression or Type D personality – but not the other. This finding indicates that diagnosis of Type D was not a function of comorbid depression and that conceptualization of depressive disorder and Type D personality may be viewed as two distinctly different categories of psychological distress (Denollet, de Jonge, et al., 2009). Another important distinction is their level of stability, with depressive symptoms referring to a mood state, as the presence of these symptoms may fluctuate over months or years (Kop, 1999), while Type D personality refers to a trait, as this personality seems to be a stable construct over time (Martens, Kupper, Pedersen, Aquarius, & Denollet, 2007; Kupper, Boomsma, de Geus, Denollet, & Willemsen, 2011). Furthermore, Type D personality and depression are differentially associated with clinical factors. For instance, one study demonstrated that the prevalence of ventricular dysfunction and female gender was lower in Type D patients without depression compared with depressed patients without Type D, indicating clinical differences between “pure” Type D and depression subgroups (Denollet, de Jonge, et al., 2009). Importantly, Type D personality independently predicts adverse health outcomes, such as increased mortality and poor quality of life, also after adjustment for depression (Denollet & Pedersen, 2008; Martens, Mols, Burg, & Denollet, 2010; Mols, Martens, & Denollet, 2010; Pedersen, Herrmann-Lingen, de Jonge, & Scherer, 2010).
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Finally, the Type D construct includes a way of coping with negative emotions, namely, nonexpression, while depression only refers to depressive feelings but not how one deals with these negative feelings. Neuroticism and extraversion/introversion reflect two traits from the “Big Five” personality classification that resemble negative affectivity and social inhibition. Neuroticism and negative affectivity share approximately 46–55% of their variance and extraversion and social inhibition 35–42% (De Fruyt & Denollet, 2002; Denollet, 2005). This indicates a fair amount of overlap between the constructs, but also indicates uniqueness. Neuroticism includes cognitive factors, such as guilt, which may be absent in Type Ds. Social inhibition may be closely related to the interpersonal dimension of introversion, such that individuals perceive the social world as threatening; they anticipate negative reactions from others such as disapproval, and therefore apply self-enhancing strategies such as inhibition of self-expression and withdrawal (Asendorpf, 1993). Social inhibition may be less related to the intrapsychic dimension of extraversion, namely, the aspects of positive affect and excitement seeking. It is relevant to address the issue of reversed causality or somatic confounding, as Type D personality is sometimes thought to develop as a consequence of physical disease. However, Type D personality is also commonly observed among individuals of the general population, with a prevalence rate of 13–25% (Aquarius, Denollet, Hamming, & De Vries, 2005; Denollet, 2005; Pedersen & Denollet, 2004), and evidence from twin studies indicates that genes may play an important role in Type D personality and its components, with 52% of individual differences in Type D personality being explained by genetic factors (Kupper, Denollet, De Geus, Boomsma, & Willemsen, 2007). In addition, the heritability estimates for both negative affectivity and social inhibition are about 50% (Kupper et al., 2011, 2007). Environmental factors, such as parenting styles, may also play a role. The prevalence of Type D personality was higher in individuals who experienced high levels of control by their parents or who felt alienated from their parents (Van den Broek, Smolderen, Pedersen, & Denollet, 2010). Furthermore, studies in cardiac samples have demonstrated that Type D personality is unrelated to indicators of disease severity (Pelle, van den Broek, Szabó, & Kupper, 2010; Schiffer et al., 2005). These findings corroborate the idea that Type D personality is a consequence of physical disease.
Assessment and Prevalence The 14-item Type D scale (DS14) is the standard measurement of Type D personality (Denollet, 2005). The DS14 is a short self-report questionnaire, which can easily be administered to patients (Fig. 9.1). The DS14 includes two seven-item subscales that assess negative affectivity and social inhibition. DS14 items are answered on a 5-point Likert scale, ranging from 0 (“false”) to 4 (“true”), with total scores for both subscales ranging from 0 to 28. Individuals that score equal to or higher than 10 on both subscales are classified as Type D. Item response theory has shown that this cutoff has the highest reliability (Emons, Meijer, & Denollet, 2007). The detrimental effect of Type D personality is not only due to the increased rate of negative
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Fig. 9.1 The Type D questionnaire (DS14)
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emotions; it is merely the combined presence of various negative emotions with high levels of social inhibition that incurs the adverse risk (Denollet, Pedersen, Ong, et al., 2006). Both subscales have good psychometric properties. Denollet (2005) reported that Cronbach’s alpha is 0.88 for negative affectivity and 0.86 for social inhibition, which indicates good internal consistency. The validity of the scales is also good, as negative affectivity correlated 0.68 with neuroticism and social inhibition correlated −0.59 to −0.65 with extraversion (Denollet, 2005). In addition, no gender differences in the prevalence of Type D personality have been shown (e.g., Barth et al., 2009). The DS14 has been validated in several languages, including Chinese, Danish, Dutch, English, German, Italian, Norwegian, and Icelandic. In cardiac samples, about one in four to one in three patients can be classified as Type D. The prevalence of Type D personality ranges from 33% to 37% in patients with peripheral arterial disease (PAD) (Aquarius et al., 2005), from 18% to 38% in patients with coronary artery disease (CAD) (Al-Ruzzeh et al., 2005; Denollet, Pedersen, Vrints, & Conraads, 2006; Martens et al., 2007; Molloy, Perkins-Porras, Strike, & Steptoe, 2008; Pedersen, Lemos, et al., 2004; Pelle et al., 2008), from 20% to 29% in patients with chronic heart failure (CHF) (Denollet, Schiffer, et al., 2009; Pelle, Pedersen, Szabó, & Denollet, 2009; Schiffer, Denollet, Widdershoven, Hendriks, & Smith, 2007; von Känel et al., 2009), from 20% to 25% in patients with an implantable cardioverter defibrillator (ICD) (Pedersen, van Domburg, Theuns, Jordaens, & Erdman, 2004; Van den Broek, Nyklicek, Van der Voort, Alings, & Denollet, 2008), and from 18% to 29% in patients receiving a heart transplant (Denollet, Holmes, Vrints, & Conraads, 2007; Pedersen, Holkamp, et al., 2006). The prevalence in healthy samples is somewhat lower, ranging from 13% to 25% (Aquarius et al., 2005; Denollet, 2005; Pedersen & Denollet, 2004).
Clinical Relevance Individuals differ in health outcomes, with personality possible serving as a determinant for these differences. Type D personality is associated with an increased risk of all-cause and cardiac mortality, independent of standard biomedical risk factors, in most (Aquarius et al., 2009; Denollet et al., 1995, 1996; Denollet, Vaes, & Brutsaert, 2000; Pedersen, Lemos, et al., 2004), but not all studies (Pelle, Pedersen, et al., 2010). Type D personality has also been linked to recurrent events, such as major adverse cardiac events in general (Denollet, Pedersen, Ong, et al., 2006; Denollet, Pedersen, Vrints, & Conraads, 2006), new MIs (Denollet & Brutsaert, 1998; Denollet et al., 2000), or life-threatening arrhythmias (Van den Broek et al., 2009). One study found that the incidence of cancer was higher among cardiac Type D patients (Denollet & Brutsaert, 1998). The risk associated with Type D is on par with the risk of established biomedical cardiac risk factors, such as left ventricular dysfunction. The detrimental effects of Type D personality on these adverse clinical outcomes have been found across different types of cardiovascular diseases, including PAD (Aquarius, Denollet, Hamming, Van Berge Henegouwen, & De Vries, 2007), CAD (Al-Ruzzeh et al., 2005; Denollet, Pedersen, Vrints, et al., 2006; Denollet et al., 1996;
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Denollet et al., 2000; Martens et al., 2010; Pedersen, Lemos, et al., 2004), CHF (Denollet, Schiffer, et al., 2009), arrhythmias (Pedersen, van Domburg, et al., 2004; Van den Broek et al., 2009), and heart transplantation (Denollet et al., 2007). Apart from identification of particular high-risk patients, it is relevant from a clinical point of view to know which factors may explain the link between Type D personality and these adverse clinical outcomes. In the context of psychosomatic research and clinical care, both behavioral and physiological pathways may play an important role. Behavioral pathways may include lifestyle factors and impaired interpersonal functioning; these will be discussed in sections Health-Related Behaviors and Interpersonal Functioning. Plausible physiological pathways may involve immune activation, blood pressure reactivity, heart rate recovery, and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Previous studies have shown that Type Ds are characterized by elevated levels of tumor necrosis factor (TNF) alpha and its soluble receptors (Conraads et al., 2006; Denollet, Schiffer, et al., 2009), indicating increased immune activation. In addition, the number of endothelial progenitor cells (EPC), which play a favorable role in wound healing and vascular repair, is also decreased in Type D patients (Van Craenenbroeck et al., 2009). Increased TNF-alpha and decreased EPC count are, in turn, associated with poor prognosis in CHF (Andreou, Tousoulis, Tentolouris, Antoniades, & Stefanadis, 2006; Feldman et al., 2000; Pompilio et al., 2009). Blood pressure reactivity to stress may also be a candidate mechanism. Although the global Type D construct was unrelated to blood pressure reactivity in college students, the components were (Habra, Linden, Anderson, & Weinberg, 2003). A recent study in CHF patients indicated that Type D personality was associated with decreased heart rate recovery during the first minute after exercise training (von Känel et al., 2009), which is associated with increased cardiovascular morbidity and mortality (Nanas et al., 2006). Type Ds may also have an increased oxidative stress burden, including decreased antioxidant levels and an increased oxidative stress ratio (Kupper, Gidron, Winter, & Denollet, 2009), which may damage all components of cells (Leopold & Loscalzo, 2009). Finally, HPA-axis activity may be disrupted, as Type D has been associated with an elevated cortisol awakening response within a few days post-MI (Whitehead, Perkins-Porras, Strike, Magid, & Steptoe, 2007) and with increased cortisol production throughout the day 4 months post-MI (Molloy et al., 2008). In addition, both components of Type D personality were related to higher cortisol reactivity in male college students (Habra et al., 2003).
Type D Personality and Patient-Centered Outcomes Mood and Health Status Empirical studies consistently show that Type D personality is related to impaired mood and health status across cardiac diseases. Type Ds generally report impaired quality of life and health status (Al-Ruzzeh et al., 2005; Denollet et al., 2000; Mols et al., 2010;
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Pelle et al., 2008; Schiffer et al., 2005), increased levels of exhaustion and fatigue (Pedersen et al., 2007; Pedersen & Middel, 2001), and feelings of emotional distress, like anxiety (Pedersen, van Domburg, et al., 2004; Schiffer, Pedersen, Broers, Widdershoven, & Denollet, 2008; Van den Broek et al., 2008; Van Gestel et al., 2007), depressive symptoms (Pedersen, Ong, et al., 2006; Pedersen, van Domburg, et al., 2004; Schiffer et al., 2005), and posttraumatic stress symptoms (Pedersen & Denollet, 2004). Clinically relevant mood problems are also more prevalent in Type D patients compared with non-Type D patients (Denollet, de Jonge, et al., 2009; Schiffer, Pedersen, Broers, et al., 2008). In addition, suicidal ideation may be more common among Type Ds (Ladwig et al., 2010). Impaired mood and health status are related to poor prognosis (Mommersteeg et al., 2009). Hence, these patient-centered outcomes are important in the context of Type D personality, but also in their own right (Spertus, 2008). In addition, patients generally are interested in the effect of treatment on their health status and quality of life (Spertus, 2008), and some patients may prefer better quality of life over prolonged survival (Stanek, Oates, McGhan, Denofrio, & Loh, 2000).
Health-Related Behaviors Health-related behaviors may reflect one mechanism by which Type D is associated with adverse health outcomes, such as mortality. Various studies have linked Type D personality to lifestyle factors. In students, Type Ds were less likely to eat sensibly, to spend time outdoors, and to avoid letting things get them down as compared with non-Type D students (L. Williams et al., 2008). Healthy males with a Type D personality more often had a sedentary lifestyle (Borkoles, Polman, & Levy, 2010), and both men and women were shown to be physically inactive (Hausteiner, Klupsch, Emeny, Baumert, & Ladwig, 2010), compared with their non-Type D counterparts. Finally, there is some evidence in cardiac patients that the prevalence of smoking is higher in Type Ds (Martens et al., 2007; Pedersen, Lemos, et al., 2004), but results are conflicting (Pelle et al., 2008; Schiffer et al., 2005; Van Gestel et al., 2007; L. Williams et al., 2008). Type Ds may also differ on their beliefs about treatment and adherence to treatment. Personality variables have been associated with adherence to cardiac rehabilitation (Hershberger, Robertson, & Markert, 1999), and specifically, Type D patients may be less likely to participate in rehabilitation. In addition, several studies suggest that Type Ds are less likely to adhere to their treatment (Brostrom et al., 2007; Williams, O’Connor, Grubb, & O’Carroll, 2011). This may be especially important in the context of CHF patients, which have to adhere strictly to their sodium-free diet and their medication. Finally, Type Ds tend to display impaired consultation behaviors and impaired self-management skills (Schiffer et al., 2007; Pelle, Schiffer, Smith, Widdershoven, & Denollet et al., 2010).
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Interpersonal Functioning The social inhibition component of Type D personality may particularly be related to difficulties at the interpersonal level, since it is known that social inhibition may impede communication between patient and physician (Roter & Ewart, 1992). Social inhibition in Type D patients may be expressed in inadequate consultation behavior and a lack of social support. These factors may be important behavioral candidates linking Type D personality to adverse health outcomes. Adequate consultation behavior is a key component in monitoring clinical deterioration and prevention of hospitalizations. Neuroticism, which is closely related to negative affectivity, has been related to poor keeping follow-up appointments in CHF (Evangelista, Berg, & Dracup, 2001). Results from both healthy individuals and CHF patients suggest that Type Ds experience difficulties in consulting health care professionals (Pelle, Schiffer et al., 2010; Schiffer et al., 2007; L. Williams et al., 2008), while – paradoxically – reporting more somatic symptoms and worrying about these symptoms (Hausteiner et al., 2010; Schiffer et al., 2007). Further, Type D patients who displayed inadequate consultation behavior were shown to be at a sixfold increased risk for impaired health status (Pelle, Schiffer, et al., 2010). Hence, an important aim of interventions should focus on teaching Type Ds to disclose their symptoms. Social support provides a buffer against the effects of stress on well-being, morbidity, and mortality, and lack of social support may augment effects of stress on health outcomes (Mookadam & Arthur, 2004). It has been reported that Type Ds have fewer social ties and experience less social support from family and friends than non-Type Ds in healthy individuals (Polman, Borkoles, & Nicholls, 2010; Williams et al., 2008) and cardiac patients (Pedersen, Spindler, Erdman, & Denollet, 2009). Further, the lack of social support partially mediated the relationship between Type D and stress (Polman et al., 2010). In addition, Type D patients without a partner experienced higher levels of distress compared with Type D patients having a partner (Van den Broek, Martens, Nyklicek, Van der Voort, & Pedersen, 2007).
Interventions in the Context of Type D Personality According to Zerhouni (2006), director of the National Institutes of Health (NIH), an “individual difference approach” to medicine is needed to precisely target treatment on a personalized basis (Zerhouni, 2006). This type of approach implies the identification of subtypes, and Type D personality may comprise a useful tool. Although Type D refers to a personality construct, this does not simply mean that interventions in the context of Type D personality may be not beneficial. Type D individuals are characterized by a distinct psychological makeup, namely, the combination of negative affectivity and social inhibition. However, the psychological problems encountered by Type D patients may also differ in nature across these patients (Denollet & Brutsaert, 1998; Schiffer, Pedersen, Widdershoven, &
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Type D personality A. Improving mood and health status
Cognitive Behavioral Therapy (CBT)
Mindfullness Based (Cognitive) Training
Relaxation Training
Pharmacotherapy
B. Improving health-related behaviors
Exercise therapy
Smoking cessation
Compliance medical regimen
Compliance lifestyle advice
C. Improving interpersonal functioning
Interpersonal Therapy (IPT)
Consultation behavior
Assertiveness training
Fig. 9.2 Overview of interventions in the context of Type D personality
Denollet, 2008; Van den Broek et al., 2008). Therefore, the main goal of interventions and psychological counseling in the context of Type D personality may focus at improving (1) mood and health status, (2) health-related behaviors, and (3) interpersonal functioning (Sher, 2005; Tulloch & Pelletier, 2008). A graphical overview of proposed interventions in the context of Type D personality is presented in Fig. 9.2. To date, three observational studies investigated the role of Type D personality in patients attending comprehensive cardiac rehabilitation. These studies demonstrated that Type D patients reported benefits in terms of improvements in health status (Karlsson et al., 2007; Pelle et al., 2008), but Type D patients still reported significantly poorer health status compared with non-Type D patients after completion of the program (Karlsson et al., 2007; Pelle et al., 2008). Moreover, scores on the DS14 did not change over time in the majority of patients (Barth et al., 2009; Binder, Kohls, Schmid, & Saner, 2007; Pelle et al., 2008). These findings were confirmed in
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a study comparing care as usual compared with expanded cardiac rehabilitation (Karlsson et al., 2007). However, because these studies were not designed to specifically target Type D personality or its correlates, generalizability is restricted. Currently, three randomized controlled trials (RCTs) in cardiac patients incorporating Type D personality are in the phase of patient enrollment. The Short-Term Psychotherapy in Acute Myocardial Infarction (STEP-AMI) trial aims at evaluating the effects of short-term psychotherapy in post-MI patients on clinical outcomes (like cardiac events and rehospitalizations, and comorbidities) and patient-centered outcomes (like health status, depressive symptoms, and social support) (Roncella et al., 2009). Second, the Stepwise Psychotherapy Intervention for Reducing Risk in Coronary Artery Disease (SPIRR-CAD) trial is a German initiative focusing on the effects of three supportive individual sessions of psychotherapy on a weekly basis in CAD patients with depressive symptoms. In addition, patients whose symptoms persist after 4 weeks receive 25 additional sessions of combined psychodynamic and cognitive behavioral group therapy (Albus et al., 2011). The effects on mood, health status, cardiovascular risk profile, neuroendocrine and inflammatory activation, heart rate variability, cardiac events, and health care utilization of this stepped intervention will be compared with patients who receive one counseling session. Finally, the WEB-based distress management program for implantable CARdioverter dEfibrillator patients (WEBCARE) trial is designed to evaluate the effectiveness of a Web-based behavioral intervention in terms of reducing anxiety and device concerns and improving quality of life (Pedersen, Spek, Theuns, et al., 2009). In this trial, the role of Type D personality as an effect modifier will be examined. In the next paragraphs, proposed interventions and psychological counseling in the context of Type D personality, aimed at improving emotional well-being, altering behavioral correlates, and enhancing interpersonal functioning, are presented (see Fig. 9.2).
Improving Mood and Health Status Cognitive Behavioral Therapy Cognitive behavioral therapy (CBT) is based on a cognitive model of depression (A.T. Beck, Rush, Shaw, & Emery, 1979) and is a time-limited and present-focused therapy (J. S. Beck, 1995). Central to CBT is the identification of negative thoughts, views, assumptions, and beliefs about themselves, the world, and the future in relation to mood and functioning (Beck et al., 1979). CBT is based on the premises that (1) important interrelationships exist between situations (having heart disease), thoughts (“my life is worthless”), and emotions (feeling depressed or anxious) (A.T. Beck et al., 1979) and (2) the changeability of these maladaptive thoughts and behaviors. The basis of CBT is cognitive restructuring, which denotes the identification of maladaptive automatic thoughts and restructuring these thoughts into more realistic and adaptive cognitions. This is achieved by the identification of automatic
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thoughts and objective feelings and detaching these from emotions. Next, patients will have to look for evidence supporting these thoughts, and since these can be refuted, more realistic explanations of emotions need to be developed (Beck, 1964). In Chap. 7, CBT in cardiac patients is explained comprehensively. Two major RCTs have been conducted in cardiac patients and have evaluated the effects of CBT on chronic emotional distress and perceived emotional support: the ENhancing Recovery in Coronary Heart Disease patients (ENRICHD) randomized trial (Berkman et al., 2003) and the EXhaustion Intervention Trial (EXIT) (Appels et al., 2005). The ENRICHD trial randomly allocated post-MI patients with depression or low levels of perceived social support to CBT or care as usual. CBT was extended with a selective serotonin receptor inhibitor (SSRI) when needed (Berkman et al., 2003). The EXIT study evaluated the effects of a comprehensive group behavioral intervention in patients that underwent a percutaneous coronary intervention (PCI) on stressors that precipitate vital exhaustion, a syndrome which is characterized by feelings of fatigue, and on support for recovery by promoting rest and making rest more efficient (Appels et al., 2005). These RCTs have shown that CBT significantly reduces emotional distress and improves social support compared with care as usual in post-MI and PCI patients, but nevertheless, no benefits were demonstrated in terms of improved survival or less recurrent cardiac events (Appels et al., 2005; Berkman et al., 2003). Despite the disappointing effects of these trials on hard medical outcomes, reducing emotional distress is nowadays considered a major treatment goal in its own right in clinical cardiology practice (Krumholz et al., 2005; Spertus, 2008). CBT may be a particular effective way of targeting the broad spectrum of negative emotions reported by Type D patients because they experience increased levels of emotional distress (Schiffer, Pedersen, Broers, et al., 2008) and poor health status (Pedersen, Holkamp, et al., 2006). CBT may also target social isolation in Type Ds, which may originate from the social inhibition component (Pedersen, Spindler, Erdman, 2009). Hence, CBT may be particularly effective in Type D patients because it may operate on the emotional and social difficulties associated with negative affectivity and social inhibition.
Mindfulness-Based Cognitive Therapy Mindfulness-based cognitive therapy (MBCT) is based on an integration of CBT with components of the mindfulness stress reduction program developed by KabatZinn (1990). In contrast to CBT, there is little emphasis on changing the contents of thoughts. Instead, the emphasis is more on changing the awareness of and associations with thoughts. Aspects of CBT included in MBCT are those designed to facilitate “decentered views,” such as “thoughts are not facts” and “I am not my thoughts” (Teasdale et al., 2000). The aim of MBCT is to teach patients increasing awareness of thoughts and feelings and to relate these to a wider, decentered perspective. Thoughts and feelings are regarded as “mental events” rather than aspects of the self or reflections of reality.
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It is assumed that the cultivation of a detached, decentered relationship to negative emotions–related thoughts and feelings is central in providing individuals with skills to prevent an escalation of negative thinking patterns (Teasdale, Segal, & Williams, 1995). Because in MBCT there is little explicit emphasis on changing contents or specific meanings of negative automatic thoughts, MBCT training can also occur in the remitted state, using everyday experience as the object of training. MBCT has been shown to be beneficial in reducing emotional distress in patients with chronic disease (Reibel, Greeson, Brainard, & Rosenzweig, 2001) and appears to be particularly effective in patients reporting chronic levels of distress (Ma & Teasdale, 2004). In addition, it has been suggested that MBCT may be more effective in decreasing residual depressive symptoms and psychiatric comorbidity and improving quality of life compared with maintenance antidepressant medication (Kuyken et al., 2008). Recently, the effectiveness of MBCT has been evaluated in CHF patients by means of a prospective cohort study. The results from the Support, Education, and Research in Chronic Heart Failure Study (SEARCH) demonstrated that an 8-week mindfulness-based psychoeducational support group was effective in reducing symptoms of anxiety and depression and increasing improving disease-specific health status compared to patients receiving usual care, and these results were maintained at 12-month follow-up (Sullivan et al., 2009). Despite improvements in patient-centered outcomes, this study failed to demonstrate effects on the combined endpoint of death and rehospitalizations (Sullivan et al., 2009). MBCT may also be effective in reducing chronic emotional distress in Type Ds. Moreover, Type D patients may feel very comfortable using MBCT because it utilizes an inward focus and does not require sharing thoughts and feelings with others. In this way, the feelings of social discomfort, a core characteristic of Type D personality, are avoided.
Relaxation Therapy Relaxation therapy may be offered in a variety of ways, including progressive muscle relaxation, relaxation imagery, autogenic training, or a combination of these ways. Stress management is often incorporated standardly in cardiac rehabilitation programs and is offered in individual or group format. In Chap. 6, techniques for stress management are described in detail for patients living with a cardiac condition. A Cochrane review evaluated 15 trials on relaxation strategies evaluating the effects on depression concluded that relaxation is better than wait-list, no treatment, or minimal treatment aimed at relieving self-reported depression, but not as effective as psychological therapies like CBT (Jorm, Morgan, & Hetrick, 2009). Hence, relaxation techniques have potential as a simple first-line psychological treatment for depression. Those who do not respond within a specific time frame need to be offered more intensive psychological treatment, like CBT. A main advantage of relaxation techniques over other psychological strategies are simplicity, low costs, the option of using a manual strategy, and short duration of training (Jorm et al., 2009).
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Relaxation therapy has shown to be effective in improving symptoms of psychological distress and health status (Collins & Rice, 1997; Hattan, King, & Griffiths, 2002; Trzcieniecka-Green & Steptoe, 1996) and decreasing the occurrence of cardiac events (Bundy, Carroll, Wallace, & Nagle, 1998; van Dixhoorn & Duivenvoorden, 1999) in patients with stable angina, MI, and CAD. In CHF, the effectiveness of relaxation therapy has only been evaluated in multicomponent interventions in elderly patients (Kostis, Rosen, Cosgrove, Shindler, & Wilson, 1994; Yu, Lee, Woo, & Hui, 2007). One study demonstrated improvements in exercise tolerance and mood states in patients with mild CHF using a multicomponent approach (Kostis et al., 1994). More recently, progressive muscle relaxation training was shown to be effective in improving anxiety, depression, and health status compared with a control group receiving supportive phone calls during the study period (Yu et al., 2007). A systematic review on this topic concluded from the results of 27 studies in cardiac patients that relaxation therapy enhances recovery from ischemic events and may contribute to improvements in secondary prevention (van Dixhoorn & White, 2005). Further, relaxation therapy was shown to improve social activities and the quality of social interactions in cardiac patients (Trzcieniecka-Green & Steptoe, 1996). Relaxation therapy may be helpful in Type D patients because this strategy may simultaneously act on both major characteristics of Type D personality. Type D patients may favor this particular type of intervention because it is associated with direct relief of emotional distress–related tension. In addition, relaxation therapy does not rely on intensive verbal social interaction between patients and health professionals, which may be likely preferred by Type Ds, as they experience social interactions as uncomfortable.
Pharmacotherapy Supplemental to psychological treatment, pharmacotherapy may be indicated to target clinical levels of emotional distress. Several trials which evaluated the efficacy and safety of SSRIs in the treatment of clinical depression in cardiac patients have demonstrated improvements in quality of life and mental health (Swenson et al., 2003; Thombs et al., 2008). However, RCTs generally demonstrated disappointing results in terms of improved survival or less recurrent cardiac events (Berkman et al., 2003; Glassman et al., 2002; Jiang et al., 2008; Lespérance et al., 2007; van Melle et al., 2007). SSRIs may also be applicable for changing broad and general personality traits as such, and not only their behavioral and psychological correlates. Several studies examined whether the treatment of depression by means of SSRIs are paralleled by changes in personality traits. A main focus in these studies has been on neuroticism and extraversion, traits with close similarities to negative affectivity and social inhibition. One clinical trial evaluated the effects of SSRIs in clinically depressed patients versus healthy controls and concluded that SSRIs evoke substantial changes in personality traits, with SSRI’s decreasing neuroticism scores and increasing extraversion scores (Du, Bakish, Ravindran, & Hrdina, 2002). More recently, an
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RCT showed that both SSRIs and cognitive therapy in patients with a major depression decreased neuroticism scores and increased extraversion scores, compared with placebo. Importantly, these alterations in personality traits did not depend on depression improvement obtained by SSRIs (Tang et al., 2009). Supplementary pharmacotherapy may be indicated in Type D patients who report clinical levels of emotional distress. Pharmacotherapy may reduce clinically relevant emotional distress and may potentially act positively on negative affectivity and social inhibition, yielding structural changes in Type D personality.
Improving Health-Related Behaviors Altering risk factors and improving health-related behaviors is nowadays considered a main goal in the clinical management of cardiac patients. In the next paragraphs, strategies aimed at altering health-related behaviors in the context of Type D personality will be discussed. Exercise Therapy Exercise training is a key component in the management of cardiac diseases, which is embedded both in cardiac rehabilitation and CBT. Exercise training has shown to be effective in improving clinical outcomes, like survival (Taylor, Unal, Critchley, & Capewell, 2006) and morbidity (Williams et al., 2006), as well as patient-centered outcomes, like quality of life (Cohen et al., 1999) and emotional well-being (Denollet & Brutsaert, 2001). Chapter 13 elaborates strategies on changing sedentary lifestyles in cardiac patients. In Type D patients, exercise training may be especially helpful in improving health outcomes, as Type Ds are less likely to engage in physical activity (Borkoles et al., 2010; Williams et al., 2008). Further, in patients attending multifactorial cardiac rehabilitation, Type D patients reported benefits in terms of physical health status after attendance (Pelle et al., 2008), which indicates that these programs improve at least subjective health in Type D patients. Smoking Cessation Smoking is a major risk factor for the development and progression of cardiac disease (Lloyd-Jones et al., 2009) and is associated with impaired health status in cardiac patients (Riedinger, Dracup, & Brecht, 2000). Hence, smoking cessation is considered a major goal of primary and secondary prevention. In Chap. 14, techniques targeting smoking cessation in cardiac patients are described in detail. The relationship between emotional distress and tobacco use has been described as dynamic, with emotional distress initially leading to tobacco use and becoming exacerbated by emotional distress over time (Orlando, Ellickson, & Jinnett, 2001).
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In post-MI patients, both anxiety and depressive symptoms have been associated with smoking relapse and lower rates of smoking cessation after hospital discharge (Kuhl, Fauerbach, Bush, & Ziegelstein, 2009; Perez, Nicolau, Romano, & Laranjeira, 2008; Thorndike et al., 2008). Overall, negative affect is closely related to smoking relapse, particularly in low distress tolerance individuals (Abrantes et al., 2008), like Type Ds. Some studies have demonstrated that the prevalence of smoking is higher in Type Ds (Martens et al., 2007; Pedersen, Lemos, et al., 2004), which may indicate that in Type Ds, smoking may be a way of coping with stressful situations. In Type D patients who fail to quit smoking, learning alternative ways to deal with negative emotions may contribute to improved health outcomes.
Compliance with Medical Regimen Drug therapy is a core component in the treatment and monitoring of cardiac conditions. Correct adherence to prescribed medications is associated with less health care use and lower costs (Esposito, Bagchi, Verdier, Bencio, & Kim, 2009). However, in the complex process of compliance to prescribed drugs, a broad range of problems may occur (like errors in timing, amount, or frequency of intake). Psychological distress has been associated with compliance to medical therapy. A meta-analysis concluded that depression is associated with a threefold increased risk of poor compliance with medical therapy in chronic disease, whereas the results on anxiety and compliance were less consistent (DiMatteo, Lepper, & Croghan, 2000). In cardiac patients, a review concluded that clinically depressed CAD patients were more likely to forget and skip medications (Gehi, Haas, Pipkin, & Whooley, 2005). Anxiety in post-MI patients has been associated better adherence to carrying sublingual nitrates (Kuhl et al., 2009). On the other hand, anxiety may also lead to poor adherence, like not taking prescribed medications because of fear of side effects. Neuroticism has been associated with poor compliance to medical regimen in CHF (Evangelista et al., 2001), and a study in sleep apnea patients found that Type Ds were less likely to adhere objectively to treatment by continuous positive airway pressure (Broström et al., 2007). Both components of Type D personality are closely linked to adherence to medications. Improved adherence to prescribed medications may be obtained by alleviating emotional distress. Further, better compliance may also be achieved by providing clear instructions and making active inquiries about understanding of information about prescribed medications because Type D patients may be distressed by inconsistent or conflicting medical information, but could be unlikely to ask questions and express their concerns, as a consequence of their feelings of social discomfort.
Compliance with Lifestyle Advice Cardiac patients are strongly recommended to implement lifestyle adjustments, like decreasing salt intake and limiting alcohol consumption. Especially in patients
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living with CHF, these lifestyle rules are strict, with fluid retention, restricted salt intake, weight monitoring, and daily inspection of lower extremities for signs of fluid retention as core activities. Self-reported adherence to these recommendations in CHF patients is known to be modest to low (van der Wal et al., 2006). Psychological distress has been related to poor dietary lifestyle adjustments in healthy individuals (Hausteiner et al., 2010) and in patients receiving an ICD (Luyster, Hughes, & Gunstad, 2009). In addition, neuroticism has been associated with poor compliance to dietary recommendations in CHF (Evangelista et al., 2001). Type D patients appear unlikely to adhere to recommendations with respect to lifestyle changes (Borkoles et al., 2010; Williams et al., 2008). Monitoring, active inquiring, and providing clear information by health care professionals may contribute to improvements in health-related behaviors. Further, recognizing and challenging emotional distress in Type D patients may also contribute to improved compliance.
Improving Interpersonal Functioning Interpersonal Therapy Interpersonal therapy (IPT) is a type of brief psychotherapy, which was originally developed as a research intervention for adult outpatients with major depressive disorder. IPT is characterized by an emphasis on the current social and interpersonal context of depression, but also acknowledges biochemical, genetic, developmental, and personality factors in the etiology of mood disturbances. IPT is founded on the premise of reciprocity between psychosocial stress and mood (Klerman, Weissman, & Rounsaville, 1984) and is, thus, especially applicable to medical settings because it acknowledges the reality of distress associated with medical conditions while encouraging patients to pragmatically move on and make the best of their future (Markowitz et al., 1998). In contrast to other types of psychotherapy using an intrapsychic approach, IPT is characterized by a more interpersonal approach. Generally, one or maximum two areas of interpersonal difficulties are identified. All areas of IPT, except for unresolved grief following the death of a beloved one, are applicable to patients living with a cardiac condition. The problem areas are defined as interpersonal role disputes (conflicts with a significant other), role transition (difficulty adjusting to changed life circumstances), and interpersonal deficits (reduced social networks and social isolation). For instance, a patient who has experienced an MI may experience difficulties with engaging in physical exercise like he or she used to, because of fear of angina, and may consequently no longer attend a regular exercise class. These difficulties may, on their part, negatively impact mood. In addition, IPT also offers the opportunity to target social problems, such as social isolation, resulting from cardiac disease. IPT has been shown to be effective in treating clinical depression in both elderly and chronically ill patients (Markowitz et al., 1998; Reynolds et al., 1999; van Schaik et al., 2006). One study demonstrated the usefulness in decreasing posttraumatic stress symptoms and symptoms of anxiety and depression, while improving
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social adjustment and generic health status. In cardiac patients, an open-label trial evaluated the efficacy and acceptability of a 12-week program of IPT in depressed patients with stable CAD (Koszycki, LaFontaine, Frasure-Smith, Swenson, & Lespérance, 2004). The results suggested that IPT may be beneficial, either alone or in conjunction with medication, in decreasing levels of depression. Moreover, 53% of the patients met the criteria for remission of depression after IPT attendance. Following these promising results, the Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial was designed to evaluate the effectiveness in a more methodologically sound way. However, despite previously promising results, the results of the CREATE-trial were disappointing, because IPT was neither successful in reducing clinical depression nor depressive symptoms, compared with clinical management (Lespérance et al., 2007). A possible explanation for these negative findings may be attributed to the study design because therapists were involved in both conditions of clinical management and IPT. Although therapists were explicitly instructed and trained not to use psychotherapeutic interventions in the clinical management condition, contamination may have occurred due to a double role of therapists. IPT may be particularly useful in the context of Type D personality because Type D patients are prone to increased emotional distress (e.g., Pedersen, van Domburg, et al., 2004; Schiffer, Pedersen, Broers, et al., 2008) and report low levels of social support (Denollet et al., 1995; Pedersen, Spindler, et al., 2009). IPT offers the possibility to target both components of the Type D personality. Emotional adaptation to cardiac disease is a core theme in IPT, and the process of emotional adaptation is often accompanied by emotional distress, which is commonly observed in Type Ds. Second, the social implications of having a cardiac condition, which are embedded in social inhibition component, are another main target of IPT. Hence, IPT may be promising in the context of Type D personality.
Assertiveness Training Type Ds cope with stressful situations by means of passive and maladaptive coping strategies, like resignation and withdrawal (Polman et al., 2010), and neuroticism and extraversion have been linked to fewer problem-solving strategies (ConnorSmith & Flachsbart, 2007). In addition, anger suppression is common in Type Ds with CAD (Denollet, Gidron, Vrints, & Conraads, 2010), indicating that feelings of social discomfort in Type Ds are directed inward and may result in dysfunctional coping. Social expectancies have been associated with assertiveness (Ames, 2008). Type Ds expect to be rejected or disapproved by others in social interactions and can, thus, be regarded as subassertive and socially anxious. Assertiveness training has been associated with better clinical depression outcomes in post-MI patients (Cowan et al., 2008). Moreover, assertiveness training improved communication skills in cancer patients (Street et al., 2010) and in high-risk individuals for mental health complaints (Timmerman, Emmelkamp, & Sanderman, 1998) and decreased social anxiety in psychiatric patients (Lin et al., 2008). Hence, assertiveness training may
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facilitate social disclosure in Type D patients, with these effects likely more pronounced in women (Barth et al., 2009). These improvements may, on their turn, contribute to improvements in emotional distress.
Consultation Behavior Adequate consultation behavior is of crucial importance in clinical management of cardiac disease. Psychosocial factors have been associated with poor consultation behavior, with Type Ds being less likely to consult their health care professional in case of symptom aggravation. Realizing changes in consultation behavior in Type D patients may result from alterations at different levels. First, health care professionals may facilitate disclosure in Type D patients about cardiac complaints by making more active inquiries about complaints and worries. Further, regular follow-up appointments may be a helpful tool to improve clinical monitoring because Type D patients are not likely to consult their specialized nurse or cardiologist in case of symptom aggravation (Pelle, Schiffer, et al., 2010; Schiffer et al., 2007). By means of regular health care professional initiated follow-ups, adequate consultation for cardiac complaints may be less compromised by the socially inhibited behavior of Type Ds. In parallel with changes in the attitude and behavior of health care professionals toward Type D patients, changes on the patient level are also needed. In Type D patients, clinical monitoring of symptoms and consulting for these symptoms may be presented as a shared investment. To obtain these changes in Type D patients, enhancing disclosure and overcoming barriers of social discomfort is required. These barriers may additionally be addressed by means of CBT, IPT, and assertiveness training.
Practical Guidelines for Clinicians How do these recommendations for interventions targeting Type D personality translate into clinical practice of behavioral medicine? In Fig. 9.3, a schematic overview of practical guidelines for clinicians is presented. A first important step in clinical care comprises recognition of high-risk patients. Using a typological personality approach, screening for Type D personality by means of the brief DS14 may facilitate and increase awareness for those patients at high risk for impaired health outcomes. Importantly, psychological risk stratification is important for both mental health care professionals and medical specialists because psychology and cardiac disease are closely intertwined. A next step is the identification of specific individual problem areas in Type D patients. As described in this chapter, difficulties may arise at different levels of functioning, i.e., mood and health status, healthrelated behaviors, and interpersonal functioning. Tailored and multidimensional interventions fitting individual needs should be provided by experienced health care professionals. As a result of the social discomfort, individual interventions may possibly obtain most optimal results in terms of improving psychosocial functioning in
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Recognize
Specify
- Identify high-risk patients (Type D personality)
- Mood and health status - Health-related behaviors - Interpersonal functioning
Intervene
- Tailored interventions - Multidimensional - Shared responsibility
Evaluate
- Effectiveness on patient-centered outcomes - Effectiveness on clinical outcomes
Fig. 9.3 Overview of practical guidelines for clinicians
Type D patients. Further, it is strongly recommended to define psychosocial interventions as a shared goal of patients and health care professionals, with both parties actively contributing to the intervention (Cowan et al., 2008). An important premise for interventions in the context of Type D personality is providing a secure environment to these patients because Type D patients are characterized by social discomfort and are unlikely to consult health care providers for their symptoms and worries (Schiffer et al., 2007). To create such a safe environment, incorporating individually tailored psychosocial care in a “normal” clinical setting may be indicated. In this way, feelings of being “different,” inherent to the social discomfort in Type Ds, can be easily avoided. Psychosocial care may for instance be embedded in comprehensive cardiac rehabilitation programs, with Type D patients being offered additional psychosocial counseling for their personal problem areas of functioning. A final recommendation in the clinical context of targeting Type D personality comprises the systematic evaluation of the effectiveness of psychosocial interventions in terms of patient-centered and clinical health outcomes. By means of systematic evaluation of psychosocial interventions, clinicians can make a valuable contribution to the evidence-based framework of behavioral medicine. In the communication with the individual patient, it is recommended to avoid the labels of “Type D,” negative affectivity, and social inhibition. Rather, it may be better to provide a description by explaining that the patient is sensitive to emotional stimuli and that he or she may probably experience feelings such as anxiety and depression, and that the patient seems to be likely to “bottle up” these emotions.
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Patients often immediately recognize this description of their psychological profile, which may give a sense of relief. In the communication with the medical team on Type D personality, it is recommended to stress that not all patients are likely to open up about their emotional well-being. A growing awareness of interindividual differences may contribute to improved referral of highly distressed patients for further exploration and tailored interventions.
Suggestions for Future Work In the last few decades, a growing body of literature reported on Type D personality in the context of cardiac disease, which has led to an improved insight in the impact of Type D on health outcomes, and possible explanatory pathways linking Type D personality to health outcomes. Nevertheless, future research is needed to resolve a number of pertinent issues. First, little is known about the causal relations between Type D personality and the onset of cardiac disease. Although several studies have addressed the role of genetics (Kupper et al., 2007), environment (Van den Broek et al., 2010), and the independence of indicators of disease severity (Pelle, van den Broek, et al., 2010; Schiffer et al., 2005), suggesting that Type D personality precedes the onset of cardiac disease, no definite answers to this question can be provided at this moment. In order to clarify the causal relationships between Type D personality and the onset of cardiac disease, longitudinal community-based cohort studies are essential. These studies should preferably include a relatively large cohort of young individuals, which allows a long-term follow-up with respect to the onset of cardiac disease over time in relation to Type D personality. The relationship between Type D personality and emotional distress has been established, but results also indicate that not all Type Ds are at increased risk for adverse health outcomes. For instance, particularly Type D patients without a partner were shown to experience increased levels of distress (Van den Broek et al., 2007). Other demographic factors – such as educational level, gender, and age – may also moderate the effects of Type D personality on health outcomes. In addition, psychological factors – such as general anxiety (Van den Broek et al., 2009) or diseasespecific anxiety (Pedersen, Spindler, Johansen, & Mortensen, 2009; Pedersen, Theuns, Erdman, & Jordaens, 2008) – and clinical factors – such as comorbidities (Pedersen, Ong, et al., 2006) – may add to the understanding of the detrimental effects of Type D personality. An evidence-based conceptual framework identifying psychosocial, demographic, and clinical factors that modify the effect of Type D personality may be developed by means of prospective clinical research. Up to now, only few studies have focused on health-related behaviors of Type D individuals, and these studies mainly included students or healthy individuals. Results suggest that Type Ds display less healthy behaviors compared with nonType Ds. Because health-related behaviors may serve as an important pathway relating Type D personality to adverse health outcomes, and may comprise an
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important treatment option in the context of Type D personality, the relationship between Type D personality and health-related behaviors in cardiac samples need to be addressed in future studies. Both research and clinical experience with respect to effective and efficient interventions in the context of Type D personality are still in their infancy. Before RCTs may be designed and conducted, observational studies may shed more light on the interventions that may be effective in Type D patients. It is important to bear in mind insights from previous studies in pitfalls of interventions aimed at improving psychosocial functioning in cardiac patients (DeMets & Califf, 2002a, b). Important issues in the design of RCTs evaluating psychosocial interventions in cardiac disease are – among others – the issue of optimal timing of delivery of these interventions, the composition of appropriate control groups, definitions of both medical and patient-centered outcomes, and the determination of which interventions to offer and their optimal combination. To conclude, Type D individuals are at increased risk for a variety of impaired health outcomes, but concrete empirical evidence that interventions in the context of Type D personality may affect both clinical and patient-centered outcomes is lacking, although evidence from observational studies appears promising. This chapter presented potential interventional strategies that may be effective in improving patient-centered outcomes, health-related behaviors, and interpersonal functioning in Type D patients. A joint avenue for both clinicians and scientists is ahead with respect to interventions in the context of Type D personality.
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Chapter 10
Stress Management with Cardiac Patients Carrie Lukens, Dicle Turkoglu, and Matthew M. Burg
My life is at the mercy of any rascal who chooses to put me in a passion. As he had himself predicted, death came suddenly, in consequence of a fit of temper at a meeting of the governors of St. George’s Hospital. When contradicted flatly, he left the board room, and in the next room gave a deep groan and fell down dead.
The first quote above is attributed to Dr. John Hunter, the esteemed cardiovascular surgeon and pathologist of the eighteenth century; the second was delivered in 1897 by Dr. William Osler as part of his “Lectures on Angina Pectoris and Allied States,” and describes the demise of this pioneering predecessor. Each quote provides a window on what we mean when we talk about stress. What stress is and how we manage it are two questions at the forefront of cardiovascular behavioral medicine, and the above quotations highlight the importance of these issues. In the following chapter, we will first provide a brief and select historical context that focuses on what we believe to be important contributions to how our thinking about stress and its management have evolved. We next provide a model for our understanding of stress that highlights what we believe to be the key elements and foci of stress management interventions. We follow with a description of various stress management techniques, with both a brief empirical grounding and a description of how that technique is accomplished. C. Lukens, Ph.D. (*) • D. Turkoglu, Ph.D. VA Connecticut Healthcare System, West Haven, CT, USA Yale University School of Medicine, New Haven, CT, USA e-mail:
[email protected] M.M. Burg, Ph.D. VA Connecticut Healthcare System, West Haven, CT, USA Yale University School of Medicine, New Haven, CT, USA Columbia University Medical Center, New York, NY, USA e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_10, © Springer Science+Business Media, LLC 2012
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Historical Perspective Early examples of stress – or some construct that we now talk about in such a summary manner – date back as far as Celsus, who in AD 30 is reported to have said, “fear and anger and any other state of mind may often be apt to excite the pulse.” It was not until the 1930s that Hans Selye, a noted endocrinologist, coined the term as applied in the manner used today. Selye’s definition of stress, a word he borrowed from his colleagues in engineering, was “the response of the body to any demand made upon it,” thereby focusing more prominently on the individual and specifically on the body. His pioneering research identified important stress response systems – the hypothalamic-pituitary-adrenal (HPA) axis – and demonstrated elements of the physiological response(s) of these systems – the general adaptation syndrome – to wide ranging physical demands, such as cold and hunger. His particular interest was in both the factors that contributed to the observed response patterns and in the limits of the underlying systems – e.g., the exhaustion of the body’s ability to respond. He elaborated an initial “alarm state” when stress is first brought to bare, a subsequent “resistance state” comprised of a more steady state response, and a final “exhaustion state,” when the systems essentially are no longer capable of maintaining a mounted response, and shut down. The psychological element was not a focus of Selye’s work at this time. Certainly, the bodily aspect of stress is implied in the earlier comments made by Hunter and Osler. It is apparent, however, that much more is implied as well. At least through our twenty-first century ears, we hear something about the context – what Selye may have called the “stressor” – and something about what the “stressed” individual brings to the “interaction” – e.g., how that individual is inclined to respond – physiologically and psychologically. Indeed, we can discern from Osler’s description of Hunter’s final moments that anger was a prominent feature of his demise. Hunter’s temper is well documented, and his own comment implies some self-awareness of how his propensity to interpret and respond to the actions of others left him in the compromised state that ended his life, something that might have been no surprise to Celsus. The second half of the twentieth century brought the psychosocial dimension to the forefront as researchers began to systematically examine the contribution of stress to heart disease. The apocryphal story is told of two cardiologists in San Francisco, Drs. Meyer Friedman and Ray Rosenman who in the 1950s, upon having their waiting room furniture replaced, were told that all but the front edges of the seats and arm rests were in excellent condition. The suggestion was therefore made to merely reupholster what they already had. The pattern with which the waiting room furniture was frayed – just at the edges, as if the seated person was waiting impatiently to be called into the cardiologist’s office – prompted what became a critical line of research. This line of research sought to identify elements of cognition, emotion, and behavior that contributed to risk for early incident CHD. Friedman and Rosenman coined the term “behavior pattern A” to describe this constellation of behaviors that could be evoked through a structured clinical examination. It is
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important to note that, while subsequent investigators and the lay press morphed this construct into a personality style, this was not consistent with the perspective of the originators or of their research. From their perspective, it was the “signs and symptoms” – overt behaviors that were evidence of “hurry sickness,” aspects of voice, style of speaking, and facial expression, all in response to clinical probes – that were paramount. These became the focus of a clinical trial designed to determine whether treating and reducing type A behavior could improve survival after myocardial infarction. Overall, their “stress management” intervention indeed affected outcomes for randomized participants. Perhaps a third body of work that expanded our thinking about stress can be attributed to Richard Lazarus and his colleagues. In the 1970s and 1980s, Lazarus and his group shifted the focus on stress to what they argued were essential elements – the cognitive and emotional. They introduced the concept of “appraisal” as a key ingredient with regard to whether a specific environmental stimulus was “perceived” or evaluated to be “stressful.” It was not merely the appraisal of the environment that was important, however. The individual was also seen to have an implicit sense of the resources they might bring to bare in responding to a perceived stressor of some degree. Thus, the individual also brought an appraisal process to their response repertoire, relative to their appraisal of the stressor. This ongoing, reciprocal system of appraisal was an important element that fully placed the individual within the ever shifting demands of the environmental context. The ongoing interaction between the individual and the environment, with each acting on the other in a dynamic interplay, has carried forward and to the greatest extent defines both the way we approach stress for cardiac patients and the approaches we teach them to manage stress on a daily basis.
Model of Stress We base our approach to stress management for cardiac patients on a cognitivebehavioral model. The model, while grounded in the conceptual work of Lazarus and the treatment literature that grew out of the cognitive psychology movement of the last 30 years, provides the treater and the patient with substantial flexibility. As seen in Fig. 10.1, the model is multifactorial and interactive, and it includes four constituents, with the environment on one side and three types of response for the individual on the other. Within this model, the individual is seen to be in a constant and steady flux of interaction with an ever changing environmental context that presents the individual with situations that may or may not necessitate anything from them. The individual has three levels of response. He or she appraises the environment ongoingly – the work of the mind – and, through that appraisal process, identifies those situations of import that do require something of them. Of course the appraisal process, by bringing along the individual’s history of experience and implicit system of values and imperatives, in part defines the situation and the degree and nature of the
202 Fig. 10.1 Cognitive Behavioral Model of Stress Demonstrating the Complex Interaction of Environment with 3 Person Variables, Mind, Body, Behavior
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demand it comprises, thus the bidirectional arrow. Inherent in the appraisal process are cognitive, or thought-based, processes and emotional processes, themselves interacting and exerting a bidirectional influence. Indeed, a cognitive framework rightly describes how feelings can be given by thoughts and vice versa. By that, we mean a particular appraisal can generate an emotional valence, which in turn reinforces a particular appraisal process over others that might otherwise arise. Additional examples of how the mind contributes to the overall nature of stress include the effectiveness of active problem solving engaged by the individual as the circumstances of the environment become apparent. Similarly, the body demonstrates both an immediate “reflex” and a more nuanced, dynamic, and sustained response that is determined in part by how the demands of the situation are cognitively and emotionally appraised. This response in turn provides input to the ongoing cognitive process(es) and begins to alter the situation. For example, the mobilization of stress response elements of the autonomic nervous system and HPA axis immediately increase cardiovascular activity, mobilize stored energy reserves, prepare the body for fight/flight, and differentially regulate blood supply to the muscles needed for a regulated and targeted response, whatever it may be. The now fully prepared and engaged physical organism, as a part of the overall person-environment entity, has altered the situational element. Similarly, the mobilized body processes contribute to the appraisal process, much in the same way that the emotional element does. For example, a racing heart vs. physical calm provokes a different class of thoughts and comparably, of feelings, while differential activation of various cognitive and emotional centers in the brain affect the ongoing appraisal process. Lastly, we come to overt, explicit behavior. This component of the individual’s response is mobilized and directed (as the physiology) by the cognitive appraisal process, alters the environment most directly, and can provide a modulation of the ongoing physical or bodily response. For example, the cardiovascular and neurohormonal
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response to more cognitively demanding situations (e.g., at work, or when engaged in difficult social exchanges) has been known for some time to be substantially greater than the metabolic needs associated with the physical concomitant of the overall response set. Indeed, one theory holds that this heightened stress response underlies in part the relationship of stress to incident CHD. A behavioral response that is more physical in nature can utilize the mobilized body and thus direct what might otherwise have damaging consequences. It is thought that exercise can serve this role, which in part is believed to underlie the stress-reducing and health-promoting consequences of this type of activity. Similarly, certain behavioral practices can compromise the ability of the body (and mind) to respond sufficiently and competently to demands. These include regular use of tobacco products and overuse of alcohol and caffeine. While the above overly brief description begins to illuminate the underlying complexity of what on paper might look to be a simple model, the good news is found in the bidirectional arrows. These arrows illustrate that an alteration in any of the four constituents of the model alter the remaining three constituents. Thus, stress management can be as multifaceted as the model itself, thereby providing the treater and the individual with a menu of choices. For the remainder of this chapter, we provide the reader with an overview of some of those choices.
What Is Stress Management? The substantial evidence that psychosocial stress contributes to incident cardiovascular disease and early mortality underlies the broad dissemination of stress management programs. The potential contribution of stress management to risk reduction is in part demonstrated by a recent meta-analysis of psychological treatment of cardiac patients in which it was found that psychological treatment, including cognitive-behavioral and self-regulation treatments which in part comprise the typical approach to stress management, can substantially improve post-cardiac-event prognosis (Linden, Philips, & Leclerc, 2007). But what exactly is stress management and what constitutes a stress management program? A cursory look at the literature reveals a wide variety of programs employed in numerous ways with differing techniques and with varying endpoints to demonstrate efficacy. Some approaches utilize relaxation therapies to enable patients to achieve physical relaxation. Others utilize a more cognitive approach to alter stress provoking thoughts. Still others utilize a more behavioral, skills-based approach so as to enhance an individual’s behavioral repertoire for addressing the demands of daily living. Often, a range of techniques are combined in one program, a “kitchen sink” approach. A recent review by Ong, Linden, and Young (2004) sought to define the amorphous concept of stress management and answer three core questions: (1) What techniques are typically used in stress management? (2) How are the protocols constituted? (3) Are they similar enough across studies to be compared? The authors were able to determine that a majority of studies used a combination of arousal
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reducing and skill-building models including relaxation, imagery, and meditation along with cognitive-behavioral therapy techniques. Different names are often given to the same techniques, further complicating matters. The modal delivery for stress management was found to consist six to ten sessions delivered to small groups, an average of 10–15 h of participant exposure during sessions, and home practice. Ong et al. concluded, however, that stress management programs are far too heterogeneous in type and delivery to compare for relative efficacy with distinct patient populations. We follow with a brief review and description of the key features or constituents of the typical stress management program.
Stress Management: Body-Focused Techniques Diaphragmatic Breathing The use of diaphragmatic or deep breathing as a relaxation technique has a long history (Lapiccirella, 1968) and is often used in conjunction with other body-focused techniques. Whether used in the context of progressive muscle relaxation, meditation, or yoga, taking a deep, “cleansing” breath is often the first instruction a patient is likely to hear when being taught any of the physically focused stress management techniques. Deep breathing refers to the act of bringing air deeply into the lungs, which in contrast to the more typical shallow breathing accomplished by flexing the chest and rib cage, is accomplished by flexing the diaphragm. To facilitate deep breathing, patients are instructed to expand the stomach area in a slow and controlled manner – which requires the more pronounced flexing of the diaphragm – so as to draw in air more deeply and more fully expand the lungs. The goal of deep breathing is not only to more fully expand the lungs but to slow the respiration rate and, in so doing, almost immediately provoke a decrease in heart rate due to vagally/ parasympathetically mediated respiratory sinus arrhythmia. When teaching deep breathing, patients may be instructed to lie down or sit comfortably on a chair with feet flat on the floor; the wearing of comfortable, loose-fitting clothing can facilitate the process. One hand is placed on the stomach while the other is placed on the chest. The patient is then instructed to inhale slowly through the nose, drawing the breath deep into the lungs, noting that with deep breathing, only the hand on their stomach should move outward while the hand on their chest should remain largely stationary, thereby indicating that the diaphragm is expanding. The patient is also instructed that exhalation through the mouth should be slow and controlled, noting that the hand on the stomach should now be moving inward as the diaphragm contracts. This continues for several minutes. Patients can at first have difficulty learning to engage their diaphragm, and some can become frustrated when they have difficulty “switching” from their more usual method of shallow, chest breathing. Practice most often will lead the patient to acquire the requisite skill.
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Several studies have demonstrated some health benefits of deep breathing alone as a stress management technique. For example, the regular utilization of this technique is associated with reduction in blood pressure even in patients with resistant or uncontrolled hypertension. Viskoper et al. (2003) found that resistant hypertensive patients who engaged in 8 weeks of guided, slow breathing had significant reductions in both office and home blood pressure. Furthermore, a recent evaluation (Kulur, Haleagrahara, Adhikary, & Jeganathan, 2009) demonstrated increased parasympathetic tone among 145 male CHD patients who regularly used diaphragmatic breathing for 1 year. This latter finding is particularly noteworthy given that low parasympathetic tone can increase risk for cardiac events in patients with CHD.
Progressive Muscle Relaxation Progressive muscle relaxation (PMR), a technique that encourages relaxation via awareness of tension in the main muscle groups and, through paradoxical means, produces relaxation, was developed by Edmund Jacobson in the 1930s (Jacobson, 1938). The method involves the alternate tensing and relaxing of each muscle group in turn. PMR is often used in concert with deep breathing techniques, with the patient instructed to take five deep breaths before tensing each muscle group. Originally, progressive muscle relaxation involved 16 muscle groups and was composed of up to nine 1-h-long sessions focusing on each (McCallie, Blum, & Hood, 2006). The Jacobson method was later adapted by Joseph Wolpe for use in systematic desensitization. Wolpe reduced the training to six 20-min sessions and two daily 15-min at-home sessions (McCallie, Blum, & Hood, 2006). Bernstein and Borkovec (1973) further modified the basic procedures by incorporating a set of “fading” procedures, moving from 16, to 7, and then to 4 muscle groups, ending with the use of relaxation by recall. When conducting a progressive muscle relaxation session, the patient starts by assuming a sitting position on a comfortable chair, with both feet flat on the floor. They are asked to close their eyes and take several slow, deep breaths before directing their attention to the first muscle group. The therapist then directs the patient to tense this muscle group and maintain the tension for 5 s, while focusing on the feeling of tension. The therapist then directs the patient to release the tension and focus on the feeling of relaxation. This is done for each muscle group in turn. The goal is for the patient to recognize the visceral feeling of tension and relaxation in the muscle group, while providing the patient with a distinct procedure for inducing a state of (relative) relaxation in that muscle group. At the completion of all the muscle groups, the patient may be asked to count backward from four, gradually moving their limbs and opening their eyes. Like deep breathing, PMR has demonstrated benefits for patients with CHD. For example, a study by Wilk and Turkoski (2001) found a reduction in resting heart rate and state anxiety and a high degree of patient satisfaction associated with PMR. Others have found that patients using this technique evidenced significantly lower blood
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pressure from pretreatment to follow-up 4 months after the end of the progressive muscle relaxation training phase (Garcia-Vera, Sanz, & Labrador, 2004).
Guided Imagery/Visualization Guided imagery involves directing the patient’s thoughts or inner focus toward an image of a safe, comfortable place such as a beach or garden. The instructions to the patient serve as prompts to include key details in the image or visualization, with a particular effort to incorporate as many senses as possible. Suggestions therefore often include what the individual would see (e.g., blue sky, gentle clouds, sun overhead), hear (e.g., the sound of waves gently breaking on the shore, of seagulls overhead, of people off in the distance), feel (e.g., the warmth of the sun, texture of the sand or ground beneath their toes, the gentle breeze on their skin), and/or smell (e.g., the faint ocean mist, the sweet perfumed air). The more detailed the visualization, the more effective the immersion into a state of relaxation can be. Patients are usually instructed in the technique during an in-person session and then given audio instructions for home practice, but guided imagery can be effectively implemented utilizing only at-home practice. As patients practice the technique and become more effective in implementing it without the audio instructions, they are often encouraged to develop their own visualizations. Results of using guided imagery as a relaxation technique in patients with cardiovascular disease are generally positive, although effect sizes appear to be smaller than with other techniques. Yung, French, and Leung (2001) compared PMR, stretch release relaxation, and cognitive imagery relaxation in men with a diagnosis of hypertension. All three therapies reduced blood pressure, but the effect size for imagery relaxation was smaller. Imagery has also been found effective for anxiety, pain, and reducing length of hospital stay when used prior to and after cardiac surgery. Halpin et al. (2002) gave interested patients who were to undergo cardiac surgery an audiotape of a guided imagery exercise in the week prior to surgery. The patients listened to the tape several times a day and while waiting on the day of surgery. There was a significant decrease in length of stay and self-reported anxiety in the guided imagery group compared to controls.
Autogenic Training Autogenic training is similar to PMR, as it involves concentration on key sensations in specific parts of the body. It is derived from the work of Johannes Schultz (1932) who found that he could create a state similar to that of a hypnotic trance by having patients focus on sensations of warmth and heaviness in their extremities; the focus on heaviness promotes relaxation of the large, voluntary muscles of the body. The focus on warmth promotes peripheral vasodilation.
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The instructional set for the patient is also similar to that used for PMR. The patient is instructed to assume a comfortable lying or sitting position and asked to focus on sensations of warmth and heaviness in different parts of the body including their arms and legs. By sitting in a “rag-doll” position, with their hands hanging downward below their waist, blood pools in these extremities, thus implicitly increasing warmth and a sense of heaviness. The patient is next instructed to take several slow, deep breaths and is led through a series of suggestions. These suggestions are repeated four times slowly, taking about 5 s to say each one with a pause of 3 s between each repetition. “My right arm is heavy…My right arm is heavy… My right arm is heavy…My right arm is heavy.” This is repeated for the left arm, both arms, right leg, left leg, both legs, and finally, both arms and both legs. Then the set is repeated substituting warmth for heaviness. These instructions are often broken down into three sets, heaviness, warmth, and both heaviness and warmth. The final set is concluded by a statement such as “I am calm and relaxed.” Research has shown autogenic training to be as effective as other forms of relaxation, with reductions in systolic blood pressure among mild to moderate hypertensives observed (Stetter & Kupper, 2002). A review by Linden (1994) found moderate pre- to posttreatment effect sizes for change in biological, psychological, and behavioral indices, similar to that seen for PMR. Linden’s review further found autogenic training to be effective in reducing systolic blood pressure in patients with essential hypertension, and self-reported anxiety, depression, fatigue, and resting heart rate in patients recovering from MI.
Meditation and Mindfulness Meditation is a process by which one attempts to generate a focused state of relaxation and awareness. As an approach specifically to stress management, meditation has been shown effective for reducing blood pressure and cholesterol, for improving endothelial function, and for decreasing anxiety, depression, and smoking behavior. There are many different types of meditation including mantra, mindfulness, and those used in yogic and tai chi practices. One popular form of mantra meditation is called Transcendental Meditation (TM). TM has its roots in the Vedic tradition and was introduced in India in 1955 by Maharishi Mahesh Yogi. It is taught by a trained teacher who uses a standardized method involving seven steps and the use of a mantra. A mantra is syllable, word, or group of words that are chanted or sung in repetition during the period of meditation. Individuals practice for 15–20 min twice a day. Once the mantra is determined, the patient selects a comfortable sitting position either on a chair or on the floor. The patient closes their eyes and begins slow, deep breathing. They then begin to chant their mantra over and over again either silently or aloud. The chant is slow and steady, often paired with in and out breaths. The patient is reminded that when thoughts begin to intrude on this relaxation, to note it and then bring their attention back to the mantra. All focus is to be given to the mantra and should be done with awareness.
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Other types of meditation include focusing on breath. In this variation, attention is fixed on the rhythmic rise and fall of the breath. When the mind begins to wander, focus is gently brought back to the breath. Counting breaths can also be used as a focus of attention. If the patient loses track, they simply start counting over. In the beginning, the patient may only be able to maintain meditation for 5 min before becoming uncomfortable or frustrated. As the patient learns ways to focus their attention and move away from intrusive thoughts, they can begin to increase the amount of time spent in meditation toward a goal of 20–30-min sessions. Mindfulness-based meditation is different from its mantra-based counterparts. It involves a process of training ones attention to focus nonjudgmentally and “in the moment.” The patient is taught to observe but not judge their moment to moment thoughts and emotions without becoming immersed in them. It is rooted in Theravada Buddhism and was popularized for use as a general stress management technique and for specific medical presentations by Jon Kabat-Zin in 1979. Some specific mindfulness techniques include focusing on an object and describing it, noting the colors, the texture, and the shadowing. Attention is wholly on the present moment and the object of attention. When other thoughts enter consciousness, they are acknowledged not suppressed or ignored, and then attention is brought back to the present. This technique can also be employed on a host of other everyday tasks such as eating or doing the dishes. The patient focuses on the task they are completing, noticing all of their senses in the moment, not thinking about the next task they will complete or what happened at work earlier that day. When these thoughts interfere with the present moment, they are again acknowledged and attention is brought back to the present moment. Meditation as a stress management strategy has had few rigorous clinical trials. A review by Ospina et al. (2008) found that most clinical trials on meditation were of poor quality with significant design flaws and threats to internal validity. Those that have been done have generally reported reductions in cardiovascular risk factors such as blood pressure and cholesterol in patients with hypertension, diabetes, and CVD. A review by Rainforth et al. (2007) reported that the TM program was superior both to other forms of meditation and other forms of stress management for reducing blood pressure and anxiety over 8 years in patients with hypertension. Results from studies of mindfulness-based meditation have also found positive results including decreased self-reported stress, anxiety, and dysphoria in a general population, and decreases in mood disturbance, anxiety and depression, and selfreported stress symptoms in cancer patients (Bishop, 2002; Baer, 2003). More rigorously controlled trials are needed to determine the merits of meditation as a stress management strategy.
Yoga and Tai Chi Yoga and Tai Chi are two forms of exercise that have in recent years come to the attention of clinicians and researchers for stress management purposes. While yoga typically involves focused and somewhat static stretching and strengthening
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exercises, Tai Chi typically involves the slow performance of a movement routine. Each can be performed privately or in groups, under the instruction of a trainer. In one study of Yoga, 42 men with CAD were randomly assigned to usual care or usual care plus yoga. At 1-year follow-up, the yoga group demonstrated significant reductions in angina, improved exercise capacity, and reductions in body weight, total cholesterol, LDL cholesterol, and triglyceride (Manchanda et al., 2000). Patients in the Yoga group also demonstrated fewer revascularization procedures and a significant regression in atherosclerotic lesions. Others have also found a reduction in blood pressure in patients practicing Yoga. Murugesan et al. (2000) randomized 33 hypertension patients to either usual care or 11 weeks of two times a day Yoga. At follow-up, Yoga was found to be as effective in lowering blood pressure as medication, a finding recently replicated (Jayasinghe, 2004). Studies using Tai Chi are less prevalent. Tsai et al. (2003) randomized 76 subjects with normal blood pressure or stage 1 hypertension to either 12 weeks of three times per week Tai Chi or a sedentary control group. They found decreased blood pressure, improved fasting lipid profiles, and decreased state and trait anxiety in the Tai Chi group compared to control. Channer et al. (1996) found a comparable effect among 126 post-MI patients. A recent systematic review by Yeh, Wang, Wayne, and Phillips (2009) found six randomized controlled trials with adequate sample size. Their review determined that a typical 12-week program of Tai Chi contributes to decreased blood pressure. Additional controlled trials of Yoga and Tai Chi are needed to determine their effectiveness and benefit for cardiovascular disease.
Stress Management: Cognitive-Focused Techniques A cognitive model of stress infers that it is the appraisal or interpretation of a situation and not the situation itself that in part provokes the emotions, physiological responses, and behaviors that we define within the interactional stress model and that are associated with the situation. These interpretations – or automatic thoughts – happen quickly and usually without awareness. While automatic thoughts may accurately appraise a situation, thereby saving time and energy in the navigation of different situations, they can also be inaccurate, erroneous, and/or unhelpful, provoking a greater experience of stress and associated physiological activation. Automatic thoughts of this kind are implicit misinterpretations of an otherwise neutral or even positive situation as threatening or stressful. Cognitive-focused stress management is a structured method by which automatic thoughts are brought to awareness and tested against evidence. Alternate appraisals or thoughts are intentionally generated and similarly tested, with the aim of transposing this more functional thinking process for the troublesome automatic thoughts that can be stress provoking. While emotions that contribute to stress are difficult to change directly, the correlated nature of thoughts and feelings means that a different set of thoughts will implicitly and immediately transform the emotions that occur with such thoughts. For example, a question regarding one’s actions from a boss or spouse can generate automatic thoughts that one is being criticized. These thoughts
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will occasion feelings of defensiveness, anger, and anxiety, and behaviors that can range from argument to withdrawal. Alternatively, thinking that the questioner is interested because of the contribution that the initial action has had will occasion feelings of pride and happiness, with consonant behaviors. In this way, automatic thoughts differ from “thinking.” The former is rapid and often unrecognized, representing in many ways the internalization of rules and experiences acquired both directly and indirectly (e.g., through the observed behaviors – often subtle – of others) throughout a person’s life. In contrast, “thinking” is a volitional activity that is dispassionate and critical in nature and can be used to objectively observe and analyze ongoing circumstances. The goal of cognitivefocused techniques is to use thinking as a means of short circuiting automatic thoughts and thereby alter the overall stress equation. Most people are generally unaware of the automatic nature of most of their thoughts, and of the correlated nature of their thoughts, feelings, and actions. An introduction to, and overview of, the cognitive model is thus very helpful. As part of this introduction, it is helpful to have the patient describe a recent scenario and have them articulate the automatic thoughts and correlated emotions they experienced at the time. A good way to elicit examples is to work backward from strong emotions or forceful actions. Since emotions like anger, sadness, or anxiety are more readily observed by patients, they are more likely to be presented as examples to illustrate the cognitive model. A patient who is unable to even provide a historical example can be asked to identify their emotions in that moment (e.g., frustration, confusion) and assisted in identifying their concurrent automatic thoughts (e.g., “I am not getting this” and “I am so stupid”). Oftentimes, cognitive distortions – which are common systematic negative biases in such beliefs – can be identified. A list of the most common types of cognitive distortions can be presented to the patient. This presentation should then be followed up by an explanation of each distortion using the patient’s own examples (c.f., Beck, 1995). Once the patient can demonstrate through personal examples their understanding of the cognitive model, the next step in this element of stress management is helping them establish a habit of monitoring and identifying their automatic thoughts and the correlated emotions that are occasioned by these thoughts. They also gradually add the monitoring of the behaviors that follow from the thought–emotion pair, and the results of these behaviors with regard to the original stressful circumstance. This can be achieved by having the individual keep a formal diary that among these factors includes a record of negative (and positive) mood episodes and the circumstances under which these episodes took place. After keeping such a record for 1–2 weeks, the next step in cognitive stress management is learning to dispassionately and critically evaluate automatic thoughts. The identified thoughts are “challenged” by examining the evidence in the environment (e.g., including the behavior of others) that does and does not support the veracity of the thought. The patient is taught a formal process of articulating these “pros” and “cons.” Additionally, this serves to identify the assumptions and beliefs through which environmental circumstances are experienced and that this prompts automatic thoughts. Such a thorough evaluation of the automatic thoughts and the
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identification of the faulty beliefs that these thoughts stem from lead naturally to the last step, which involves the generation of alternate thoughts that are more accurate, helpful, and adaptive. This step can be as easy as asking the patient, “What would be another way of thinking about this that would be more helpful?” When the patient is having difficulty responding to this question, the therapist can use Socratic questioning to facilitate the process. If the patient is unresponsive to Socratic questioning, a behavioral experiment to test the original thought or belief might be useful. For example, a patient who has the belief “If I am late in turning my work in, I will be publicly humiliated by my supervisor” might be asked to turn in some work late purposefully to put his original unhelpful automatic thought to test. With repeated practice, the patient learns to incorporate this new set of skills for utilizing cognitive elements in an overall approach to stress reduction. Ascertaining the efficacy of cognitive stress reduction techniques alone is difficult, though certainly the evidence base for these techniques in the treatment of anxiety, depression, and anger is well documented (c.f., Roy-Byrne et al., 2010; Gibbons et al., 2010). As part of an integrated approach to stress management, these approaches have been shown to reduce type A behavior with improved post-MI event-free survival (Friedman et al., 1982, 1987) and reduce the occurrence of mental and emotion provoked myocardial ischemia and both improve event-free survival (Blumenthal et al., 1997) and reduce health-care costs (Blumenthal et al., 2002).
Stress Management: Behaviorally Focused Techniques Structured Problem Solving Within the context of the interactional stress model, the manner in which an individual behaviorally responds to demands that arise during the day, and the effectiveness of their responses can serve to increase or reduce the demands that individual is subject to. Sometimes an individual’s response to real problems can be shortsighted or consequent to an interpretation of the demands that is emotional in nature. Some patients can be deficient in problem solving in general, while some others are temporarily perplexed by a problem because they are overwhelmed by a large number of concurrent demands. Structured approaches to problem solving can be helpful in managing these multiple and complex demands. A structured approach to problem solving was articulated by Goldfried and D’Zurilla almost 40 years ago (D’Zurilla & Goldfried, 1971), and this approach has been put to effective use for the treatment of depression in general medical populations (Unützer et al., 2002) and in patients after acute coronary syndrome (Davidson et al., 2010). Within this framework, effective problem solving is broken down into five steps: 1. Defining the problem. The first step for effective problem solving is to objectively and specifically define the problem, pinpointing essential elements – including
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whether it is really under the individual’s control – rather than defining it in global terms. It is helpful to emphasize the behavioral aspects of the problem to bring it more to the observable realm and, as necessary, to break down a large problem into smaller constituent parts. Lastly, it is important to establish realistic and achievable goals for the defined problem. Brainstorming – generating multiple solution alternatives. The second step in effective problem solving is generating multiple solution alternatives to the articulated problem. At this point, it is imperative to communicate to the patient that the goal during brainstorming is to come up with as many alternatives as possible and to specifically not judge or evaluate them at this point. A minimum of three alternatives is essential. This promotes flexibility in thinking, which is a vital skill to master for tackling future problems. Weighing the pros and cons. Following the compiling of multiple solution alternatives, the patient and therapist engage in a discussion to carefully and objectively identify the advantages and disadvantages of each possible problem solution. Some things to consider are the practicality of the solution, whether or not the patient currently possesses the skills to implement this solution, and the financial, energy, time, and emotional cost of the solution. It is helpful at this point to have the patient list these advantages and disadvantages, so as to help organize the discussion and the selection process. Selecting and implementing a response. The third step is to select the best approach based on the review of the pros and cons and implement that solution. Evaluating the outcome. Finally, the fourth step involves an evaluation of the outcome of the solution that was implemented. Was the problem solved? Did new elements of the problem emerge? Where do things stand now? Based on such an objective evaluation, the patient can move on to the next problem, make adjustments to their originally selected solution, or abandon that solution and reconsider other alternatives as needed. Essentially, this step entails a regeneration of the complete problem-solving approach.
Of note, the results of randomized trials of problem-solving therapy with medical populations demonstrate that this behaviorally focused approach to stress management can be taught easily, quickly, and with brief sessions. Thus, problem-solving therapy can provide an overall important element to stress management.
Time Management Most people are faced with multiple demands that must be addressed in a parallel rather than sequential manner. Furthermore, many of the demands are complex and involve multiple elements and multiple steps. Being able to “schedule” demandrelated activities in an effective manner allows an individual to respond more effectively to the multiple demands that they face. In time management – like effective problem solving – demands are broken down into discrete behavioral elements, and,
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in so doing, a structure is provided for knowing when things have been accomplished and where they stand along that route toward accomplishment. While not fully consistent with its “title,” time management is really more focused on results than on time alone. While time is an abstract concept, results are concrete and observable. Time merely comes into play when we have as a goal the production of some result by some point “in time” – but it is the result that is most essential. Results, since they are objective and observable, can be tracked, and their completion acknowledged. In focusing on results rather than time, an additional aim is to explicitly incorporate the patient’s goals. Encouraging patients to identify short, intermediate, and long-term goals allows them to bring an awareness concerning what they want as they engage with the demanding circumstances they encounter. It allows the patient to place these demanding circumstances within a larger context while providing them an awareness of the choice and influence they bring to these demands. Goals can be “nested” in that the accomplishment of a larger or longer term goal is based on the earlier accomplishment of a short-term or smaller goal. Thus, “subgoals” serve two functions. They are mileposts along the way of achievement and provide incentives to keep directing effort toward the large goal by providing reinforcement and feedback. Subgoals thereby highlight accomplishments along the way to the ultimate goal. To manage results, it is important to define goals that are “SMART”: specific, measurable, attainable, realistic, and occurring within time. Another key concept in time or results management is defining priorities for one’s goals. Priorities allow patients to make educated decisions about where to allocate their limited efforts. A similar key concept for results management involves differentiating between urgency and importance. Each day, situations arise that have urgency to them. By definition, these situations demand our immediate attention; however, urgency does not equal importance. Focusing attention, effort, and time on urgent yet unimportant tasks is a common time management mistake that leads to poor results management. In such situations, prioritization of goals as discussed earlier is helpful. This raises the question of how to identify priorities. Identifying an individual’s values allows them to distinguish between what is important and what is merely urgent. Values can be articulated by thinking about them or can be identified by studying existing goals because often values are inherent in goals.
Communication Skills Training While not usually contextualized as an approach to stress management, most demanding situations involve communication, and therefore clear communication can go a long way toward reducing or preventing stress. We define three important elements to effective communication: Active listening – is the basis of good communication, bringing together the effort of openly listening to what another is saying, which requires the absence of any under-
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lying agenda, and reflecting what was heard to insure a match between what was spoken and what was heard. The specific components of active listening can include: 1. 2. 3. 4. 5. 6. 7.
Listening without interrupting Maintaining good eye contact and nonverbal encouragement such as nodding Observing the speaker’s nonverbal cues Reflection: checking for accuracy in hearing and understanding Use of open-ended questions to probe the speaker for detail Summarizing and clarifying Responding
Nonverbal communication – involves the implicit or explicit use of facial expression and body posture/movement during communication. Awareness of what the face and body communicates when one is speaking is essential, as these can undermine or reinforce one’s words. Appearing calm, in control, and interested in the other person during verbal exchanges can enhance the effectiveness of communication bidirectionally, particularly regarding requests being made or responded to. Similarly developing an awareness of one’s facial expressions and body posture when speaking provides one with tools to mitigate any emotional charge that is unhelpful when one is communicating and/or enhance the impact and clarity of one’s message. Speaking style – is particularly important when making or responding to demands and requests. Styles include passive, aggressive, passive-aggressive, and assertive. Assertiveness is perhaps the most effective method for communicating effectively. Briefly, assertiveness involves clearly stating one’s request and needs. It also involves an acknowledgement of the other person’s perspective when making requests and stating one’s needs and making sure the listener understands the nature of the request or response being made. Assertiveness is important when making requests and when responding to requests, with the freedom to decline a request without appealing to excuses. Role-playing can be helpful in learning communication skills. Some barriers to assertiveness that may need to be problemsolved by therapist and patient involve fear of rejection and various forms of distorted thinking (e.g., black/white, “should”, mind reading, etc.). Patient should also be reminded of some of the blocks to effective communication. These include: (a) Me-too statements: dismissing what the other person is saying by coming up with an example from one’s life (b) Moralizing, preaching, being judgmental (c) Inappropriate questions that are only asked in order to satisfy the listeners curiosity and do not add to the discussion (d) Advice giving when not specifically asked (e) Interrupting (f) Defensiveness: inability to flexibly think through what is being said
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(g) Hearing only facts but not feelings: being overly concerned with the facts of a conversation while not paying enough attention to the emotional intent of the speaker (h) Hearing what is expected and not what is said (i) Automatic dismissal In short, using open listening and clear speaking ensures that both parties involved in communication will be aware of each other’s points of view, requests, and needs, thereby facilitating the alleviation and/or prevention of stress. Case Illustration John was a 52-year-old married man with three children. He was employed as a manager at a local grocery store, working in a supervisory capacity. During routine screening while in hospital for an acute MI, he explained that since his promotion to manager last year, he has been under overwhelming stress at work. His recent health concerns were now added to that tension. John had been referred to a local cardiac rehabilitation program, and as an adjunct that program John was able to participate in a six-session stress management program that met weekly for 1 h. This program taught a range of cognitive-behavioral skills that covered body, behavioral, and cognitive-focused techniques Session 1 During the first session, John and the other four individuals in the group were introduced to each other and the group leader. During the session, the group participants were introduced to the cognitive-behavioral stress model, and the group leader used this to describe how stress affects not only the body, physiologically, but thoughts, emotions, and behaviors as well. The group leader then reviewed the topics that would be covered in subsequent sessions to address these areas. The remainder of the first session was used to teach diaphragmatic breathing, with the leader demonstrating the proper technique and having group members practice. Before having them practice, she had each person rate their level of relaxation on a scale from 1 (the lowest) to 10 (the highest). John rated his level of relaxation at 4. During practice, he had difficulty flexing his diaphragm and became frustrated. The leader told John to imagine that he had a balloon inside his stomach that was filling with air. After several more minutes, John was able to expand his stomach more consistently. The leader described to the group that many people normally breathe using shallow chest breathing and that it would take time and practice to be able to perform diaphragmatic breathing regularly. After 10 min of practice, she had each person again rate their level of relaxation. John rated himself at a 7. The homework assignment for the next week was to practice diaphragmatic breathing twice per day for 5–10 min each time, noting level of relaxation before and after.
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Session 2 Session 2 started with a review of the homework from the previous week. John reported that he was still having difficulty flexing his diaphragm consistently but was getting better. He noted that his level of relaxation usually increased by two to three points each time. After checking in with each group member, the leader then quickly reviewed diaphragmatic breathing and had everyone practice for 5 min before moving on to the new topic for the week, time management skills. The key concepts of time management – focusing on results rather than time, identifying priorities, and using the acronym “SMART” to help articulate goals (specific, measurable, attainable, realistic, time based) – were introduced. John volunteered to describe a typical work day in which he often has more tasks to complete than he has time for. The leader worked with John on ways to prioritize the tasks for the day, break down larger tasks into smaller, more manageable pieces, and then organize them so he could work more efficiently. For example, John reported that he wasted a lot of time going back and forth from one end of the store to the other during the course of the day to complete different tasks. By prioritizing tasks each morning, John could see what needed to be accomplished and then complete several tasks that were in the same part of the store at one time. The homework for the next week was to continue to practice diaphragmatic breathing twice daily for 5–10 min and to use the SMART goal worksheet during the week as an aid in utilizing time management skills.
Session 3 Session 3 started with a review of the homework from the previous week. John reported that his diaphragmatic breathing was continuing to get easier although he still occasionally had some difficulty with flexing his diaphragm. He also noted a three to four point improvement each time. John reported that he was having success using time management skills. He was spending 10–15 min each morning prioritizing tasks and organizing them so that he could be more effective and efficient. He also realized that he often took on tasks that were more appropriately accomplished by others. He was still not able to complete as many tasks as he wanted during the day, which led to higher levels of stress toward the end of the day, but noted improvement in his overall stress levels each morning. The focus of the third session was on communication skills. The leader discussed the importance of using an assertive style of communication in order to communicate your needs and wants. Using an assertive style reduces stress in the interaction as it is respectful of each person and is more likely to result in your getting your needs met, unlike in aggressive or passive styles which can often lead to anger and resentment. The leader gave examples of each style and discussed examples of common blocks to effective communication. John noted that his style of communicating with his subordinates was often passive, which resulted in his requests being ignored. His frustration would then reach a “boiling point” so that he became aggressive, often yelling by the end of the day. John went on to provide an example of a request
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he typically had to make of subordinates at work. He role-played with another group member and practiced making the request using an assertive style. The end of the session was spent introducing progressive muscle relaxation (PMR). The leader used a bottom-up approach, with tension and relaxation of the feet first, all the way up to the head. John’s level of relaxation was at a 5 before the practice and he noted that it was a 10 after. Participants were given a CD which contained a guided progressive muscle relaxation exercise. Homework for the next week was to practice using assertive communication when making requests and to practice PMR twice daily.
Session 4 During the review of homework, John reported that he really liked progressive muscle relaxation and was usually able to achieve complete relaxation by using the technique. He also reported success making assertive requests at work, describing not only that his subordinates were completing tasks more readily but that the overall tone of interactions had “cooled down.” He also reported that because he was better at delegating tasks, he was able to accomplish more at work, which led to an overall reduction of his stress levels. The new technique for the session – cognitive restructuring – was then introduced. The leader reviewed the stress model to reiterate how stress, the body’s physiological response, thoughts, emotions, and behaviors are all interconnected. She then introduced the first part of cognitive restructuring, automatic thoughts, and described how they are related to our emotions and can ultimately produce and increase stress, using examples from group members. John identified a situation where his boss said he wanted to speak with John later in the day. John reported has automatic thoughts as, “I must have done something wrong” and “He’s probably going to fire me.” He experienced high levels of negative emotions and overall stress for the rest of the day until he was able to speak with his boss, who had just wanted to see how he was transitioning back to work since his MI. The group discussed how John’s automatic thoughts had left him feeling unnecessary stressed. The group members were given a thought record to monitor their automatic thoughts in situations during the next week. They were also asked to keep track of their emotions during those situations, and of the outcome (i.e., their behavior). They were also told to continue practicing PMR twice per day using the CD and rating their level of relaxation before and after.
Session 5 During homework review, John reported continued success using PMR. He also described several situations during which he had automatic thoughts – catastrophic in nature – that increased his stress. The leader used these examples to introduce the next part of cognitive restructuring: evaluating and changing negative automatic
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thoughts. Using a worksheet that listed questions for testing the accuracy and “groundedness” of automatic thoughts, she described how to examine the evidence in support of, and not in support of, a given thought. She then described how to use the evidence to articulate a more realistic thought for that situation. Using examples from their homework, group members practiced these processes. John chose to practice using an argument he had with his wife the previous week. He had forgotten it was his turn to pick up their daughter from soccer practice and was 25 min late. His wife had asked him why he had been late, and their conversation eventually spiraled into an argument. John had identified his automatic thoughts – “I’m the worst father ever” and “My wife would never do something so irresponsible” – and his emotions: guilt, shame, and anger. The outcome had been behaving defensively toward his wife’s questions, which led to an argument. The group evaluated John’s automatic thought, “My wife would never do something so irresponsible,” by asking him what evidence he had for and against it. John stated that his wife was a wonderful mother, she was very organized and made a point of being on time for things, and that she would call if she was going to be late. With some prompting from the group that no one was perfect, John was then able to come up with an example of a time when his wife had been irresponsible. After examining the evidence for and against John’s automatic thought, the leader then had John articulate a new, more realistic thought to replace his old one. He stated it was more accurate to say, “I wasn’t very responsible in forgetting to pick up my daughter but it could happen to anyone. I will write things down in the future to help me remember.” He also was able to describe that he loved his children, and to describe overwhelming evidence of this. Guided imagery relaxation was introduced in the last part of the session, with a CD given out for home practice. Homework was to practice evaluating negative automatic thoughts and replacing them with more positive and realistic thoughts.
Session 6 During homework review, John reported some success identifying his negative automatic thoughts quickly and a growing ability to evaluate them and replace them with alternative thoughts. The leader explained that with continued practice, John and the others would get better, but that they would likely always have situations where their automatic thoughts “got out of hand.” The analogy she presented was that of a discipline – the idea is to work on it ongoingly. She then reviewed the techniques they had learned and had each person create their own stress management plan. John identified PMR as the most effective body-focused technique for him. He noted that at work, he was becoming more aware of when his shoulders and neck muscles were tight and tense. He would then tense and relax these muscle groups and noted that he became less stressed immediately. He also felt it would be useful to do a full-body PMR when he came home from work so he would be more relaxed throughout the evening. He also reported ongoing success using time management skills at work and planned to continue to prioritize and break down tasks each morning. He still reported higher stress levels at work than he would like due
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to the fact that he still had more tasks to complete than he could each day. John acknowledged that he was getting better at using assertive communication but that he still needed to work with this. He made this technique a priority to practice more. Finally, John reported that cognitive restructuring was helpful in reducing his stress levels, especially at home. He identified this as another technique for continued practice. Each group member wrote down their personalized stress management plan which they then took home with them at the end of the session. The session ended with each acknowledging what they had accomplished together.
Conclusions Rather than providing an exhaustive description of the many approaches to stress management, the above focused review most specifically described notable practices that address the physiological, behavioral, and cognitive elements of stress. Other approaches to be found in the literature include massage, aromatherapy, music therapy, and acupuncture to name a few. Although these techniques may offer some benefit, the evidence base for their use as a stress management strategy for CVD is spare. Other forms of stress management with a substantial literature base that are not described here include biofeedback, which has shown some benefit for patients with Raynaud’s disease, and more generally, as an approach that can assist patients in learning to use relaxed breathing for stress reduction. Research has found that although biofeedback is more effective than no treatment at all for hypertension, additional treatment elements such as deep breathing, meditation, or imagery are needed to achieve significant blood pressure reductions (Nakao et al., 2003). This, along with the fact that biofeedback is often expensive due to the associated equipment needs, demonstrates that biofeedback may not be a cost-effective approach to managing stress in patients with cardiovascular disease. In determining what stress management program is best for you to utilize with your patients, there are many things to consider beyond relative efficacy. Choosing the best program depends more on other factors such as what you are trying to accomplish, what endpoints you are looking to effect, and what constraints individual patients are under.
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Ong, L., Linden, W., & Young, S. (2004). Stress management: What is it? Journal of Psychosomatic Research, 56(1), 133–137. Ospina, M. B., Bond, K., Karkhaneh, M., Buscemi, N., Dryden, D. M., Barnes, V., Carlson, L. E., Dusek, J. A., & Shannahoff-Khalsa, D. (2008). Clinical trials of meditation practices in health care: Characteristics and quality. Journal of Alternative and Complementary Medicine, 14(10), 1199–1213. Rainforth, M., Schneider, R., Nidich, S., Gaylord-King, C., Salerno, J., & Anderson, J. (2007). Stress reduction programs in patients with elevated blood pressure: A systematic review and meta-analysis. Current Hypertension Reports, 9(6), 520–528. Roy-Byrne, P., Craske, M. G., Sullivan, G., Rose, R. D., Edlund, M. J., Lang, A. J., Bystritsky, A., Welch, S. S., Chavira, D. A., Golinelli, D., Campbell-Sills, L., Sherbourne, C. D., & Stein, M. B. (2010). Delivery of evidence-based treatment for multiple anxiety disorders in primary care: A randomized controlled trial. Journal of the American Medical Association, 303, 1921–1928. Schultz, J. H. (1932). Das Autogene Training-Konzentrative Selbstentspannung. Leipzig: Thieme. Stetter, F., & Kupper, S. (2002). Autogenic training: A meta-analysis of clinical outcome studies. Applied Psychophysiology and Biofeedback, 27(1), 45–98. Tsai, J. C., Wang, W. H., Chan, P., Lin, L. J., Wang, C. H., Tomlinson, B., Hsieh, M. H., Yang, H. Y., & Liu, J. C. (2003). The beneficial effects of tai chi chuan on blood pressure and lipid profile and anxiety status in a randomized controlled trial. Journal of Alternative and Complementary Medicine, 9, 747–754. Unützer, J., Katon, W., Callahan, C. W., Williams, J. W., Hunkeler, E., Harpole, L., Hoffing, M., Della Penna, R. D., Hitchcock Noël, P., Lin, E. H. B., Areán, P. A., Hegel, M. T., Tang, L., Belin, T. R., Oishi, S., & Langston, C. (2002). Collaborative care management of late-life depression in the primary care setting: A randomized controlled trial. Journal of the American Medical Association, 288, 2836–2845. Viskoper, R., Shapira, I., Priluck, R., Mindlin, R., Chornia, L., Laszt, A., Dicker, D., Gavish, B., & Alter, A. (2003). Nonpharmacologic treatment of resistant hypertensives by device-guided slow breathing exercises. American Journal of Hypertension, 16(6), 484–487. Wilk, C., & Turkoski, B. (2001). Progressive muscle relaxation in cardiac rehabilitation: A pilot study. Rehabilitation Nursing, 26(6), 238–243. Yeh, G. Y., Wang, C., Wayne, P. M., & Phillips, R. (2009). Tai chi exercise for patients with cardiovascular conditions and risk factors. Journal of Cardiopulmonary Rehabilitation and Prevention, 29, 152–160. Yung, P., French, P., & Leung, B. (2001). Relaxation training as complementary therapy for mild hypertension control and the implications of evidence-based medicine. Complementary Therapies in Nursing & Midwifery, 7(2), 59–65.
Chapter 11
The Effects of Meditation and Yoga on Cardiovascular Disease Sonia Suchday, Maria Dziok, Miriam Katzenstein, Erica Kaplan, and Michelle Kahan
Cardiovascular disease is a chronic illness with physiological, behavioral, and psychosocial components implicated in the etiology and course of the disorder. Given its multifaceted nature, management of cardiovascular disease needs to be multidimensional and include attention to all risk factors. Research has indicated that modification of one risk factor (e.g., diet) does not lead to automatic benefits to other risk factors (e.g., exercise) (Prochaska, Nigg, Spring, Velicer, & Prochaska, 2010). Hence, attention needs to be focused simultaneously on both physiological and psychological components. For example, medical regimens need to be augmented by lifestyle changes that include diet and exercise. Psychosocial variables such as depression, hostility, and stress also play a key role in morbidity and mortality associated with cardiovascular disease and need to be independently managed. An explicit focus on techniques that involve concurrent physiological and psychological interventions makes mind-body therapies effective and appealing in dealing with cardiovascular disorders. Mind-body medicine is the most widely used domain of complementary and alternative medicine among the US population for treatment of medical conditions (NIH, 2004). Examples of mind-body medicine include meditation, yoga, relaxation, visual imagery, biofeedback, qigong, cognitive-behavioral therapies, support groups, tai chi, and spirituality. This chapter will focus on the most widely studied and used interventions, specifically, yoga and meditation.
S. Suchday, Ph.D. (*) • M. Dziok, Ph.D. • M. Katzenstein, M.A. • E. Kaplan, B.A. • M. Kahan, M.S., M.A. Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, Yeshiva University, 1300 Morris Park Avenue, Bronx, NY 10641, USA e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_11, © Springer Science+Business Media, LLC 2012
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Epidemiologic Evidence Mind-body therapies have wide use among patients in the management of cardiovascular disease. According to a recent study, approximately one-third of patients with acute coronary syndrome practice some form of mind-body medicine (Leung, Tamim, Stewart, Arthur, & Grace, 2008). The use of these therapies tends to be more common among nonwhite women with higher levels of education, who exercise regularly, and have a history of smoking and poor mental health (Leung et al., 2008). Mind-body therapies also have a significant impact on risk factors such as insulin resistance which may worsen the disease (Innes, Vincent, & Taylor, 2007).
Introduction: Defining Meditation and Yoga Meditation (dhyan) and yoga in India and other Eastern cultures have been around by some accounts for several centuries. They are not necessarily considered to be two distinct and separate entities. Collectively, they are considered to be a way of life and a part of daily living. Practice of a yoga and meditation lifestyle is harmony between the mind, body, and spirit, enabling individuals who adhere to their principles to face life with equanimity. Breath (pranayama) is considered to be an essential element of both practices. Committed practitioners of yoga begin their day with 1–2 h of practice which includes yoga, meditation, and breathing exercises. This early morning practice is thought to induce a state of contemplative awareness that is brought to bear on all situations encountered during the day. Practice of yoga is also traditionally augmented by a moderate vegetarian diet that is free of intensive spices that are considered harmful to health and well-being. Spiritually, the practice of yoga also entails the philosophy of Karma or the policy of engaging in right action regardless of provocation and disengagement with reward and benefit calculations associated with action (Jayasinghe, 2004). The Eastern system of medicine, Ayurveda, regularly utilizes principles of yoga, meditation, and pranayama for their therapeutic benefits in treating diseases and achieving optimal health and wellbeing. It is important to note that the traditional practice of this way of life does not view yoga, meditation, or pranayama as prophylactic treatments but rather views them as a way of optimal functioning. Western cultures have adopted these Eastern practices as an alternative or complement to allopathic or Western medicine to treat disease and also as a recreational activity, a form of exercise, and a stress management technique. Yoga and meditation are regarded as powerful mechanisms for preventing illness via their beneficial impact on stress. Regardless of the scientific validity of yoga and meditation, overwhelming anecdotal evidence has pointed to this positive, stress-mitigating effect. Still, an important difference to note between Eastern and Western perspectives on yoga and meditation is that Western perspectives have viewed them as supplemental techniques rather than a way of life.
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Meditation The major challenge in operationally defining yoga and meditation is that Western society has popularized many different forms, including mantra meditation, mindfulness meditation, hatha yoga, raja yoga, etc. (Ospina et al., 2008; Innes et al., 2007). For the purposes of this chapter, definitions of two of the most popular forms of meditation are provided: transcendental meditation and mindfulness meditation. Transcendental meditation (TM): The basis of TM is mantra meditation, which refers to meditation practices in which a repeating mantra (word, sound, symbol) is the main component. The underlying idea is that repetition of the word, symbol, or sound prevents other cognitive activity allowing focused attention. In addition to TM, other forms of mantra meditation include relaxation response (RR), clinically standard meditation (CSM), and Acem meditation (Ospina et al., 2008). Currently, there are many meditation practices used in combination with other relaxation techniques such as progressive muscle relaxation (PMR), autogenic training, and biofeedback. Mindfulness meditation: Mindfulness is defined as attention on the present moment – observation without judgment. Mindful meditation involves an enhanced awareness or cognizance of the body, thoughts, emotions, and surroundings without questioning or judgment and with acceptance (Baer, 2003). Mindfulness meditation does not restrict attention to a single stimulus such as a word, mantra, or object. Instead, the focus is simply on observing the ongoing stream of internal and external stimuli, nonjudgmentally, as it unfolds, without trying to change, escape, or avoid it (Baer, 2003). For example, a practitioner may focus on the breath, heartbeat, thoughts, proprioceptive sensation, and external auditory and visual stimuli. Mindfulness meditation is the pervasive practice in the USA and is considered to be a secular form of meditation independent of religious and cultural origins. Mindfulness meditation incorporates guided imagery, breathing exercise, light yoga, and other techniques. The best know therapies that have integrated mindfulness meditation include mindfulness-based stress reduction (MBSR, Kabat-Zinn, 1990), mindfulness-based cognitive therapy (MBCBT, Segal, Williams, & Teasdale, 2002), dialectical behavior therapy (DBT, Linehan, 1993a, b), and acceptance and commitment therapy (ACT, Hayes, Strosahl, & Wilson, 1999). Vipassana meditation and Zen meditation also embody principles of mindfulness meditation (Ospina et al., 2008). Regardless of the modality in which it is used, research on the concept of mindfulness has identified the following components that comprise experience: (a) not reacting to internal experiences (emotions, thoughts, etc.); (b) attention to sensations, perceptions, thoughts, and feelings; (c) awareness of actions/behaviors; (d) description of experiences in the present moment; and (e) not judging experiences (Lutz, Greischar, Rawlings, Ricard, & Davidson, 2004).
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Yoga Yoga is an ancient mind-body discipline that is thought to be a way of life in conjunction with meditation. Throughout history, specifically in countries like India and Tibet, yoga, with its focus on integration of the mind, body, and spirit, has been viewed as a pathway to achieve full human potential and even enlightenment. Yoga couples muscular activity (asanas) with attention focused inward (dhyan) assisted by breathing that is regulated (pranayama) to create a state of contemplation (LaForge, 1997). The idea behind yoga is that over years of practice, this induced contemplative state is maintained as practitioners interact with the world around them (LaForge, 1997). Such a state is crucial in examining the contrast between yoga and other Eastern forms of activity and traditional body-centered aerobic and muscular fitness (LaForge, 1997). The practice of yoga has been rising steadily in Western industrialized countries during recent decades. There are many forms and branches of yoga, but most of them are comprised of different elements of postures, attention, and breath. Of the seven major branches of Hindu yoga, hatha (forceful) yoga, raja (classical) yoga, and mantra yoga are perhaps the best known and most widely practiced forms. Each type of yoga may emphasize different aspects. For example, hatha yoga and raja yoga emphasize specific postures (asanas) which include active and relaxed poses along with breath regulation (pranayama), concentration (dharana), and meditation (dhyan). Hatha yoga is the version most commonly practiced in the Western industrialized world and includes many different styles (e.g., Iyengar, Kundalini, Ashtanga, Integral, and Bikram yoga). It also incorporates mantras or chants, cleansing exercises (kriyas), and specific hand gestures (mudras) (Innes et al., 2007).
Therapeutic Mechanisms Rehabilitation after a cardiac event generally includes diet, exercise, and psychosocial interventions – including stress management interventions – in addition to pharmaceutical managements of the disease. Interestingly, traditional forms of yoga and meditation practice also involve dietary, psychosocial, and physical components – asanas (physical posture), dhyan (meditation), pranayama (breathing exercises), and diet (moderate vegetarian diet). Overall, meditation and yoga are described as multifaceted processes that affect cognitive, sensory, affective, and biological processes (Newberg & Iversen, 2003). Research on yoga and meditation has examined effects on overall well-being as well the effects on patients who have coronary heart disease (CHD), diabetes mellitus, essential hypertension, cancer, etc. Recent literature has also focused on the beneficial impact of these techniques on chronic disease risk factors such as obesity, elevated blood pressure, blood glucose, and cholesterol (Yang, 2007). In addition to physiological factors, research has also indicated links between the practice of yoga and meditation and psychological well-being.
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Psychological Pathways Psychological pathways associated with cardiovascular disorders include depression, anger/hostility, anxiety, and stress. Stress, one of the most prominent risk factors, is a function of psychosocial, behavioral, and physiological factors, including biological and genetic components, that interact throughout the lifespan (McEwen & Gianaros, 2010). Evidence shows that these pathways independently contribute to the risk of developing cardiovascular disease after controlling for traditional risk factors (Figuedero, 2009). Popular culture frequently points to yoga and meditation as ideal methods for stress relief. The 2008 Yoga in America Study determined that Americans spend $5.7 billion on yoga classes and yoga products such as equipment, clothing, DVDs, books, and magazines. In addition, the amount of people that say they are interested in yoga has nearly tripled in the last 4 years. Many websites such as “yogaawakening.com” and “onlinemeditation.org” advertise yoga and meditation as proven methods to decrease stress and anxiety (Yoga Journal, 2008). Extant scientific literature confirms the efficacy of yoga and meditation in relieving stress (Rozanski, Blumenthal, Davidson, Saab, & Kubzansky, 2005) to positively impact cardiovascular health. Empirical evidence also points to major depressive disorder (MDD), generalized anxiety disorder (GAD), perceived hostility, and anger as catalysts for both coronary events and CHD. Prevalence of depression has been seen in individuals with CHD (Lett et al., 2004), and depressive symptoms have been found to predict the metabolic syndrome (a constellation of risk factors for CHD) in middle-aged women (Raikkonen, Matthews, & Kuller, 2007). In addition to depression, recent data has shown that anxiety is also associated with CHD. Patients with CHD and a diagnosis of either MDD or GAD are at more than two times the risk for cardiac events (Frasure-Smith & Lesperance, 2007). A study by Goodwin, Davidson, and Keyes (2009) determined that CHD is associated with increased likelihood of any anxiety disorder after adjusting for depressive disorders as well as GAD, panic disorder, or specific phobias. Extant research also links prevalence of hostility and anger to prevalence of CHD and the frequency of recurrent cardiac events (Rozanski et al., 2005). Particularly notable is that all of these aforementioned psychological conditions can be alleviated through yoga and meditation. Thus, it is likely that mind-body therapies may positively impact cardiovascular health via a variety of psychological mechanisms.
Meditation Transcendental meditation (TM) has been shown to have a beneficial impact on psychosocial stress and anxiety, as well as smoking, and alcohol abuse (Rainforth et al., 2007). Over the years, mindfulness techniques have often been used to enhance many stress management programs. Mindfulness-based stress reduction (MBSR) was first
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developed by Jon Kabat-Zinn at the University of Massachusetts Medical Center in 1990. MBSR is a standard 8-week program that combines mindfulness meditation techniques, as well as light yoga and psychoeducational discussions to reduce stress and coping (Olivo, Dodson-Lavelle, Wren, Fang, & Oz, 2009). Research has shown that MBSR reduces symptoms of anxiety, depression, and fatigue (Carlson & Garland, 2005; Carlson, Speca, Patel, & Goodey, 2003; Carlson, Speca, Patel, & Goodey, 2004; Carlson, Ursuliak, Goodey, Angen, & Speca, 2001; Carlson, Speca, Patel, & Goodey, 2003; Speca, Carlson, Goodey, & Angen, 2000). Kabat-Zinn et al. (1992) reported that among patients with GAD and panic disorder (with or without agoraphobia), the 8-week MBSR program resulted in a reduction of anxiety and depressive symptoms. Notably, this reduction in symptoms was maintained over 3 years (Miller, Smith, Turner, Guijarro, & Hallet, 1996). TM has also been studied in relation to its effect on the psychological correlates of cardiovascular disease. A study by Jayadevappa et al. (2007) showed that TM decreased depressive symptoms in an African-American population living with congestive heart failure. In studies conducted on medical students, nursing students in a graduate program, and premedical students who are all at extremely high-risk stress and stress-related disorders, 1 month of mindfulness meditation training was compared to somatic relaxation. Results showed both groups exhibited less distress and had an enhanced positive mood compared to the control group who did not receive any intervention. However, mindfulness meditation was more effective than somatic relaxation at enhancing positive mood states and reducing distractive thoughts, and was also more effective in reducing ruminative thoughts and behaviors compared to a control condition (Jain et al., 2007; Shapiro, Schwartz & Bonner, 1998). Additionally, among women diagnosed with cardiovascular disorders, 8 weeks of mindfulness meditation led to reductions in anxiety, sadness, and anger compared to women who did not participate in the program (Tacon, McComb, Caldera, & Randolph, 2003). Collectively, these studies indicate the powerful effect meditation can have on psychological well-being among people who do not have an identified disease and are in chronically stressful situations (e.g., medical school) and among patients that have CHD. Studies using global psychological measures provide evidence that mindfulness improves all aspects of psychological functioning. It appears that mindfulness meditation is as effective as progressive muscle relaxation (a technique for reducing anxiety by alternately tensing and relaxing muscles) or psychotherapy. Finally, it is hypothesized that mindfulness enhances self-regulation of symptoms in the long term (Kabat-Zinn, Lipworth, & Burney, 1985).
Yoga Yoga promotes feelings of well-being that alleviate the effects of stress. In 2004, West and colleagues conducted a study comparing hatha yoga with African dance using salivary cortisol, a measure for stress levels (West et al., 2004). They found that cortisol levels decreased among individuals participating in hatha yoga, evidencing yoga’s relaxing effects. Treatment for GAD using Ashtanga yoga exercises
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is remarkably effective, particularly among women experiencing both depression and GAD (Javnbakht, Hejazi Kenari, & Ghasemi, 2009). The efficacy of the yoga intervention depends on enhanced bodily awareness resulting in being mindful of anxiety and tension (Javnbakht et al., 2009). Enhanced awareness of anxiety and physiological responses leads to deliberate attempts at relaxation, benefiting health and well-being. Research comparing yoga therapies with traditional exercise in areas of focus and concentration found that yoga significantly decreased the time needed to perform certain concentration tasks (Manjunath & Telles, 2001). These research studies further support the notion that yoga exercises allow the participant to identify and attend to their concerns, thereby increasing mindfulness and making health issues easier and more realistic to manage. Thus, yoga’s fundamental nature helps practitioners to lead a psychologically healthy lifestyle that effectively mitigates many risks for cardiovascular problems.
Physiological Pathways Mind-body therapies act through a variety of physiological pathways to lessen the risk of CHD and improve cardiovascular health. Existing literature suggests that meditation may have a beneficial effect on CHD risk factors, disease markers, and clinical events. It may also decrease myocardial ischemia, carotid atherosclerosis, and mortality rates (Paul-Labrador et al., 2006). Yoga impacts cardiovascular health by reducing activation and reactivity of the sympathoadrenal system of the HPA axis, alleviating the effect of stress and fostering multiple positive effects on neuroendocrine status, metabolic function, and related inflammatory responses (Innes et al., 2007; McEwen & Gianaros, 2010) In summation, an extensive review of extant literature has elicited that yoga and meditation affect cardiovascular health via neurological, biochemical, autonomic, and pulmonary functioning.
Neurological Functioning: HPA-Axis Regulation/Stress Buffering Responses to stress – both the perception and appraisal of threat and coping physiological and behavioral responses – are controlled by a complicated neurobiological network of brain structures that include the hypothalamus, amygdala, and the prefrontal cortex. Based on developmental history, these structures regulate stress appraisal and physiological/behavioral stress responses. Over a short period of time, these processes are effective in helping the individual adapt to and cope with stress. However, as time progresses, these systems can become maladaptive due to overactivation. This systemic failure due to overuse or “wear and tear” is referred to as allostatic load (McEwen & Gianaros, 2010). Yoga and meditation have a beneficial impact on perceptual and physiological responses to stress, thus reducing the allostatic load or wear and tear on an individual. Data has indicated that yoga helps to regulate the HPA axis, evidenced by a reduction of cortisol and catecholamines (Innes et al., 2007; Kamei et al., 2000; McEwen, 1999). Similarly, meditation/relaxation practices
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that have a nonexplicit spiritual component (e.g., yoga, TM, or Zen meditation) have been shown to effectively lower stress hormone levels (Seeman, Dubin, & Seeman, 2003). TM practice modulates neurophysiologic, neuroendocrine, and physiologic mechanisms associated with stress and is associated with significantly reduced systolic and diastolic BP similar or greater to effects of other lifestyle modifications, including weight-reducing diet, aerobic exercise, alcohol restriction, and sodium restriction (Rainforth et al., 2007). Vagal Nerve Stimulation The vagus nerve, the longest cranial nerve, connects the limbic system to various areas in the body, including the heart. It acts to lower heart rate and calm the body, or deactivate the “fight or flight” response. Vagus nerve stimulation is a procedure that has recently been introduced to improve symptoms of depression and seizure activity in individuals who do not respond to medication. A stimulator is implanted in these individuals in order to improve activity of the left vagus nerve in the neck. Surprisingly, there have been particular mind-body therapies that have shown similar stimulation to the vagus nerve. In 2006, Paul-Labrador and colleagues found a relationship between meditation practice and vagus nerve stimulation, suggesting that meditation produces a cholinergic effect and buffers against the effects of chronic stress (Innes et al., 2007). Similarly, yoga enhances parasympathetic output and shifts the autonomic nervous system balance in favor of the parasympathetic system, leading to increased cardiac-vagal function (Innes et al., 2007). Yoga and meditation may compensate for adverse systematic changes related to cardiovascular disease by buffering the effects of chronic stress and repairing sympathovagal balance, or the autonomic control resulting from sympathetic and parasympathetic activities (Innes et al., 2007). Brain Anatomy Current research has focused on utilizing PET and fMRI technology to explore the neurological and neurochemical effects of meditation and yoga. These studies have established a direct relationship between meditation and certain neurological structures. Hippocampal activity (which as aforementioned is directly linked to HPA activation) is found to be significantly increased by meditation practice (Lazar et al., 2000). A study by Lazar et al. (2000) determined that meditation leads directly to increased hypothalamic activity and to increased GABA transmission (Newberg & Iversen, 2003), both of which can help mitigate the risk of cardiac events. Biochemistry: Hypertension Hypertension is a term used to describe elevated blood pressure with systolic blood pressure levels greater than 140 mmHg and diastolic blood pressure levels greater
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than 90 mmHg. It has been established as a major risk factor for cardiovascular disease, with risk increasing significantly even in prehypertensive individuals, who are generally defined as having a systolic blood pressure of 130–139 mmHg and a diastolic blood pressure of 85–89 mmHg (Vasan et al., 2001). Yoga and meditation are effective techniques that lead to significant reductions in blood pressure among adults (Rainforth et al., 2007) and youth (Barnes, Treiber, & Davis, 2001). Compared to the effects of yoga and meditation, other behavioral therapies such as simple biofeedback, relaxation-assisted biofeedback, progressive muscle relaxation, and stress management training did not elicit this same blood pressure effect (Rainforth et al., 2007).
Meditation and Blood Pressure In studies utilizing TM, results showed decreasing heart rate and resting ambulatory blood pressure in both normal and cardiac at-risk youth (Barnes, Davis, Murzynowski, & Treiber, 2004; Barnes, Johnson, & Treiber, 2004). Three months of consistent TM practice twice a day for 15 min lead to significant reductions in cardiovascular reactivity to stress (a hypothesized marker for CHD) among young people with high-normal BP (Barnes et al., 2001). Even among adult participants, meditation practice leads to lower blood pressure and lower blood pressure reactivity to stress (Seeman et al., 2003). Efficacy of TM in lowering blood pressure has led to its consideration as both a legitimate recommendation for patients with elevated BP to prevent the development of essential hypertension, and as a treatment option among those diagnosed with essential hypertension and CHD (Rainforth et al., 2007).
Yoga and Blood Pressure Numerous studies have supported the significant relationship between yoga practice and BP regulation in a variety of populations. Rates of hypertension were significantly lower in a group of yoga-practicing individuals than in a normal exercise control (Murugesan, Govindarajulu, & Bera, 2000). One study determined that 11 weeks of yoga practice for 1 h/day had the same effect as pharmacological therapy in regulating blood pressure in healthy adults between the ages of 33 and 65 (Murugesan et al., 2000). In addition to the beneficial effects of overall yoga practice on blood pressure, specific yoga postures such as the head-up or headdown tilt were found to be especially effective in restoring baroreflex sensitivity, (a reflex triggered by pressure changes), the lack of which is a major cause of hypertension (Selvamurthy et al., 1998; Jayasinghe, 2004). Research also indicates that yoga practice is also useful in managing complications resulting from chronic elevated blood pressure, particularly left ventricular hypertrophy (Jayasinghe, 2004). In a sample of healthy young adults, ages 17–18, 2 weeks of Sarvangasana yoga, a type of yoga where the head is down and the body is up, contributed to a significant decrease in left ventricular volume, an indicator for strong heart muscles
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(Konar, Latha, & Bhuvaneswaran, 2000). Thus, research suggests that yoga practice has benefit as both a treatment and prevention measure for hypertensive, borderline hypertensive, or healthy individuals.
Lipid Levels Elevated levels of serum cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides have been identified as primary risk factors for CHD, and improving these risks is associated with CHD prevention (Manninen et al., 1992). While most research leans toward treatment with diet and exercise or prescription medications, yoga and meditation may improve lipid levels in its participants. Manchanda et al. (2000) found that among men with angiographically identified CHD, a 1-year yoga and lifestyle change intervention that included diet and exercise lead to a significant decrease in serum total cholesterol, LDL-C, and triglyceride levels. In fact, it has been suggested that yoga and lifestyle interventions may slow the process of atherosclerosis (Manchanda et al., 2000). In addition to impacting favorably on lipid levels among CHD patients, a brief 8-day yoga intervention showed lowered total triglycerides, lowered LDL-C, and elevations in high-density lipoprotein cholesterol (HDL-C) levels among individuals at high risk for CHD (Bijlani et al., 2005). The 3–4-h intervention in this study included yoga exercises, individualized counseling, and group support and lectures about yoga practices for daily living (Bijlani et al., 2005). Using a variety of cardiovascular disease markers, Vyas and Dikshit (2002) compared long-term, short-term, and nonmeditators using raja yoga meditation. Individuals’ total cholesterol levels were significantly improved in both long-term and short-term meditators as compared to nonmeditators; however, HDL-C levels were not significantly different among groups. Vyas and Dikshit (2002) suggest that this significant change was due to participants’ ability to cope with stress. Interestingly, while most research suggests diet modification or use of prescription drugs to treat this type of hyperlipidemia, almost all participants in this study were vegetarian, effectively eradicating diet as a potential cause for elevated lipid levels. In 2008, Vyas, Raval, and Dikshit used a similar protocol with postmenopausal women noting similar results with LDL-C and total cholesterol levels.
Blood Glucose Levels Consistently elevated levels of blood glucose are considered a primary risk factor for heart disease and can lead to the progression of type 2 diabetes mellitus. While much is known about treatment, treatment adherence for improving glycemic control can be difficult for some individuals to maintain. A combination of medical treatment and yoga/meditation may be suggested for both prediabetic individuals and those diagnosed with type 2 diabetes mellitus. In a 40-day yoga intervention
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designed specifically for individuals with type 2 diabetes mellitus, a yoga lifestyle intervention that included both practices in yoga asanas and pranayama led to reductions in fasting blood glucose as well as postprandial blood glucose levels. Researchers focused on controlled breathing, believing that such practices might influence the mechanism for glycemic control (Singh, Malhotra, Singh, Madhu, & Tandon, 2004). Among healthy adults, Bijlani and colleagues (2005) found lower levels of fasting plasma glucose after individuals participated in a 3–4 h yoga lifestyle intervention study for only 8 days. This further supports the notion that yoga can be used in conjunction with Western medicine to assist with cardiovascular illnesses, via glycemic control improvements in those with type 2 diabetes mellitus.
Autonomic Regulation Meditation and yoga may affect the cardiovascular system via autonomic pathways. Cardiovascular reactivity may be decreased through calming the sympathetic reaction to stress, and poststress cardiovascular reactivity may be improved by increasing parasympathetic activation. For example, Kubota et al. (2001) have shown that participants who practiced a Zen meditation task requiring sustained attention had an increase in both peripheral sympathetic and parasympathetic activity during the task. Moreover, they found that as frontal midline theta rhythms increased, the sympathetic nervous system slowed. In their 40-day yoga intervention mentioned previously, Singh et al. (2004) noted a decrease in participants’ corrected QT intervals, a test which diagnoses for cardiac autonomic neuropathy. In general, parasympathetic nervous system activation can ameliorate stress responses.
Pulmonary Functioning Researchers have tested pulmonary levels and exertion rates among individuals participating in meditation and yoga as compared to traditional exercise. In a group of 30 healthy males, Agarwal and Gupta (2006) determined that peak expiratory flow rate improved those practicing TM over both a physical activity and control group. Compared to a normal exercise control, adults who practiced yoga showed significant improvement in terms of vital lung capacity and improved aerobic capacity (Ray et al., 2001). In a study performed with 20 community teens (aged 12–16), half were randomly assigned to a yoga intervention while the others was assigned to a physical activity intervention involving activities in a garden (Telles & Srinivas, 1998). Researchers suggested that garden activities paralleled those in yoga (e.g., stretching and bending), with the exception of the bodily awareness and relaxation that are unique to yoga practice. Results suggest that those individuals in the yoga intervention reduced their breathing rate compared to unchanged breathing patters in the physical activity group. The following schematic summarizes the physiological and psychological mechanisms by which yoga and meditation impact cardiovascular health (Fig. 11.1).
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S. Suchday et al. Therapeutic Mechanisms Physiological Mechanisms • • • • • •
Neurological Functioning (HPA-Axis) Biochemistry (Blood Pressure) Autonomic Regulation Blood Glucose Levels Lipid Levels Pulmonary Functioning
Psychological Mechanisms • • • • •
Mood Disorders Anxiety Disorders Perceived hostility/anger General level of stress Concentration/awareness
YOGA / MEDITATION
Fig. 11.1 Therapeutic mechanisms
Clinical Example The following is the description of a structured 8-week mindfulness meditation course conducted in postoperative cardiac patients. Patients typically met once a week at a group meeting where meditation and mindfulness skills were taught and practiced. The group was located in the same facility where patients received cardiac rehabilitation. The location of the group within the cardiac rehabilitation facility led to increased referrals and attendance among participants. Frequently, patients with chronic and complicated medical histories have difficulty with adherence to any regimen due to problems with transportation, chronic pain, and fatigue. Hence, the convenient location of the group facilitated consistent attendance among group members. Despite the fact that attendance is emphasized, it is helpful to structure the course so that each week offers skills in a noncumulative manner to enhance participation among patients with chronic difficulties who would benefit the most from the intervention. Although the following is a typical, time-limited group format, the content can be modified for use among individuals as well as condensed or expanded in duration. During the first session, members introduced themselves to each other. They were then educated about the concept of meditation and mindfulness as well as the interaction between stress, affect, and cardiovascular function. They were encouraged to discuss how meditation can be helpful in their own lives, specifically for regulating emotions such as anger and anxiety. A portion of the introduction also included discussion about the importance of practice in the development of mindfulness skills. Many patients become discouraged when first practicing
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mindfulness, as they are not able to quiet their racing mind or they have a difficult time staying awake. In these cases, patients are reassured that ongoing ruminative thoughts and fatigue are normal processes. Developing mindfulness takes time, and when one falls out of practice, whether it be over the course of seconds or years, one can simply begin in a new moment, with no judgment. The next few sessions consisted of both guided practice and discussion. Initially, it is beneficial for the duration of practice to be a few minutes in length, as many patients are new to mediation. As the weeks progressed, patients improved in their ability to meditate in longer durations. Exercises conducted during each class included focusing on the breath and describing it objectively. Some patients that also have pulmonary complications find it difficult to deepen their breathing. In these cases, patients were encouraged to not change, rather just focus on their breath. Exercises can also include focusing on heartbeat or pulse sensations. Doing this may cause emotional reactions that need to be discussed. For example, one patient had feelings of anger and frustration toward their cardiovascular system because he perceived that it had failed him and it was diseased. This patient was encouraged to discuss his experience. The use of guided positive imagery with focus on the cardiovascular system also may be helpful in these cases. Following exercises focusing on the breath and emotional reactions, the facilitator expanded the practice to paying attention and objectively labeling external sounds, smells, tastes, and touch as well as to internal sensations such as pain and thoughts. Patients were encouraged to find a visualization that they found helpful in letting go of thoughts, such as ocean waves, a balloon, or clouds. These visual images are generally considered to be inconsistent with stress. One thing to consider is that some individuals find it difficult or frightening to meditate because they are uncomfortable with losing control. This is especially true among patients with histories of trauma. In these cases, patients have found it helpful to keep their eyes open during meditation to promote feelings of safety. Additional sessions focused on other meditation techniques such as focusing on word or mantra, counting, or guided imagery. Facilitators have found it helpful to write copies of their favorite scripts for slow reading, if he or she finds it uncomfortable to improvise. During discussion, it was helpful for individuals to identify ways they could apply these techniques in their daily lives. For example, one patient spoke about applying the techniques he learned at his place of employment. Although his job caused him great psychological stress, he was unable to consider other options due to familial and financial reason. With assistance from the group, he was able to identify a quiet location that he designated as his place for 60 s of mindful breathing during lunch or particularly stressful moments. Occasionally, meditation practice elicited distressing emotions and thoughts in patients, and these thoughts were mentioned in discussion. Some common topics included struggles with body image or weight loss, lack of social support, the existence of pain, and marital problems. One particular rumination that surfaced within
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groups of postoperative cardiac patients somewhat frequently is fear of sudden death. The facilitator encouraged using mindfulness to cope with these thoughts, experiencing the thought as just another transient sensation in the body. However in many cases, the group spent some time discussing these issues as the depression and anxiety associated with these stressors greatly influence cardiovascular function. The group assisted each other in developing insight into the nature of the problem identified ways of coping. If a qualified mental health professional is not present or if the patient needs more intensive treatment, a referral to a qualified professional may be necessary.
Rationale for Treatment Approach Currently, focus on combating heart disease and promoting heart health has shifted from a pharmacological paradigm toward an emphasis on behavioral modification and an overall healthy lifestyle. The European Prospective Investigation into Cancer and Nutrition (EPIC) study, published in the archives of internal medicine, surveyed 23,153 German individuals to determine that adhering to four simple healthy lifestyle factors – not smoking, having a BMI lower than 30, performing 3.5 h/week or more of physical activity, and adhering to healthy dietary principles – significantly lowered the risk of developing chronic diseases such as myocardial infarction, diabetes, stroke, and cancer (Gonzalez, 1997). Similarly, the INTERHEART study isolated nine risk factors that account for over 90% of the risk of acute myocardial infarction. The nine factors – smoking, lipids, hypertension, abdominal obesity, diet (fruits and vegetables), physical activity, alcohol consumption, diabetes, and psychosocial factors – are consistent worldwide across both sexes and at all ages in all regions. This study also advocated that approaches to prevention should take a behavioral approach and that lifestyle change is the best way to prevent heart attacks (Yusuf et al., 2004). The strength of mind-body therapies lies not only in empirical support but in logistical advantage. Yoga and meditation programs are appropriate for both men and women of all ages. Empirical support exists for adolescents, adults, and older adults, with positive outcomes found in all three age groups. Yoga and meditation are also both cost-effective and can be used for individuals from lower socioeconomic groups who cannot afford to keep up with potentially expensive medication regimens. In addition, several common cardiovascular medications have unpleasant side effects that are not a risk of mind-body therapy. Furthermore, research suggests that yoga and meditation may positively impact six of the nine INTERHEART factors and therefore are comprehensive treatments as well as effective preventative measures (Tables 11.1, 11.2).
Sample
Yoga intervention
Control/ comparison
Yoga lifestyle intervention reduces blood pressure in HIV with CVD risk factors Cade et al. (2010)
60 adults with HIV
20 weeks of supervised yoga
Heart rate variability
Fasting plasma glucose, serum lipid profile, subjective well-being, and anxiety
Outcome measure(s)
Standard of 2-h oral glucose care – regular tolerance test with visits to insulin monitoring, physician with body composition, no change fasting serum lipid/ in physical lipoprotein profile, activity or resting blood medication pressure, CD4 count and plasma HIV RNA, SF-36, and health-related QOL inventory
Comprehensive 98 subjects 8-day outpatient None lifestyle 20–74 years course, 3–4 h education (26 with of teaching and program based HTN, 25 lifestyle on yoga with CHD) education Bijlani et al. (2005) Effects of yoga 42 healthy 2 days of separate None based males ages sessions of relaxation 18–48 years cyclic techniques on meditation and heart rate supine-rest variability counterbalSarang and Telles anced (2006)
Study (selected recent studies)
Table 11.1 Summary of yoga studies Methodological appraisal
Clinical comments
(continued)
Significant improvement No control group, Evidence for in serum lipid profile in short-term improvement of patients with initial study biomarkers and cholesterol of greater subjective than 200 mg/dL. well-being Significant improvement through yoga in subjective well-being Heart rate increased Changes in Sitting yoga is a during yoga postures reactivity may form of exercise and decreased during be due to and increases guided relaxation and relaxation sympathetic after CM. Sympathetic imagery not reactivity. activity dominated effects of yoga Guided during yoga postures itself relaxation and parasympathetic reduced dominated during rest physiological arousal Resting systolic and Small sample Yoga can lower diastolic blood pressures size, low blood pressure in improved more baseline CVD prehypertensive (p = 0.04) risk adults with HIV in the yoga group. plus mild-moderImmune and virological ate CVD risk status was not adversely factors affected
Results
Effects of a 46 healthy multimodality adults natural medicine program Fields et al. (2002)
54 healthy adults
Effect of yogic exercises on physical and mental health Ray et al. (2001)
Aerobic training
Wait list control group
Control/ comparison
12 months of yoga plus diet and walking
Blood pressure and sympathetic/ parasympathetic markers
Blood pressure and sympathetic/ parasympathetic markers
Methodological appraisal
Clinical comments
Small sample size, Restorative yoga was participants effective in not blind, increasing the study not long energy level of enough to adults with measure metabolic outcomes, not syndrome generalizable to other interventions No significant change in Small sample Sympathetic and blood pressure between size, effects parasympathetic groups and significant may be due to markers were positive finding in aerobic differentially sympathetic markers activity of effected, yoga suggesting separate mechanisms Lower sympathetic Effects may not Noteworthy activity in yoga group be generalizimprovements on vs. initial control, able to both physiologiimproved flexibility, and medical cal and psychological populations psychological functioning parameters Significant changes on all Small Multimodality indices when compared sample size programs to the control group significantly reduce atherosclerosis – important focus for the future
Results
BMI, blood pressure, Trend of reduced blood insulin sensitivity, pressure (p = 0.07), a plasma glucose, significant increase in SF-36, PSS, CES-D, energy level (p < 0.009), physical activity, and and trends of improvenutrition ment in well-being (p < 0.12) and stress (p < 0.22)
Outcome measure(s)
Usual care, diet, Insulin-resistance exercise, indices, blood education, and pressure, and blood supplements lipids
10 months of hatha No yoga until yoga month 6
6 weeks of yoga training
26 healthy adults
Effects of aerobic exercise training and yoga on the Baroreflex Bowman et al. (1997)
Yoga intervention
15–90 min yoga sessions over 10 weeks
Sample
Restorative 26 underweight yoga in adults overactive with metabolic adult men syndrome and women Cohen, Chang, Grady, and Kanaya et al. (2008)
Study (selected recent studies)
Table 11.1 (continued)
57 prehyperten- 12 weeks of sive and Iyengar yoga stage I hypertensive adults
Enhanced usual care (dietary supplementation)
Flexibility, aerobic exercise
Control/ comparison
Iyengar yoga versus usual care on blood pressure in patients with preHTN to stage I HTN Cohen et al. (2009)
3 months of hatha yoga
Yoga intervention
1. Physical exercise, 2. Sodium intake reduction 3. Control
30 healthy adults
Sample
Community based 113 prehyper8 weeks of yoga RCT of tensive and for 30–45 min/ non-pharmahypertensive day on at least cological young 5 days/week interventions adults in prevention (20–25) of HTN Saptharishi et al. (2009)
Effects of Hatha yoga and Omkar meditation on cardiorespiratory performance Harinath et al. (2004)
Study (selected recent studies)
Blood pressure
Blood pressure
Blood pressure and sympathetic/ parasympathetic markers
Outcome measure(s)
Methodological appraisal Clinical comments
Significant change in Small sample size Positive outcome of blood pressure between study suggests groups and significant hatha yoga may decrease in sympathetic/ be beneficial to parasympathetic improve markers autonomic balance, respiratory performance, and overall well-being There was no significant No method to Low attrition rates in change (SBP/DBP: standardize or this intervention 0.2/0.5 mmHg) of blood quantify the suggest that pressure in control magnitude of patients are group. Physical exercise the intervenamenable to was most effective tion per the completing (considered individuindividual lifestyle ally); salt intake modification reduction and yoga were programs also effective No differences between High attrition Difficult to assess groups at 6 or 12 weeks rates, difficult outcome of study but significant yoga regimen, differences study needed in blood pressure at 24 h to run longer between groups
Results
154 AfricanAmerican men and women (49 ± 10 years) 54 exp 44 ctrl
A randomized control trial of stress reduction in the treatment of hypertension in African Americans during 1 year Schneider et al. (2005)
TM or PMR
Health education
Health education
100 adolescents (16.2 ± 1.3 years) 50 exp 50 ctrl
Impact of stress reduction on ambulatory BP in African-American adolescents Barnes et al. (2004)
TM
Health education
Control/ comparison
Impact of TM on CV Adolescents TM function at rest and (15–18) during acute stress in with adolescents with high-normal high normal BP BP Barnes et al. (2001) 17 exp 18 ctrl
Table 11.2 Summary of meditation studies Study (selected recent Meditation studies) Sample intervention
Net change in BP *BP recorded at 3,6,9, and 12 months posttreatment
Net change in BP Change in HR CO at rest and in response to two stressors (simulated car driving/ interpersonal social stressor) *All changes recorded pre-post intervention Net change in BP *BP recorded at pretest, 2- and 4-month posttest, and 4-month follow-up
Outcome measure(s)
TM group: Greater decrease in SBP and DBP relative to PMR and health education Decreased use of antihypertensive medication (increased use in other two groups)
TM group: greater decrease in resting SBP TM group/driving stressor: greater decrease in SBP, HR, CO reactivity TM group/interpersonal stressor: greater decrease in SBP reactivity TM group: greater decrease in daytime SBP and DBP
Results
RCT Adequate baseline BP assessment Use of control Duration = 1 year
RCT Adequate baseline BP assessment Use of control Duration = 4 months
RCT Adequate baseline BP assessment Use of control Duration = 2 months Majority AfricanAmerican adolescents (n = 34)
Methodological appraisal
TM decreases BP in AfricanAmerican adolescents at risk for development of hypertension TM decreases BP over 1 year in AfricanAmericans TM had greatest effect (relative to PMR and Health education) in women
TM has a positive impact on cardiovascular functioning at rest and during certain stressors in adolescents with high-normal BP
Clinical comments
240 S. Suchday et al.
The effect of simplified 70 patients w/ Yang style TC Usual care TC on improvement CHF (simplified of cardiac function (LVEF range not 24 forms) for in patients with heart specified); 12 weeks failure NY Heart Assoc Wei and Liu (2004) Classes II–III Effects of TC and Elderly pts. (avg Yang style TC Strength/ resistance training age = 69) 61% (simplified resistance on CV risk factors in hypertension, 24 forms) for training elderly Chinese 59% impaired 12 weeks with subjects glucose theraband; Thomas et al. (2005) tolerance, usual 14% diabetes activity mellitus
Benson’s relaxation response
Patient education, usual care
Control/ comparison
A relaxation response 95 patients with randomized trial on moderatepatients with chronic severe Heart failure chronic Chang et al. (2005) heart failure
Meditation intervention Health education
Sample
Effects of a randomized 103 participants TM control trial of TM with stable on components of CHD the metabolic 39 exp syndrome in subjects 45 ctrl with CHD Paul-Labrador et al. (2006)
Study (selected recent studies)
BP Cholesterol Fasting glucose Hemoglobin
LVEF
QOL Exercise capacity
Net change in BP Lipoprotein profile Insulin resistance
Outcome measure(s)
Clinical comments
The Effects of Meditation and Yoga on Cardiovascular Disease (continued)
JADAD = +3 (Yeh et al., 2009)
JADAD = +1 (Yeh et al., 2009)
RCT TM decreases BP in Adequate baseline patients with BP assessment CHD Use of control group TM may modulate Duration = 16 weeks physiological responses to tress and improve CHD risk factors RCT Limited but possible Single-blind study clinical Duration of significance: 15 weeks short relaxation response intervention can improve some QOL aspects
Methodological appraisal
RCT Some significant bias that may impact results (Yeh, Wang, Wayne, & Phillips, 2009) Lower DBP w/TC Longitudinal Lower SBP w/ RCT theraband Very little bias that No change in total may impact cholesterol, LDL, results (Yeh HDL, or triglycerides et al., 2009) Lower fasting glucose and lower hemoglobin A1 in all groups
RR versus usual care: significantly better QOL change scores in peace-spiritual scales, emotional QOL RR versus patient education: no significant difference Increased LVEF
TM group: Decreased SBP Decreased insulin resistance Decreased heart rate variability
Results
11 241
Short-term autonomic and CV effects of mindfulness body scan meditation Ditto et al. (2006) *Study #2
Short-term autonomic and CV effects of mindfulness body scan meditation Ditto, Eclache, and Goldman (2006) *Study #1
Study (selected recent studies)
Table 11.2 (continued)
Meditation intervention
32 healthy Body scan young adults meditation (23 women, (7 W, 3 M) 9 men) Progressive muscular relaxation group (7 W, 3 M) 30 healthy Mindfulness young adults meditation (15 M, 15 W) Meditation first: (8 w, 7 m) Novel first: (7 w, 8 m)
Sample
Audiotape of a popular novel
Wait-list control group (sat quietly) 9 women, 3 men
Control/ comparison
Heart rate Cardiac RSA BP Impedance cardiography measures
BP (mmHg) Heart rate (beats/min) Cardiac respiratory sinus arrhythmia (RSA)
Outcome measure(s)
Methodological appraisal
No significant Random assignment differences in BP Heart rate lower in control Meditation = larger baseline to treatment Inc in RSA (largest RSA change) Increase in RSA while Within subjects meditating design Decrease in cardiac Counterbalancing pre-ejection period during meditation Females = larger decrease in DBP during meditation Men = larger increase in cardiac output during meditation
Results
Simultaneous increases in cardiac parasympathetic and sympathetic activity may explain lack of effect on heart rate Similarities and differences in physiological responses to body scan meditation and other relaxing activities
Numerous physiological changes occur during body scan meditation
Clinical comments
242 S. Suchday et al.
Meditation intervention
23 AfricanTranscendental American meditation patients at least 55 years old, recently hospitalized with class II or III CHF and with an ejection fraction of <.40.
Sample Health education
Control/ comparison 6-min walk test Generic and diseasespecific healthrelated quality of well-being Perceived stress CES-D Rehospitalizations Brain natriuretic peptide Cortisol
Outcome measure(s)
Methodological appraisal
TM: Change in outcome Improvement on walk from baseline, test 3–6 months Improvement on SF-36 posttreatment subscale Improvement on Minnesota Living with Heart Failure scale Decrease on CES-D Fewer rehospitalizations
Results TM improves overall quality of life and functional capacity of AfricanAmerican CHF patients
Clinical comments
CV cardiovascular, Exp experimental group, ctrl control, TM transcendental meditation, BP blood pressure, SBP systolic blood pressure, DBP diastolic blood pressure, HR heart rate, CO cardiac output, PMR progressive muscle relaxation, TC Tai Chi, LVEF left ventricualar ejection fraction, CHD coronary heart disease, QOL quality of life, CHF coronary heart failure, RCT randomized control trial, RSA respiratory sinus arrhythmia, JADAD JADAD scoring/Oxford quality scoring system * Organizational purposes
Effectiveness of TM on functional capacity and QOL of African-Americans with CHF Jayadevappa et al. (2007)
Study (selected recent studies)
11 The Effects of Meditation and Yoga on Cardiovascular Disease 243
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Summary/Conclusions Various forms of meditation and yoga may be used in conjunction with Western medicine as research suggests powerful benefits among cardiac patients. Although frequency and duration may influence results, both short-term studies of just 8 days (Bijlani et al., 2005) and long-term studies of 5 years (Bharshankar, Bharshankar, Deshpande, Kaore, & Gosavi, 2003) have yielded positive results. However, chronological factors can influence adherence as increased frequency and duration may deter participants from continuing. There are major empirical limitations in the current research regarding the effectiveness of yoga and meditation in cardiovascular disease. Several meta-analyses indicate a strong need for more rigorous research in this area. In fact, in a notable meta-analysis conducted for the National Center for Complementary and Alternative Medicine, only 10% of studies were considered to be of good quality (Ospina et al., 2008). Specific limitations include selection bias, exposure to multiple interventions, lack of agreement in defining terminology, and few longitudinal studies (Ospina et al., 2008; Rainforth et al., 2007). It is clear however that the psychological and physiological benefits for patients who practice mind-body medicine can have direct and indirect improvement on overall health.
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Selvamurthy, W., Sridharan, K., Ray, U. S., Tiwary, R. S., Hegde, K. S., Radhadrishan, U., & Sinha, K. C. (1998). A new physiological approach to control essential hypertension. Indian Journal of Physiology and Pharmacology, 42(2), 205–213. Shapiro, S. L., Schwartz, G. E., & Bonner, G. (1998). Effects of mindfulness-based reduction on medical and premedical students. Journal of Behavioral Medicine, 21(6), 581–599. Singh, S., Malhotra, V., Singh, K. P., Madhu, S. V., & Tandon, O. P. (2004). Role of yoga in modifying certain cardiovascular functions in type 2 diabetic patients. The Journal of the Association of Physicians of India, 52, 203–206. Speca, M., Carlson, L. E., Goodey, E., & Angen, E. (2000). A randomized, wait-list controlled clinical trial: The effect of a mindfulness meditation-based stress reduction program on mood and symptoms of stress in cancer outpatients. Psychosomatic Medicine, 62, 613–622. Tacon, A. M., McComb, J., Caldera, Y., & Randolph, P. (2003). Mindfulness meditation, anxiety reduction, and heart disease: A pilot study. Family & Community Health, 26(1), 25–33. Telles, S., & Srinivas, R. (1998). Autonomic and respiratory measures in children with impaired vision following yoga and physical activity programs. International Journal of Rehabilitation and Health, 4(2), 117–122. Thomas, G. N., Hong, A. W. L., Tomlinson, B., Lau, E., Lam, C. W., Sanderson, J. E., & Woo, J. (2005). Effects of Tai Chi and resistance training on cardiovascular risk factors in elderly Chinese subjects: A 12-month longitudinal, randomized, controlled intervention study. Clinical Endocrinology, 63, 663–666. Vasan, R. S., Larson, M. G., Leip, E. P., Evans, J. C., O’Donnell, C. J., Kannel, W. B., & Levy, D. (2001). Impact of high-normal blood pressure on the risk of cardiovascular disease. The New England Journal of Medicine, 345, 1291–1297. Vyas, R., & Dikshit, N. (2002). Effect of meditation on respiratory system, cardiovascular system and lipid profile. Indian Journal of Physiology and Pharmacology, 46(4), 487–491. Vyas, R., Raval, K. V., & Dikshit, N. (2008). Effect of raja yoga meditation on the lipid profile of post-menopausal women. Indian Journal of Physiology and Pharmacology, 52(4), 420–424. Wei, L., & Liu, H. Y. (2004). The effect of simplified Tai Chi on improvement of cardiac function in patients with heart failure. Chinese Journal of Clinical Rehabilitation, 7, 1460–1461. West, J., Otte, C., Geher, K., Johnson, J., & Mohr, D. C. (2004). Effects of hatha yoga and African dance on perceived stress, affect, and salivary cortisol. Annals of Behavioral Medicine, 28(2), 114–118. Yang, K. (2007). A review of yoga programs for four leading risk factors of chronic diseases. Evidence-Based Complementary and Alternative Medicine, 4(4), 487–491. Yeh, G. Y., Wang, C., Wayne, P. M., & Phillips, R. (2009). Tai chi exercise for patients with cardiovascular conditions and risk factors. Journal of Cardiopulmonary Rehabilitation and Prevention, 29, 152–160. Yoga Journal (2008). 2008 Yoga in America study. California: Dayna Macy. Yusuf, S., Hawken, S., Onupuu, S., Dans, T., Avezum, A., Lanas, F., INTERHEART Study Investigators, et al. (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet, 364(9438), 937–952.
Chapter 12
Job Stress and Overcommitment in Cardiac Patients En-Young Nicole Cho and Roland von Känel
Introduction This chapter summarizes the current knowledge about the relationships between job stress and heart diseases, particularly coronary heart disease (CHD). In recent decades, job stress seems to have increased in modern societies, while the nature of work and employment underwent significant changes. For instance, there has been a shift in the prevalence of health-adverse work environments from material to mental and emotional stressors (Siegrist & Rödel, 2006; Marmot, Theorell, & Siegrist, 2002; Schrijvers, van de Mheen, Stronks, & Mackenbach, 1998). Computer-based information processing is part of a growing number of job profiles, and the service sector continues to increase. In a macroeconomic context, with the advent of globalization, work pressure has increased considerably along with growing job insecurity and job loss (Siegrist & Rödel, 2006). Moreover, women and elderly people comprise a growing proportion of the work force. Part-time working and flexible work
E.-Y.N. Cho, M.D. Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital, and University of Bern, Freiburgstrasse, CH-3010 Bern, Switzerland R. von Känel, M.D. (*) Division of Psychosomatic Medicine, Department of General Internal Medicine, Inselspital, Bern University Hospital, and University of Bern, Freiburgstrasse, CH-3010 Bern, Switzerland Psychocardiology Unit, Cardiac Prevention and Rehabilitation, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, and University of Bern, Bern, Switzerland e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_12, © Springer Science+Business Media, LLC 2012
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arrangements have also increased. A significant proportion of middle-aged men and women are no longer participating in the labor market partly due to early and involuntary retirement (Brugiavini, 2001). Early retirement is often consequent to job stress–related mental and physical diseases, including cardiovascular diseases (CVD). For instance, the burnout syndrome is understood as a complex of symptoms, primarily exhaustion, in response to prolonged emotional and interpersonal stress at work (Maslach, Schaufeli, & Leiter, 2001). The prevalence of burnout among North American residents fluctuates between 18% and 82% (Prins et al., 2007). Importantly, not all work is carried out in organizations such that work stress issues are also relevant for the self-employed and even those who work in the home, all of which may also be at risk for overwork and associated exhaustion. Chronic states that are characterized by exhaustion, profound fatigue, and feeling burned out are to be considered serious stress consequences because they are accompanied by many medical problems, particularly an increased CHD risk, as well as high economic costs (Melamed, Shirom, Toker, Berliner, & Shapira, 2006). Effort-reward imbalance at work (van Vegchel, de Jonge, Bosma, & Schaufeli, 2005; Tsutsumi & Kawakami, 2004; Kuper, Singh-Manoux, Siegrist, & Marmot, 2002; Stansfeld, Bosma, Hemingway, & Marmot, 1998; Stansfeld, Fuhrer, Shipley, & Marmot, 1999; Ostry, Kelly, Demers, Mustard, & Hertzman, 2003) was positively related to psychosomatic health symptoms, such as self-reported impaired health (Stansfeld et al., 1998; Niedhammer, Tek, Starke, & Siegrist, 2004; Godin & Kittel, 2004; Pikhart et al., 2001), poor well-being (de Jonge, Bosma, Peter, & Siegrist, 2000), and depression (Tsutsumi, Kayaba, Theorell, & Siegrist, 2001). In British civil servants of both sexes, effort-reward imbalance and negative aspects of close relationships at work predicted poor physical, psychological, and social functioning. Psychological demands at work in women and low emotional support in men predicted poor functioning as well. Thus, an even balance between efforts spent and rewards obtained at work appears to be a crucial aspect to maintain mental health–related quality of life in white-collar workers (Stansfeld & Candy, 2006). High-strain work was associated with reduced vitality and mental health as well as with increased pain and risks of both physical and emotional role limitations. Isostrain work (i.e., high strain and low work-related social support) increased these risks further. The lack of work, redundant tasks, and boredom are also increasingly acknowledged as imposing strain particularly on white-collar workers due to low satisfaction with one’s work. Job insecurity also predicted lower subjective health status. Impaired well-being is more likely to be reported in low qualified jobs. In female employees, low decision latitude, high job demands, and low work-related social support were all associated with poor health status at baseline and also with greater functional decline in the subsequent 4 years. Groups with partly unique qualities of job stress are middle managers who experience demands both from above and below in the job hierarchy. The greatest functional decline was observed in jobs characterized by iso-strain (Amick et al., 1998). Overcommitment at work was linked with musculoskeletal pain (Sprigg, Stride, Wall, Holman, & Smith, 2007; Joksimovic, Starke, von dem Knesebeck, & Siegrist, 2002), depression
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(Tsutsumi et al., 2001; Watanabe, Irie, & Kobayashi, 2004; Bonde, 2008; Rockenbauch, Meister, Schmutzer, & Alfermann, 2006), mental disorders (Stansfeld & Candy, 2006), psychosomatic complaints (van Vegchel et al., 2005; Godin & Kittel, 2004), and self-reported health in men (Niedhammer et al., 2004). Overcommitment in German residents explained the greatest percentage of life dissatisfaction well before effort-reward imbalance and organizational issues (Rockenbauch et al., 2006). The number of working hours is related to the perceived work stress which in turn is caused by an imbalance between effort and reward at work. Effort-reward imbalance and overcommitment are strong predictors of physical and mental health as well as life satisfaction in young physicians. These relationships should be a matter of concern as they might particularly herald increased risk of burnout. Job stress may not only affect cardiovascular health but a sick heart may also impact a person’s functioning in his or her job. For instance, return to work is an important behavioral and functional measure of recovery from disease (Picard et al., 1989; Rost & Smith, 1992). Intriguing research shows that – if patients believe that their myocardial infarction will have serious and long-lasting consequences – a slower return to work and higher levels of disability are predicted, too (Petrie, Weinman, Sharpe, & Buckley, 1996). The way patients make sense of their heart attack can strongly influence their trajectory of recovery (Leventhal, Meyer, & Nerenz, 1980). The cognitive representation of the illness consists of five main domains: identity (the name and symptoms that the patient identifies as part of the illness), the cause of the illness, the timeline for the illness (how long the patient thinks it will last), the amount of control the patient perceives he or she has over the illness, and the perceived consequences of the illness on the patient’s life (Lau & Hartman, 1983; Leventhal et al., 1984). More recent research added illness coherence (how well the patients feel they understand the illness), perceptions of treatment control (how much treatment is needed to control the illness), and the emotional representation (how much patients are emotionally affected by the illness) to assessments of illness perceptions (Kaptein & Broadbent, 2007). Perceptions of greater damage to their heart more accurately predicted the patients’ return to work status than any of the biomedical risk factors (Broadbent, Petrie, Ellis, Ying, & Gamble, 2004). Attributions to the cause of myocardial infarction, such as chronic stress or smoking, have also been linked to return to work (Bar-On, 1987; Bar-On, Gilutz, Maymon, Zilberman, & Cristal, 1994; Billing, Bar-On, & Rehnqvist, 1997a) and to lifestyle behaviors (Billing, Bar-On, & Rehnqvist, 1997b; French, James, Horne, & Weinman, 2005; Weinman, Petrie, Sharpe, & Walker, 2000). Patients who view their heart condition as highly symptomatic and suffer from severe consequences, those who feel that they understand their condition and can control it, and those who see lifestyle as a cause of the heart disease are all more likely to attend cardiac rehabilitation (French, Cooper, & Weinman, 2006; Cooper, Lloyd, Weinman, & Jackson, 1999). Previous research has shown that a brief hospital-based psychological intervention after MI can successfully change illness perceptions and improve recovery, including faster return to work (Petrie, Cameron, Ellis, Buick, & Weinman, 2002).
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Definition of Job Stress Theories on job stress differ in defining and quantifying the “distress” elements of the work environment. Traditionally, the discipline of working and organizational psychology has emphasized the role of (objective) working conditions and the working environment for health and well-being (Mohr & Udris, 1997; Ulich, 2001; Levi et al., 2000). More recently, specific conditions of chronic work stress and their impact on physical health were examined applying different theoretical models (Semmer & Mohr, 2001; Siegrist, 2002; Karasek & Theorell, 1990). Two prominent models have gained particular attention as they allow clinicians and researchers alike to operationalize the relationship between job stress and adverse health outcomes. The first model is the job-strain model, proposed by Karasek and Theorell (1990), in which “job demands,” “job control,” and “social support” are identified as critical dimensions of the working environment. The second one is the effort-reward imbalance and overcommitment model that was developed by Siegrist (1986, 1996).
The Job Demand/Control and Social Support Model In 1979, Karasek introduced the demand-control or “job-strain” model (Karasek, 1979) which has become one of the most frequently used models for psychosocial working conditions and health in job stress research (Karasek & Theorell, 1990; Karasek, 1979). The job-strain model postulates that a combination of high psychological demands with low control at work (“high strain”) leads to mental and physical illness (Karasek, Baker, Marxer, Ahlbo, & Theorell, 1981; Karasek et al., 1988). The two core dimensions of the model – “psychological job demands” and “decision latitude” or “control” – were later supplemented with a third dimension of social support at work (Johnson & Hall, 1988; Johnson, Hall, & Theorell, 1989). Persons with high job strain and low support (so-called iso-strain) are at highest risk of adverse health outcomes. For example, assembly line workers, unskilled industrial workers, city bus or tram drivers, and low-level clerical workers are faced with high-strain workplace conditions. The dimension of psychological demands refers to the quantity of work, the mental requirements, and time constraints such as time pressure, work pace, and deadlines. The decision latitude dimension comprises a person’s possibility to influence his or her own work by exploring new methods and ways of accomplishing the job, possibilities for learning, taking responsibility, being independent, developing and using own skills and knowledge, and experiencing variation at work (Lundberg, 2000). Interactions of high versus low levels of decision latitude with high versus low levels of psychological demands generate four different psychosocial work characteristics: high-strain jobs (high demands and low control), active jobs (high demands and high control), low-strain jobs (low demands and high control), and passive jobs (low demands and low control). The job-strain model emphasizes the interaction between demands and control in causing adverse health outcomes: High psychological demands do not impair health
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per se, but they produce adverse health effects if they coincide with a low level of decision latitude (high strain). That situation produces passivity, learned helplessness, and lack of participation at work (Schnall, Landsbergis, & Baker, 1994). A favorable work situation is constituted if high demands are combined with high decision latitude (active job). This favorable condition is a characteristic for many high-status jobs (i.e., CEOs and managers) and is associated with active learning and development of job skills (Schwarzer, Knoll, & Rieckmann, 2003). Employees who have few demands placed on them along with a low level of control become passive workers as they are stuck in a so-called passive job. Finally, a work situation characterized by low demands and high control is defined as a low-strain job. Low-strain and active work environments constitute the most favorable work conditions with regard to the employee’s health (Karasek & Theorell, 1990). Typical questionnaire items to test the job-strain model are “My job requires working very hard” (job demands) and “On my job, I have very little freedom to decide how I do my work” (job control). Lack of social support (social isolation) was added as a third dimension to the model. It defines the very critical work situation of “iso-strain,” i.e., high-demand jobs with little autonomy and low support (Johnson & Hall, 1988). Social support has long been a potentially moderating variable in the case of high demand and low control (Karasek & Theorell, 1990; Johnson & Hall, 1988; Johnson et al., 1989). Work-based social support as a concept includes the support people receive from colleagues and supervisors at the workplace. Social support usually distinguishes between instrumental and emotional support (Schwarzer et al., 2003). Instrumental support is direct assistance in completing a task or reaching a goal, for example, if an employee receives guidance or practical assistance from a supervisor. Socioemotional support places the emphasis on the face-to-face interaction with another person. A distinction is usually made between coworker support and support from a superior (Karasek & Theorell, 1990). Social support outside of work, such as support from family or friends, is usually not included in the model, although it should be considered that this type of social support has, for instance, also been related to CHD risk (Barth, Schneider, & von Känel, 2010). Social support at work can mediate the relationship between working conditions and well-being in different ways. For instance, social support can act as a “stress buffer” and thereby alleviate the adverse effects of psychological and psychophysiological challenges on health (Karasek & Theorell, 1990). If social support is considered for the job-strain model, there will be eight types of work stress. There are the four original types named above and their combinations with or without social support at the workplace.
The Effort-Reward Imbalance and Overcommitment Model In 1986, the effort-reward imbalance (ERI) model was introduced by Siegrist (1986) in order to predict and explain the incidence of CVD explained by job stress. The ERI model has its origin in medical sociology and emphasizes the principle of social reciprocity according to which the employee invests efforts and expects rewards (Marmot, Siegrist, Theorell, & Feeney, 1999). In other words, the ERI model assumes
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that the imbalance between high effort spent and low rewards received at work is likely to elicit recurrent negative emotions and sustained (biological) stress responses particularly relevant to the pathogenesis of coronary heart disease in exposed employees (Siegrist 1996, 2002). Examples of questionnaire items to assess ERI are “I have constant time pressure due to a heavy workload” (effort), “I have many interruptions and disturbances in my job” (effort), “My job promotion prospects are poor” (reward), and “I experience adequate support in difficult situations.” The workplace offers opportunities to acquire self-efficacy (e.g., successful job performance), self-esteem (e.g., recognition), and self-integration (e.g., belonging to a significant group). According to the model, effort at work is spent as part of a social contract that ideally guarantees adequate reward (Siegrist, 1986; Siegrist & Peter, 2000). Rewards are distributed by three types of work-related rewards: money, esteem, and status control. Low promotion prospects, forced job change, job instability, and job insecurity are all examples of poor status control. High-effort low-reward conditions are maintained (1) if employees have no alternative choice in the labor market (e.g., due to low level of skills, lack of mobility, and a precarious labor market), (2) if employees accept this imbalance for strategic reasons (e.g., expecting future gains), and (3) if the employee exhibits a specific cognitive and motivational pattern of coping with demands characterized by excessive work-related commitment (“overcommitment”) (Siegrist, 2002). Overcommitted employees underestimate the demands and overestimate their coping resources while not being aware of their own contribution to the imbalance between effort and rewards (Siegrist, 2002). Examples of questionnaire items to assess overcommitment are “Work rarely lets me go, it is still on my mind when I go to bed” (inability to withdraw from work) and “I easily get overwhelmed by time pressures at work” (disproportionate irritability). Overcommitment is seen as a set of attitudes, behaviors, and emotions based on the cognitive and motivational elements of the former type A coronary behavior pattern reflecting an exorbitant ambition in combination with the need for approval and esteem (Hanson, Schaufeli, Vrijkotte, Plomp, & Godaert, 2000; Siegrist, 1998). The scale overcommitment comprises items that originally derived from the construct of “need for control” (i.e., need for approval, competitiveness, disproportionate irritability, and inability to withdraw from work). With the concept of overcommitment, the ERI model encompasses not only situation-specific and work-related extrinsic dimensions (i.e., efforts and rewards) but also a person-specific intrinsic component (Siegrist, 2001). Figure 12.1 illustrates the ERI and overcommitment model (Siegrist, 1996). The ERI model posits three hypotheses which allow clinicians and researchers to characterize three specific job stress constellations which may impact on health (van Vegchel et al., 2005): (a) The extrinsic ERI hypothesis: Adverse health effects are a result between a mismatch between high effort and low reward at work. (b) The intrinsic overcommitment hypothesis: Adverse health effects are a result of personal commitment that leads to continued exaggerated effort in a low-reward working environment (i.e., even if ERI is absent).
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Extrinsic (situation)
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Overcommitment (need for control and approval)
High effort
Low reward
demands obligations
money esteem security/career opportunities
Fig. 12.1 The effort-reward imbalance model (according to Siegrist, 1996)
(c) The interaction hypothesis: The relatively highest health risk would be expected in workers with high overcommitment (constellation 2) who experience ERI at work (constellation 1). Clear conceptual and methodological differences exist between the two models. The job demand/control model is restricted to the structural aspects of the psychosocial work environment if the effort-reward imbalance model includes both extrinsic (situational) and intrinsic (personal) characteristics. Additionally, the two different theoretical stress orientations (control vs. reward) have different implications for policy. Whereas the control paradigm points to the division of labor, the reward paradigm addresses the issue of distributive justice and fairness (De Vogli, Ferrie, Chandola, Kivimäki, & Marmot, 2007).
Other Models of Job Stress Kasl (1992) suggested that occupational stressors can be considered a long-term risk for health and well-being if the following four conditions are met: (1) the stressful situation is chronic, (2) an adaptation is difficult because permanent adaptation and concentration is required, (3) there are serious consequences associated with failure to meet demands, and (4) the problems affect other spheres of living, resulting in cumulative effects. In the long run, a vicious circle of increasing vulnerability that diminishes resources may ensue, while the individual needs more resources to meet the external challenges (Schönpflug, 1987). Workplace unfairness may also have detrimental consequences for cardiovascular health (De Vogli et al., 2007). One line of occupational research puts a particular focus on (subjective) person-specific conditions, such as – to name a few – negative affectivity (Watson & Clark, 1984; Watson & Pennebaker, 1989), type A behavior pattern (Contrada et al., 1982; Krantz et al., 1988), type D personality (Pedersen & Denollet, 2003), or self-regulatory processes such as optimism and goals (Schwarzer, 1999). Moreover, a state of profound fatigue (so-called vital exhaustion) that is accompanied by irritability, general malaise, and demoralization has been introduced as one consequence of long-lasting demands at work which exceed an individual’s coping resources (Appels, 2004).
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Epidemiologic Evidence Job Stress as a Predictor of Incident Coronary Heart Disease Few studies have investigated whether high job stress is a predictor of recurrent cardiac events. In contrast, in a review of 33 studies, several studies reported job strain as a risk factor for incident CHD (Eller et al., 2009). However, interactions between situation- and person-specific stressors and resources enhance the complexity of the relationship between work and cardiac health (Mohr & Semmer, 2002; Levine & Ursin, 1991). The fact that traditional risk factors account for approximately two thirds of cases of CHD at best has stimulated increasing interest in the relationship between psychosocial factors and CHD. Five areas – chronic stress, socioeconomic status (SES), personality, depression, and social support – have been most thoroughly examined in this regard (Rozanski, Blumenthal, Davidson, Saab, & Kubzansky, 2005). The worldwide executed Interheart Study investigated almost 25,000 patients with myocardial infarction and controls. They found that psychosocial risk factors explained 33% of the population-attributable risk of myocardial infarction above and beyond classic CVD risk factors (Yusuf et al., 2004). In the Interheart Study, psychosocial stress was assessed in terms of stress at work and at home, financial strain, and major life events in the past year; locus of control and depression were also assessed. Specifically, patients with myocardial infarction reported higher relative risk of job stress than controls with odds ratios of 1.38 (99% CI 1.19–1.61) for several periods of work stress and 2.14 (1.73–2.64) for permanent stress at work. All analyses adjusted for age, sex, geographic region, and smoking (Rosengren et al., 2004). Most research on the association between ERI at work and health concerned CHD, including first-time myocardial infarction, chronic heart failure (CHF), and systemic hypertension (Marmot et al., 2002; van Vegchel et al., 2005; Tsutsumi & Kawakami, 2004; Siegrist, 2002; Siegrist & Peter, 2000). A recent review summarized data from 24 studies which focused on CVD outcomes (van Vegchel et al., 2005) and found that high-effort low-reward conditions were repeatedly associated with a 1.2–8.9-fold increased greater relative risk of incident coronary events (Bosma, Peter, Siegrist, & Marmot, 1998; Kivimaki et al., 2002; Niedhammer et al., 1998; Siegrist, Peter, Junge, Cremer, & Seidel, 1990; Peter, Alfredsson, Knutsson, Siegrist, & Westerholm, 1999). Overcommitment has also been associated with a 1.2–4.5-fold increased relative increased risk of developing or dying from CVD (Kristensen, 1996). As yet, about 50 job stress studies have been published with CVD as the primary endpoint, one third of which were conducted prospectively. The majority of these empirical studies support the notion of an association between particularly low decision latitude and risk of CVD. Few studies have investigated the interaction between job demands and job control, with some studies suggesting that job strain is associated with a 1.2–5.0-fold increased CVD risk. The literature on job strain and CVD has been reviewed by several authors (Schnall et al., 1994; Belkic,
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Landsbergis, Schnall, & Baker, 2004; Kristensen 1989, 1996). Table 12.1 gives an overview of findings from large-scale epidemiological studies. One major problem regarding the evidence of an association between job strain and CHD is that even the best-designed prospective studies have failed to take into account the cumulative effects of early life factors which may have an effect on Table 12.1 Literature overview on job stress and cardiovascular disease risk Authors (year) Study population and design Main findings Karasek 1,461 Swedish male workers; Job demands increase the risk of developing et al. (1981) prospective cohort CHD symptoms and signs and premature CHD-CVD death. Low decision latitude is also associated with increased risk of CVD Alfredsson, Spetz, 958,096 men and women, Men employed in occupations where a high and Theorell 20–64 years; prospective proportion reported a combination of hectic (1985) cohort work and few possibilities to learn new things were more frequently hospitalized for MI than other working men Siegrist, Peter, 416 men, blue-collar workers; Men with high ERI had a significantly Junge, Cremer, prospective cohort greater 4-year progression of atheroscleand Seidel rosis. High OC was associated with (1990) increased risk of CVD Siegrist, Peter, 416 male blue-collar workers; High ERI predicts fatal or non-fatal CVD Motz, and prospective cohort (acute MI, stroke). High OC was Strauer (1992) associated with increased risk of CVD Siegrist and Peter 416 male blue-collar workers; High ERI at work was positively associated (1994) prospective cohort with coronary events Lynch and Krause 1,797 Finish men; prospective High ERI at work was positively associated (1997) cohort with the occurrence of coronary events Appels, Siegrist, 79 male acute MI patients, Chronic workload distinguished between and de Vos 132 controls; retrospective MI patients and controls (1997) cohort Bosma 10,308 civil servants; CVD symptoms and risk factors were et al. (1998) prospective cohort positively associated with high ERI and low job control Hammar, Swedish men and women An increased incidence of MI was found for Alfredsson, (8,833 cases, 24,913 (young) men and women in occupations and Johnson controls); case–control characterized by low decision latitude. (1998) study For men this increase was seen primarily in combination with high psychological demands (high job strain) and low social support at work Joksimovic 106 men with CHD; OC was an independent predictor of et al. (1999) prospective cohort coronary restenosis after percutaneous coronary angioplasty Kivimäki 812 factory employees (varies High ERI at work was positively associated et al. (2002) from foundry work to with the occurrence of coronary events. administrative work); High OC was associated with increased prospective cohort risk of CVD (continued)
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Table 12.1 (continued) Authors (year) Study population and design Kuper, SinghManoux, Siegrist, and Marmot (2002) Peter, Siegrist, Hallqvist, Reuterwall, Theorell, and SHEEP Study Group (2002) Guimont et al. (2006)
Kivimäki et al. (2006) Kornitzer et al. (2006) Aboa-Eboulé et al. (2007)
Main findings
10,308 civil servants; prospective cohort
High ERI was positively associated with the risk of coronary events
951 workers with MI, 1,147; retrospective cohort
High ERI was positively associated with the risk of coronary events. | High OC was associated with increased CVD risk
8,395 white-collar workers; prospective cohort
Exposure to cumulative job strain had a significant effect on systolic blood pressure among men. Men and women with low social support at work had higher risk for elevated blood pressure 83,014 employees; review Observational data suggest an average 50% and meta-analysis of excess risk of future CHD among prospective cohort studies employees with work stress 21,111 middle-aged European Job strain predicted acute coronary events men; prospective cohort with the psychological demands scale emerging as the important component 972 men and women, Chronic job strain after first MI was 35–59 years, returned to associated with an increased risk work after first MI; of recurrent CHD prospective cohort 4,707 women, 3,063 men, Social support at work was an independent from Sweden; prospective predictor of MI and stroke among cohort women
André-Petersson, Engström, Hedblad, Janzon, and Rosvall (2007) Ohlin, Berglund, 448 men and women; Rosvall, and prospective cohort Nilsson (2007) De Vogli 5,726 British men, 2,572 et al. (2007) British women; prospective cohort Alves, Chor, 1,819 women; crossFaerstein, sectional cohort Werneck, & Lopes (2009) Leineweber 2,755 men; prospective cohort et al. (2009)
Job strain in men, but not in women, predicted blood pressure increase at 6.5 years of follow-up Unfairness was an independent predictor of increased coronary events and impaired health functioning Job strain was associated with hypertension
Covert coping with unfair treatment at work was associated with risk of incident MI or cardiac death ERI was associated with coronary artery lesions
Xu, Zhao, Guo, 320 Chinese; cross-sectional Guo, and Gao cohort (2010) CHD coronary heart disease, CVD cardiovascular disease, ERI effort-reward imbalance, MI myocardial infarction, OC overcommitment
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stress perception in adulthood (Stansfeld et al., 1998, 1999). These early influences on both adult CHD risk and stress perception could confound evidence regarding the status of job strain as a risk factor for CHD in adult populations. Indeed, it is unclear whether part of the association between job strain and CHD may be attributable to influences from childhood or adolescence. The Cardiovascular Risk in Young Finns Study (Kivimäki et al., 2007) prospectively examined in men whether biological, familial, and socioeconomic risk factors in adolescence contributed to the association between job strain and adult carotid artery intima-media thickness, a marker of atherosclerosis and valid preclinical marker of CHD (O’Leary & Polak, 2002; van Trijp et al., 2006; Tzou et al., 2005). Most of the adolescent risk factors predicted adult intima-media thickness. A dose– response relation was also seen between higher job strain and greater intima-media thickness after adjustment for age. Nonetheless, there have been several nonconfirmatory findings concerning job strain and CVD outcomes within large-scaled studies (Hlatky et al., 1995). Following a selection process with a predefined set of criteria, Belkic and colleagues recently reviewed 17 longitudinal studies of which 9 were case-controlled and 8 were crosssectional ones (van Vegchel et al., 2005). The authors concluded that there is a strong and consistent evidence for an association between exposure to job strain and CVD, especially among men. Additional evidence was provided between job strain and CVD among men for prevalence of MI and self-reported angina pectoris (Belkic et al., 2004). The association between chronic work stress with CHD was strongest among participants aged under 50 (working population) (Britton et al., 2008). At least, as far as the dimension of low decision latitude is concerned, this conclusion is in line with other reviews on the job-strain model (Schnall et al., 1994; Siegrist & Peter, 2000; Landsbergis et al., 2001), with findings which are most consistent for men, blue-collar workers, and in populations under the age of 55. Several studies looked at risk of job stress for CVD in women only. For instance, women experiencing financial strain over the past year had an increased risk of recurrent events, that is, the combination of all-cause mortality, new acute myocardial infarction, and unstable angina pectoris during the follow-up. Financial strain was a predictor for recurrent events among women with CHD, independently of commonly used SES indicators, such as education and household income (Georgiades, Janszky, Blom, László, & Ahnve, 2009). Epidemiological studies have shown that vital exhaustion is an independent risk factor of incident CHD and recurrent coronary events in both men and women (von Känel, Bellingrath, & Kudielka, 2009a). Vital exhaustion has been shown to also predict new cardiac events after successful coronary angioplasty (Kop, Appels, Mendes de Leon, de Swart, & Bär, 1994). It has been identified as an independent risk factor for adverse health outcomes, including CVD (Melamed et al., 2006; Levine & Ursin, 1991; Rozanski, Blumenthal, & Kaplan, 1999). In occupational research, there are studies demonstrating a relationship between working conditions (working overtime, excessive workload, adverse physical work conditions, adverse coworker behavior, qualification potential, and social support by coworkers) and
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vital exhaustion (Rozanski et al., 1999). Particularly, working overtime has been found to predict both vital exhaustion and myocardial infarction (von Känel, Bellingrath, & Kudielka, 2009b). Excess fatigue and feelings of general malaise have been found by many researchers to be prevalent precursors of myocardial infarction and sudden cardiac death. The idea behind the construct of vital exhaustion stemmed from an interest to understand the nature of the feelings of unusual tiredness and fatigue which were commonly reported among patients having antedated a recent MI. Ad Appels (Appels & Mulder, 1989) who originally conceptualized the vital exhaustion concept followed the reasoning of postulating a prolonged period of perceived uncontrollable stress that results in a state of vital exhaustion. Therefore, it has been suggested that vital exhaustion is a mental state at which people arrive if their resources for adapting to stress are broken down.
The Pathophysiology of Job Stress Job stress may cluster with established cardiovascular risk factors (smoking, excessive alcohol consumption, physical inactivity, unhealthy food habits, obesity, and diabetes) and other psychosocial risk factors for CHD (e.g., depression, sleep disorders, burnout, low social support), which are also associated with partly distinct pathophysiology. Job stress has also been associated with increased blood pressure over the working day (Steptoe & Willemsen, 2004) and development of the metabolic syndrome (Chandola, Brunner, & Marmot, 2006). Both are strong risk factors of CVD. Moreover, cardiac patients with job stress show poorer compliance with cardiac regimens (Antonovsky 1979, 1987; Udris, 1990). Comparably, little is known about the psychobiological mechanisms through which job stress might increase the risk of atherosclerosis initiation, progression, and manifestation in form of clinically overt CVD. Nonetheless, several potential pathways involving cerebral processing of job stress with accompanying negative affect, the hypothalamic pituitary adrenal (HPA) axis and autonomic nervous system, as well as vascular and circulating biomarkers of increased atherosclerotic risk have been proposed (Fig. 12.2). Applied research strategies to identify such psychophysiologic mechanisms include ambulatory monitoring in naturalistic settings, experimental studies, analyses of innovative biomedical markers in high-risk groups in epidemiological studies (e.g., nested control studies), and brain imaging studies. With regard to the latter, the neural correlates of rewarding experiences, of stimuli that predict reward, and of violation of expected rewards have recently been studied. Omission of an expected reward was shown to be associated with a relative decrease of cerebral activation in dopaminergic brain areas. Enhanced brain activation in distinct areas of the dopaminergic reward-sensitive system was interpreted as a compromised ability of adapting brain activation among those suffering from chronic social reward frustration (Siegrist et al., 2005). In the past years, several biological markers have been examined as potential mediators, such as hypertension and systolic blood pressure (Peter & Siegrist, 1997;
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Fig. 12.2 Psychoneuroendocrine-immune interactions relevant to atherosclerosis
Peter et al., 1998; Steptoe, Siegrist, Kirschbaum, & Marmot, 2004; Vrijkotte, van Doornen, & de Geus, 1999; Vrijkotte, van Doornen, & de Geus, 2000), atherogenic lipids (e.g., increased total cholesterol, high concentration of low-density cholesterin) (Peter et al., 1998), impaired fibrinolysis (e.g., decrease in activity of profibrinolytic tissue-type plasminogen activator (t-PA) and increase in activity of antifibrinolytic plasminogen activator inhibitor (PAI-1)) (Peter et al.; Vrijkotte et al., 1999), ambulatory blood pressure, heart rate, and heart rate variability (Vrijkotte et al., 2000), and cortisol (Steptoe et al., 2004; Wirtz et al., 2010). Specifically, overcommitment has been related to an impaired fibrinolysis (Vrijkotte et al., 1999), exaggerated cardiovascular reactivity (Vrijkotte, van Doornen, & de Geuset al., 2004), blood pressure (Vrijkotte et al., 2000, 2004), higher LDL cholesterol (Siegrist & Matschinger, 1989) (in women), and elevated morning (Steptoe et al., 2004) and post meridiem (Wirtz et al., 2010) cortisol levels and predicts restenosis after coronary angioplasty in cardiac patients (Joksimovic et al., 1999). Effort-reward imbalance was related to elevated blood pressure (Vrijkotte et al., 2000), atherogenic lipids (Peter et al., 1998), impaired fibrinolysis (Siegrist, Peter, Cremer, & Seidel, 1997), and decreased serum levels of high-density lipoprotein (HDL).(Irie, Tsutsumi, Shioji, & Kobayashi, 2004) Regarding the job-strain model, several studies found associations between demand or control and the prevalence of cardiovascular risk factors like hypertension, atherogenic lipids, and fibrinogen (Schnall et al., 1994; Peter et al., 1999). In a review of 18 studies, job strain was mainly defined as a mismatch between job demands and decision latitude (i.e., job control) or as an imbalance between effort spent and reward obtained at work moderated by a personality trait of overcommitment to work (von Känel et al., 2001). There emerged a reliable association between high job stress and a prothrombotic milieu reflected by elevated
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procoagulant molecules (i.e., fibrinogen and clotting factor VII (FVII)) and reduced fibrinolytic capacity (i.e., decreased t-PA activity and increased PAI-1). Many studies found this association independent of potential confounders. However, factors related to the metabolic syndrome largely accounted for a positive relationship between job strain and PAI-1 which was found in women, but not in men (Brostedt, de Faire, Westerholm, Knutsson, & Alfredsson, 2004). While most studies were cross-sectional, FVII, FVIII, and fibrinogen levels as well as ADP- and thrombin-induced platelet aggregation were increased in accountants during a period of increased workload compared to a calm period (Frimerman, Miller, Laniado, & Keren, 1997). In teachers, high overcommitment was associated with prolonged hypercoagulability of the blood in response to acute psychosocial stress, particularly during the recovery period (von Känel et al., 2009b). Plasma fibrinogen might be a particularly important mediator linking job stress with increased risk of CHD (Theorell, 2002). A cross-sectional study on 16,335 male and 5,084 female workers aged 35–54 years from 24 Belgian enterprises found positive relationships between job demands and fibrinogen for men in the lowest educational level and between job strain (i.e., high demands and low control) and fibrinogen in men, but not in women (Kittel et al., 2002). Job strain was also positively associated with plasma fibrinogen levels in Japanese men, but not in women. The relationship between high job demands and elevated fibrinogen in men survived adjustment for potential confounders, including total cholesterol and C-reactive protein (Hirokawa, Tsutsumi, Kayaba, & Jichi Medical School Cohort Group, 2008). In male Belgian workers, a negative association was found between job control and fibrinogen independent of sociodemographic factors, traditional cardiovascular risk factors, and medications (Clays et al., 2005). Although this work may suggest that men are particularly susceptible to exhibit increase in fibrinogen with job stress, relationships have been found for both sexes depending upon the particular country and male/female ratio in the studies (Theorell, 2002; Tsutsumi, Theorell, Hallqvist, Reuterwall, & de Faire, 1999). Job control seems more consistently related to fibrinogen than job demand perhaps because job control may contribute to the above discussed inverse relationship between socioeconomic status and fibrinogen (Steptoe & Willemsen, 2004). In a previous systematic review, the cortisol awakening response showed a positive association with job stress and a negative one with fatigue, burnout, and exhaustion (Chida & Steptoe, 2009). Less control at work predicted higher cortisol levels even on weekends, suggesting impaired physiological recovery from job stress (Berset, Semmer, Elfering, Amstad, & Jacobshagen, 2009). Positive associations between early morning cortisol levels and job stress have been reported for the and ERI models alike (Alderling, Theorell, de la Torre, & Lundberg, 2006; Kunz-Ebrecht, Kirschbaum, & Steptoe, 2004; Steptoe, 2000). Contrasting results have been obtained for the ERI model with blunted (Peter & Siegrist, 1997; Bellingrath, Weigl, & Kudielka, 2008; Bellingrath & Kudielka, 2008; Wirtz, Siegrist, Rimmele, & Ehlert, 2008), heightened (Steptoe et al., 2004), or unchanged salivary cortisol levels and HPA axis response in relation to job stress (Siegrist, 1998; Irie et al., 2004). More studies examining the two models simultaneously with regard to salivary cortisol
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levels in order to potentially explain these differing results are clearly needed (Hurwitz Eller, Netterstrøm, & Hansen, 2001). This seems important because the two models combine complementary aspects of a stressful work environment (Maina, Bovenzi, Palmas, & Larese Filon, 2009). Anticipatory cognitive stress appraisal seems to modulate monocyte inflammatory activity following stress (Wirtz et al., 2007). Job stress also seems to alter specific serum catecholamine metabolites (brain-derived neurotrophic factor, plasma 3-methoxy-4-hydroxyphenylglycol levels) in healthy persons (Mitoma et al., 2008). General life stress was associated with poorer cardiovascular recovery. However, regarding the sympathetic and parasympathetic nervous system, there were no direct associations between job stress and hemodynamic stress reactivity or recovery (Chida & Hamer, 2008).
Behavioral Approach(es) to the Management of Job Stress There is a dearth of literature to describe the development and implementation of preventive interventions aimed at reducing psychosocial stressors at work (i.e., high demands, low decision latitude, low social support, and low reward) and associated health effects. A review covering 20 years of literature of job stress preventive interventions concluded that interventions mostly target individuals rather than work organization by implementing stress management programs instead of decreasing adverse psychosocial work factors (Kompier & Kristensen, 2001). Many authors argue that organizational approaches are more effective and showed longer-lasting benefits than individual approaches (Bond & Bunce, 2001). There are indeed work reorganization outcome studies which have tested for relationships between improvements in job control and stress-related outcomes. For example, Parker et al. (1997) found a significant relationship between increases in control and job satisfaction 4 years after a chemical processing plant instituted strategic downsizing in association with an “empowerment initiative.” Unfortunately, many of these studies (Cordery, Mueller, & Smith, 1991; Murphy & Hurrell, 1987; Pierce & Newstrom, 1983; Wall & Clegg, 1981) lack the inclusion of a comparison group and a follow-up period, thus making interpretation of findings problematic. Those few studies using these two essential design features (Griffin, 1991; Jackson, 1983; Landsbergis & VivonaVaughan, 1995; Wall, Kemp, Jackson, & Clegg, 1986) do not provide encouraging support for the effectiveness of control-promoting and work reorganization initiatives on stress-related outcomes. In fact, only the studies by Wall et al. (1986) and Griffin (1991) appear to have demonstrated that such a program can significantly improve stress-related outcomes at a final observation point by using a longitudinal and quasi-experimental design. Specifically, Wall et al.’s (1986) intervention of instituting autonomous workgroups significantly improved intrinsic job satisfaction at their 30-month follow-up, and Griffin’s (1991) intervention, which sought to increase autonomy and other work characteristics (e.g., task identity), improved
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supervisors’ evaluations of subordinates at 48-month follow-up. Schaubroeck et al. (Schaubroeck, Ganster, Sime, & Oilman, 1993) demonstrated that a work reorganization intervention could improve job satisfaction of supervisors in a business division of a university. However, their intervention, involving a role-clarification program, did not try to achieve these outcomes by increasing people’s work control. Bunce and West (1996) as well as Bond and Bunce (2000) conducted two studies which demonstrated that an intervention could improve people’s well-being by encouraging them, if possible, to reduce their own work stressors (e.g., asking for clarification regarding one’s expected roles). Nevertheless, in studies assessing improvements in individual psychosocial work factors, significant decreases between 9% and 55% in symptoms associated with mental health, such as depression and anxiety and sick leave, were observed (Bond & Bunce, 2001; Morel-Kopp et al., 2009). A participative action research intervention significantly improved people’s mental health, sickness absence rates, and self-rated performance at a 1-year follow-up. Increase in job control served as the mechanism or mediator by which these improvements occurred (Bond & Bunce, 2001). Whether job stress–targeted interventions improve cardiovascular health and even mortality is currently unknown. However, in terms of cardiovascular risk markers, a 60-h training session of managers in psychosocial work environment factors aimed at improving employee well-being resulted in lowered serum cortisol after 1 year in employees (but not in the managers) (Theorell, Emdad, Arnetz, & Weingarten, 2001). A parallel line of behavioral cardiology research suggests that treatment of psychosocial factors might indeed result in favorable changes of cardiovascular risk profile. For instance, in depressed outpatients without CVD, treatment with psychotherapy and antidepressants seemed equally effective in reducing increased platelet activation (Morel-Kopp et al., 2009). In patients with stable CHD, stress management improved endothelial dysfunction (Blumenthal et al., 2005). However, another study found that it did not alter blood clotting compared to usual care (Claesson et al., 2006).
Clinical Approach to the Individual Patient with Job Stress If planning any kind of interventional approach at the workplace, it has to be taken into account that stress is a highly individual process (Siegrist, 2002; Lazarus & Folkman, 1984; Lazarus 1991, 1999; McEwen, 1998). In terms of managing the patient with heart disease and job stress, job-related stressors and resources are relevant for the development of coping strategies, such as feelings of coherence (Antonovsky 1979, 1987) or perception of social support (Siegrist & Peter, 2000). In general, job stress–related therapy must cover several dimensions. Specific behavioral interventions targeting job stress–related factors, such as reducing job demands and increasing job control, are available to support the patient in this challenging endeavor. A behavioral treatment approach should systematically assess the following five main factors which are known contributors to job stress (Table 12.2).
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Table 12.2 Suitable (open) questions for the clinical assessment of job stress Job stress: five main factors Suitable open question Job demands What does your job require from you? How many hours per week are you working? What about working on weekends? Job control How much control do you have over your work? When do you get a break during working hours? Social support at work How do you perceive support from your co-workers and your supervisor? Reward at work What type(s) of reward do you perceive at work? What about your career opportunities? Overcommitment to work How important is your work to you? If I would ask your partner how engaged a worker you are, what would she or he tell me?
Table 12.3 Suitable intervention approaches Targets Interventions Role of the employee Reduction of job demands Avoid making overtime, take a break, adhere to time schedule, learn to delegate tasks Increase of social support at work Seek out for social support from co-workers/supervisors Correction of overcommitment Improve stress management skills, question self-demanding to work expectations and requirements, (re)establish a work-life balance Role of supervisor Increase of work autonomy
Increase of social support at work Increase of reward at work
Allocate responsibilities, enable professional training, let employees participate in decision-making and job operation processes Estimate achievements, create a positive work atmosphere, prevent workplace bullying Enable professional development, engage in verbal appreciation, increase salary, initiate staff wellness programs
Based on these factors, an individual explanatory model can be developed with the patient. In a next step, the patient will be asked to actively suggest feasible modifications of his or her explanatory model for perceived job stress. The therapist may support this process by asking the patient: “Did you already try actively to establish a contact with your boss? Are you able to have lunch break? Do you have the opportunity to get professional training in work activities where you feel overstrained? How do you manage to distract from work? How are you maintaining your worklife balance?” In a next step, small but clearly defined changes which are realistically achievable in a predictable period of time should be set. It is important to mention that general fatalism toward job strain (“today’s working conditions are not changeable in any ways”) is out of place. Possible intervention approaches for the employee and/or his or her supervisor are listed in Table 12.3. If practicable, the therapist may ask the patient for his or her agreement to get in contact with the boss or supervisor. Furthermore, the supervisor may participate in
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a therapy session. In general, such participation is of high value for the ongoing therapy process and should be well prepared by both therapist and patient. Self-reflection about individually stressing job situations may be enhanced by one-on-one interviews (What did the patient contribute to interpersonal conflicts at work? What are the individual mechanisms involved in a patient’s high disposition for overcommitment (e.g., need for being loved and accepted which can only be achieved through being successful in his or her job)? What does the patient expect from his supervisor?). The therapist may want to examine work-related unrealistic expectations, challenge distorted views, generate more adaptive explanations, help the patient adopt a more flexible coping style, enhance sense of control, reframe and practice supportive self-talk, and guide the patient in anger management. The therapist should particularly appeal to anger and disappointment of the patient toward employer and colleagues, caused, for example, by unsuccessful application for a job promotion. Sometimes a job change can make sense particularly in deadlocked situations. Further unspecific stress management activities like regularly performed relaxation exercises, noncompetitive endurance sports, informal meetings with good friends, and a short and refreshing afternoon nap will balance an overactive sympathetic nervous system and distract from work-focused thoughts and rumination about these. Overall, the therapist should encourage a general healthy lifestyle in terms of regular physical activities, quitting smoking and excessive alcohol consumption, intake of a balanced diet rich in vegetables and fruit, and sleep hygiene. Other important sources of work stress and possibilities to coping may also be conveyed to the individual patient, the typical self-talk that underlies driven behavior and associated values and assumptions; the distinction between hard work (and being healthily tired) versus chronic overwork; the recognition of fatigue symptoms early on and their management; work as avoidant coping for anxiety, low selfesteem, and relationship difficulties; changing work practices, resuming part-time, light duties; charter of rights where relevant; referral to vocational officers and social work; and working for extra money “just because it is there to be earned.” Support by pharmacological means may be temporarily indicated, especially in the presence of comorbid conditions like depression, anxiety disorders, sleep problems, burnout, and musculoskeletal pain to symptomatically improve mood, sleep, and pain. Basic supportive psychotherapy should accompany such pharmacological interventions to improve, for instance, sleep hygiene and alternative pain management skills like relaxation techniques. The therapist should regularly acknowledge and validate the patient’s feelings that the job situation might be difficult and hard to bear. At the same time, it is essential to encourage the patient to think about realistic ways to change the situation. According to the concept of “work-life balance,” the patient should incorporate the attitude that other life areas apart from work, like sports, a recreational hobby, or social activities, are worth to maintain or sometimes resume. Other relevant stressors that are not related to the job (e.g., marital and family stress) should also be identified as they may aggravate job stress and thus the overall level of distress. In this context, many studies identified a stable social network as one of the key components for successful stress management.
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Eventually, as clinicians treating cardiac patients with job strain, it is important to note that “the stressed doctor” has a negative influence on the atmosphere at his or her workplace, which, in turn, contributes to the patient’s feeling of being stressed at the hospital (Billing et al., 1997a). Training and support of clinicians by a professional could reduce and prevent job strain and so improve physicians’ and patients’ quality of life.
Clinical Example Mr. M., a 51-year-old man with known CHD for 5 years, was referred by the cardiac outpatient rehabilitation specialist to the Psychosomatic Division of the Department of General Internal Medicine after his second myocardial infarction in October 2009. Reasons for referral were persistent intermittent chest pain, left shoulder pain, and abnormal exercise tolerance, all of which were not explainable by the patient’s CHD. During cardiac rehabilitation, he was found to be overactive and to overcommit frequently. As part of routine work-up of psychosocial risk factors for CHD, a self-rated psychocardiogram was obtained at the beginning of cardiac rehabilitation (Fig. 12.3). As can be seen, Mr. M.’s psychocardiogram revealed low physical quality of life and high scores for vital exhaustion. Critically high scores were also found for negative affectivity and social inhibition from the type D (“distressed”) personality questionnaire. At hospital entry, Mr. M. reported to have suffered from invalidating chest pain irradiating to the left shoulder for more than 15 years. He reported that pain was regularly accompanied by feelings of fear, anger, insecurity, and diffuse abdominal sensations. He emphasized that he was able to distinguish between these chronic complaints and symptomatic CHD. Mr. M. had a history of hypertension, type II diabetes, and hypercholesterolemia. His daily medication was perindopril 5 mg, hydrochlorothiazide 25 mg, atenolol 25 mg, aspirin 100 mg, and simvastatin 20 mg. Mr. M. was a former smoker and had a family history of premature CHD. In 2004, he had experienced a first myocardial infarction but completely recovered and resumed work. Concerning his professional situation, the patient worked as a manager of several nursing homes. Over the last years, he had been living separated from his wife and children. At the beginning of the hospitalization, Mr. M. could not accept his situation of being sick and was cynical and anxious about therapeutic progress and further examinations. Physical exams, laboratory tests, electrocardiogram at rest, stress ergometry, orthostatic test, chest X-ray, as well as further evaluation by diverse subspecialties revealed all normal results. There was no evidence for a new ischemic cardiac event. He was more relaxed when he was told the normal results of the examinations and subsequently gained security about his complaints. Mr. M. showed apparent difficulties in coping with perception of psychophysiological reactions to stress (e.g., palpitations, thoracic sensations), which he tended to interpret as potential harbingers of a recurrent cardiac event. A structured biofeedback program helped him to keep within recommended heart rates while exercising.
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PsychokardiogrammΘ
prae
risik factor
ressource
somatic score
-1.95
low well-being
high well-being
psychological score
-0.45
low well-being vital exhaustion
high well-being
-1.96
strong
vital
social support
-0.09
low negative affectivity
strong
-1.35
strong social inhibition
low type D -0.59
strong
communicative
hostility
0.00
strong advoidant coping
peaceful 0.79
strong palliative coping
low
-0.53
low depression
strong
-0.81
depressive fear
content
-1.00
anxious positive affectivity
courageous
-0.89
few positive feelings negative affectivity
many positive feelings
-2.01 many negative feelings
few negative feelings
effort/reward
-0.23
dysbalance overcommitment strong -5
-4
-3
balance
-1.13 -2
low -1
0
1
2
3
4
5
*z-value healthy range
threshold limits
<1 standard deviation
critical value
Fig. 12.3 Psychocardiogram example
By this, Mr. M. was able to improve his physical condition. Psychocardiology work-up during hospitalization revealed that the patient had been facing high job demands during the last 3 years as a consequence of ongoing reorganizations at work. He complained of low decision latitude feeling that he was exploited by his institution which wanted him to implement new regulations as issued by a steering agency. For years, Mr. M. had been struggling for his position while exercising high efforts. Interestingly enough, while his psychocardiogram revealed high overcommitment,
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it did not show much evidence for clinically relevant effort-reward imbalance. However, the discrepancy between the patient’s self-rated perception of job stress and respective information obtained by a semistructured interview clearly highlights the importance of the latter in a clinical context. The patient also reported low social support at work from coworkers or supervisors and that his future occupational position was unclear. Seemingly consistent with his type D personality characteristics, he had socially withdrawn and was reluctant to talk about stress at work, his marital conflict, and negative emotions triggered by his current life circumstances. During the 12-week cardiac rehabilitation outpatient program, Mr. M. was seen for six sessions by the psychocardiologist with whom Mr. M. discussed his engaged working style and job demands. It became apparent that “all his life” Mr. M. had been trying to compete with his father who used to be a very successful entrepreneur for whom his family-owned firm was the meaning of life. Mr. M. sadly had the sense that he never had been accepted by his father who, when Mr. M. was 30 years old, died from cancer, not before having uttered his disappointment about the fact that Mr. M. had declined early on to become his successor in the firm. It was very much relieving for Mr. M. to realize that his attempt to prove his father that, as a son, he was equally hardworking, was a major drive behind his behavior to adopt more work than he could realistically handle. Mr. M. agreed upon a work schedule that would allow him to spend more time for his work-life balance, including time for progressive muscle relaxation. As a concrete means to implement this intent, he contacted his supervisor telling him that he would immediately lay down the responsibility for two nursing homes. To the astonishment of Mr. M., his supervisor accepted this announcement without any rejections. Mr. M. confirmed that this experience had assured him that his work was appreciated even at a level of effort spent he had previously perceived as being too low to be valued by his father.
Summary This chapter provided an overview about job stress in cardiac patients, particularly those with CHD. An impressive amount of research has been accumulated during the last 30 years. It strongly suggests that job stress is an important risk factor for CHD. While this link may partly be explained by poor lifestyle of individuals under high job strain and associations of work stress with additional psychosocial risk factors for CVD, psychophysiologic pathways directly linking job stress with atherosclerotic mechanisms are also increasingly identified. Two job stress models – the job demand/control and social support model as well as the effort-reward imbalance and overcommitment model – have most widely been used in job stress research and provide also a suitable framework for individual behavioral approaches to the (cardiac) patient with job stress. While quality of life and mental health of employees benefit from job stress interventions on the organizational and individual level clearly, it remains currently unclear whether cardiovascular morbidity and mortality can be prevented by such interventions.
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Chapter 13
Managing Sleep Problems Among Cardiac Patients Jaan Reitav
Introduction Sleep problems are common among cardiac patients, and treating them is important to both risk reduction and quality of life. This chapter will review the evidence supporting this statement and educate the cardiac frontline health-care provider (physician, psychologist, nurse) about how to manage these problems. The epidemic of obesity in North America is paralleled by an epidemic of sleeplessness. In 1900, the average American slept for 9 h a night. The intervening century has seen the invention of the light bulb, electricity in every home, the digital revolution, and the proliferation of a 24/7 consumer society. Each advance has meant less sleep and more disrupted sleep. The average American adult today sleeps 6–7 h a night, while the recommended minimum sleep for adults remains at 8 h a night. In 2005 (National Institutes of Health State of the Science Conference statement on Manifestations and Management of Chronic Insomnia in Adults), the joint offices of NIMH and Medical Applications of Research (NIH) sponsored a conference on clinical management of chronic insomnia in adults. The panel reviewed clinical research in a number of areas, among them the evidence of the consequences, morbidities, comorbidities, and the public heath burden associated with chronic insomnia. The consensus statement released by the committee highlighted that insomnia is an independent risk factor for many health conditions, among them cardiac problems, and that it must be managed as an independent comorbid condition, rather than as a feature of other conditions, like depression.
J. Reitav, Ph.D., C.Psych., C.B.S.M. (*) University Health Network, Toronto Rehabilitation Institute, Cardiac Rehabilitation and Secondary Prevention Program, Toronto, Canada Department of Clinical Diagnosis, Canadian Memorial Chiropractic College, Toronto, Canada e-mail:
[email protected] E.A. Dornelas (ed.), Stress Proof the Heart: Behavioral Interventions for Cardiac Patients, DOI 10.1007/978-1-4419-5650-7_13, © Springer Science+Business Media, LLC 2012
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One follow-up to the conference was the release of the report from the Institute of Medicine of the National Academies (Colton & Altevogt, 2006), which recognized that sleep disorders are commonly undiagnosed, called for primary care providers to screen and treat these problems more aggressively, and provided the resource material to accomplish this goal. In addition, the American Board of Medical Specialties has recently approved a certificate of added qualifications in sleep medicine for family doctors. The American Psychiatric Association is currently revising and releasing the fifth edition of the Diagnostic and Statistical Manual (DSM). The revisions highlight that sleep disturbances must be evaluated and managed. The first circulated drafts for the DSM-V have included at least seven new diagnoses of sleep disorders, and throughout, the DSM highlights the importance of managing comorbid sleep problems. Paradoxically, while all this has been happening in the sleep world, the cardiac rehabilitation literature has been sleeping. Sleep disturbances are still not considered a risk factor for cardiac disease. In the past 30 years, sleep disturbance has rarely been mentioned as a risk factor to be managed among cardiac disease, even in passing. For example, the INTERHEART study (Yusuf et al., 2004), probably the most comprehensive international study of cardiac risk factors, conflated sleep with stress. They did not measure sleep directly, but included it in their measure of stress (Rosugren et al. 2004). Four decades of epidemiological evidence has established that sleep disturbances are linked with mortality from cardiac and other causes (Prior, Francis, & Reitav, 2009). The past decade has been the most exciting, as the pathophysiological mechanisms behind increased cardiac risk are now being unraveled through basic and clinical research. All of these developments have set the stage for a serious review of the lack of attention paid to sleep and have provided a theoretical foundation for the development of targeted clinical interventions for heart patients. Until 2008, none of the guidelines for cardiac rehabilitation (CR) ever mentioned management of sleep disorders as an important part of clinical treatment of the heart patient (Somers et al., 2008). That will change. The present chapter provides health-care providers with the background context and the clinical strategies needed to work with sleep problems among cardiac patients. Among the topics reviewed will be understanding “normal” sleep among older adults, review of principles of assessment and diagnosis, and presentation of behavioral principles useful in management of the two most common sleep disorders. Behavioral and psychological principles are powerful and effective with older patients (C. M. Morin et al., 2006) and will continue to be an indispensible part of the armamentarium of all health providers treating cardiac patients. Management of sleep problems in this population is an important application of health psychology to a population with a serious disease burden. A full understanding of the principles outlined will require additional reading in physiology, pathophysiology, and behavioral sleep medicine. This chapter aims to provide the interested reader with the historical and scientific background needed to begin this longer journey.
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Reviewing the existing literature on behavioral interventions with sleep in cardiac patients reveals a curious paradox. The most common sleep disorder found among cardiac patients, insomnia, has continued to be ignored, while treatment of sleep apnea has, at least, finally begun to be recognized as the serious health problem that it is. The present chapter will present the clinical approach developed by this author to assess and manage the most common sleep disorders among cardiac patients. This material is based on 25 years of experience in working with sleep disturbances generally, and the past five focused on developing better interventions for cardiac patients specifically. It builds on my training as a clinical and health psychologist, as well as specialty training in behavioral sleep medicine. It is an introduction to an area that is sure to get a great deal more attention in the years to come. The interventions described in this chapter have been developed at the University Health Network, Toronto Rehabilitation Institute’s Cardiac Rehabilitation (CR) Program. This CR Program has a 40-year history of innovation in treating heart patients and currently treats over 1,600 patients each year. The majority of patients have had myocardial infarctions (MIs), cardiac surgery, or angioplasty, but programs for heart failure, heart transplant, diabetic, and stroke patients are also offered. This chapter will introduce the reader to the core strategies and clinical skills that this author has found to work well in a CR population.
Epidemiological Evidence Population-Based Studies of Normal Sleep “Normal sleep” is difficult to define and can vary from person to person, yet normative references are essential to make determinations about clinical status. In the case of a phenomenon as inherently variable as sleep is, a clear grasp of normative values is essential for clinical assessment. The best reference point for clinicians working with an older population is the Sleep Heart Health Study (Walsleben et al., 2004), a normative study of 470 subjects 40–91 years of age. The study cohort had an average of 15 years of education, had a 25 BMI, and was 65.1% female. The occurrence of various chronic health conditions was retained in the sample to provide more realistic norms. The baseline rates for significant comorbid conditions were different for males and females. Their sample was composed of 306 women and 164 men. However, the baseline rates of both cardiovascular disease markers and sleep problems among men were twice that of women, across the board. Habitual snoring was present among 11% of women and 25% of men; diabetes, 2% and 8%; previous MI, 2% and 7.5%; presence of ongoing angina, 3% and 6%; and hypertension, 26% and 35%, respectively. Of importance for the clinician is the presence of cardiac disease among this normative sample. The existence of a representative amount of chronic disease in the cohort makes these sleep norms a reasonable comparator for clinical work.
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The take home message is that the sleep of the normative group (even when the normative group includes a representative amount of chronic illnesses) does not result in any suggestion of clinically disturbed sleep. The findings from this study suggested that the sleep of older adults was predictably consistent, and most participants report waking refreshed and energized. Self-reported sleep duration on weekdays was 7.2 h a night and 7.7 h on weekends. The sleep lab tests of these participants showed that the average older person has a sleep latency (SL, or time taken to fall asleep) of just under 20 min, and they have a sleep efficiency of 85% (SE, they are in bed for just over 8 h a night, and estimate they sleep for 7.2 h). Self-reported total sleep time (TST) each night was slightly higher than what was observed in the sleep laboratory. The sleep lab test indicated the average person slept 6.2 h, and the 50th percentile was 6.4 h. Overall, for older healthy adults, their TST was a shade below the criterion typically used to define insomnia for younger adults (sleeping less than 6.5 h) (Edinger et al., 2004). Clinical insomnia can be defined as persistent occurrence of difficulties falling asleep (SL > 30 min), staying asleep across the night (wakes after sleep onset [WASO] >30 min; ³2 WASO per night; and SE < 85%), and TST < 6.5 h. While the average older person sleeps at or just below the threshold for insomnia in TST and is vulnerable to multiple awakenings, most older adults fall asleep quickly, have good sleep efficiency, awaken refreshed, and do not have problems getting through the day. Most elderly do not meet the criteria for insomnia just because they are older (Ohayon, Carskadon, Guilleminault, & Vitiello, 2004). Age-related changes in sleep appear to be relatively modest based on the findings from this study. For every decade after 40, TST decreases by 6 min and SE decreases by 1.6%. In other words, for the average person, sleep duration will decrease by about 30 min from age 40 to age 90! In absolute terms, this is not a great deal of change, but somewhere toward the end of those 50 years, night time sleep alone no longer feels adequate for sustaining daytime activity without a nap. In conclusion, age gradually diminishes both the quantity and quality of sleep, and men are more affected.
Prevalence of Sleep Problems Among Cardiac Patients A review of the epidemiological studies examining the impact of sleep dysregulation on cardiac symptoms, events, and cardiac deaths provides four primary lines of evidence relating impaired sleep with cardiac mortality. These converging lines of evidence are: 1. 2. 3. 4.
The health risks of shift workers (intermittently misaligned sleep) Studies of short and long sleepers (inadequate or excessive sleep) Insomnia among heart patients (chronically dysregulated sleep) Sleep apnea studies (chronic sleep disorder)
All studies indicate sleep disturbance is a serious risk factor increasing cardiac risks.
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Health Consequences of Shift Work Boggild and Knutsson reviewed studies of shift work and cardiovascular disease (CHD). The evidence indicated a 40% increase in risk for CHD among shift workers compared to day workers. The odds ratio for shift workers having a myocardial infarct was 1.3 for both men and women (Boggild & Knutsson, 1999).
Population-Based Studies of Sleep Duration and Coronary Artery Disease (CAD) An extensive population-based literature has investigated the relationship between sleep duration and mortality. These studies were recently reviewed (Prior et al., 2009) and provide strong evidence that short duration sleepers (£5 h of sleep per night) have a higher risk of coronary events (adjusted relative risk [RR] confidence interval [CI] 1.45 < RR < 1.79). Long sleepers (³9 h of sleep) showed the same pattern (adjusted RR CI 1.38 < RR < 1.79). These effects persist even when subjects with diabetes and hypertension are excluded from the analysis. The mechanisms underlying these findings are the subject of ongoing research. The most active area of current research is defining the impact of circadian rhythms of basic physiological functions on cardiac functions (see next section). It has been estimated that compared to 8-h sleepers, the 5% of the population who sleep less than 5 h have a 39% increased risk of congestive heart disease, while the 21% who slept 6 h had an 18% increased risk compared to those sleeping 8 h. More specifically, the younger subjects (£60) where more impacted by shorter sleep (relative risk of cardiac events, RR = 1.62 vs. 1.43), while the older adults (>60) were more impacted by longer sleep (RR = 1.39 vs. 1.82) for having a cardiac event.
Insomnia Prevalence of Insomnia in a Prospective Series of MI Patients Twenty years of research have established that heart patients report more sleep disturbances. In 1987, Appels reported that sleep complaints were very common among patients who had had a myocardial infarct. In the weeks and months leading up to their cardiac event, 50% of their patient sample reported insomnia. They noted that this incidence was higher than that of 33% reported by patients hospitalized with other medical conditions. Both of these are much higher than recent estimates of about 12% of a community-based sample reporting insomnia (M.M. Ohayon, 2002). Carney assessed the frequency of sleep disturbance in a prospective, consecutive series of patients with new incidence MIs. Seventy consecutive MI patients <70 years old were assessed with the Diagnostic Interview Schedule protocol for standardized assessment for both depression and insomnia (Carney, Freedland, & Jaffe, 1990).
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They found that 39% of MI patients reported insomnia in the preinfarct period: three times the usual community prevalence! Of the insomnia patients, half met the DSM-III-R criteria for major depressive disorder, and the other half did not. In addition, insomnia patients were neither more nor less likely than others to be taking medications known to affect sleep; nor was insomnia related to either age or comorbid medical conditions. The authors concluded, “If insomnia and depression play an etiologic role in MI, it is still unclear whether depression is the crucial factor, or if sleep disturbance, secondary to or independent of depression, is of primary importance” (Carney et al., 1990, p. 607). We are still unable to answer this key question, as there have been no studies measuring both variables independently.
Sleep Duration Combined with Daytime Distress and CHD The link between short sleep and hypertension and short sleep and CHD has been further clarified recently. Vgontzas and colleagues conducted an epidemiological study of 1,741 randomly selected community-dwelling men and women (Vgontzas, Liao, Bixler, Chrousos, & Vela-Bueno, 2009). All subjects had a polysomnographic sleep study. Subjects were clustered into three groups: (1) ³6 h sleep (50% of cohort), (2) 5–6 h (25% of cohort), and (3) <5 h (25% of cohort). “Insomnia” was defined as any subject who had a subjective sleep complaint for the past year, or longer. The highest risk of hypertension was in the insomnia groups who were ALSO short sleepers: (1) <5 h (odds ratio [OR] = 5.1) and (2) 5–6 h (OR = 3.5). They concluded that the risk of hypertension among insomniacs is equal to the risk found among sleep-disordered breathing patients. The same methodology has now also been applied to the 10,264 men (56%) and women (44%) in the Whitehall II cohort (Chandola, Ferrie, Perski, Akbaraly, & Marmot, 2010). Data was available for both sleep duration and complaints of disturbed sleep. Separately, and in combination, these two variables increased heart disease in these patients across a 15-year period. Both variables showed a dose– response relationship with incident coronary heart disease, and this relationship was evident in both males and females. When statistical corrections were computed, removing confounding variables (age, sex, and ethnicity) and mediating variables (hypertension, cholesterol, BMI, diabetes, and smoking) neither factor alone (short sleep or disturbed sleep) was related to CHD. However, the combination of both predicted onset of verified CHD across 15 years. After adjustment for confounding variables, the relative excess risk these patients carried due to interaction (RERI) of disturbed short sleep was 37% higher than for the other groups (p < 0.05). When all of the other standard risk factors (hypertension, diabetes, smoking, BMI, and cholesterol) were also removed, the RERI was still 26% higher for these men and women but was not statistically significant (p = 0.10).
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Sleep Apnea (SA) Among MI Patients Hung enrolled 101 consecutive male survivors of a first MI into a study to assess the relationship between sleep apneic events and MI. All patients had a polysomnographic study (Hung, Whitford, Parsons, & Hillman, 1990). The apnea index (AI) was higher among the MI survivors than age-matched controls. After adjustment for age, BMI, hypertension, smoking, and cholesterol levels, the top quartile of AI among the MI group (AI > 5.3) was an independent predictor of MI. The relative risk (RR) for MI between the highest and lowest quartiles of AI was 23.3 (95% CI 3.9–139.9). The increased incidence of apneic events does not necessarily translate into actual cardiac events in the immediate post-event period. Marin followed 55 OSA patients and 196 non-OSA patients in the ICU after their MI (Marin, Carrizo, & Kogan, 1998). During the first complete day in the ICU, MI survivors were monitored continuously for both ECG and SpO2. While there was no difference in total number of incident MI complications, length of stay, or 30-day mortality, the OSA patients did have more PVCs and couplets during their sleep recordings.
Among Heart Failure (HF) Patients Five studies investigating the prevalence of SA have been reported (Javaheri, 2010). In total, 1,250 consecutive patients with systolic HF were included in the cohort. A full 50% of HF patients had an AHI ³ 15: 30% due to central sleep apnea (CSA) and 20% due to OSA. Javaheri highlighted that it is unusual for HF patients to report feeling sleepy. But when given an objective test of sleepiness, they demonstrate intense sleepiness! The above finding has two critical clinical implications. Firstly, that sleep apnea is under diagnosed in this population. To properly evaluate sleepiness, clinicians should routinely ask HF patients to also do a simple behavioral test of wakefulness such as the Maintenance of Wakefulness Test. Secondly, because continued adherence to positive airway pressure (PAP) treatment is usually dependent on the patient having a clear sense of feeling more alert when using the machine, these patients DO NOT feel any better. Knowing HF patients are more likely to stop treatment, the clinician can take a more proactive approach with education of these patients. Early recognition and treatment of sleep-disordered breathing is important, not only because it reduces mortality, but also because recurring hypoxic episodes causes irreversible decrements of executive functions (Simmons & Clark, 2009). Cell deaths in mammillary bodies (memory functions) and cerebellar structures (movement, coordination, and processing speed) have all been documented. The accumulating evidence documenting a causal relationship between OSA and cardiovascular and cerebrovascular events has led the American Heart Association (AHA) and the American College of Cardiology (ACC) to release a joint position paper summarizing research evidence relating sleep apnea and cardiac health
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(Somers et al., 2008). This document concluded that OSA is an independent risk factor for CHD. In addition, the AHA proposed that the standard clinical criterion for treating SA (AHI ³ 15) be set at AHI ³ 5 in the HF population. Adoption of this criterion would mean that about two-thirds of HF patients would meet criteria for PAP treatment. The paper concluded that strong empirical support linking SA with MI and stroke mandates routine screening for SA. Finally, another recent AHA Scientific Statement (Riegel et al., 2009) has advocated strongly for a self-care approach, as a way of involving patients more fully in their treatment. Self-care was defined as “a naturalistic decision-making process” that patients could be taught to maintain their well-being and respond to symptoms more promptly when they occur. The authors argue that improving sleep in HF patients is likely to improve cognitive functions, and improved cognitive functions are more likely to result in improved self-care. This hypothesis is testable but has yet to be evaluated (Riegel & Weaver, 2009).
Circadian Distribution of Vascular Events Despite the increased risk evident in all four lines of evidence reviewed above, sleep disturbances have not been considered risk factors in clinical work with cardiac patients. The clinical evidence establishing increased risk from sleep is further bolstered by consideration of the timing of cardiac and vascular events. For example, depression and anxiety do not have a recurring diurnal cycle, but circadian rhythms do, by definition. The evidence that cardiac these events are not only more frequent among those with disturbed sleep, but also that these events are not random, but clustered at predictable points in the recurring circadian (sleep-wake) cycle. Cardiac Deaths, Myocardial Infarcts, Angina, and Thrombotic Strokes Muller was the first to describe a clear circadian distribution of myocardial infarcts, with most deaths occurring between 7 and 11 am (Muller et al., 1987). Figure 13.1 bottom row clearly demonstrates clear circadian patterns for myocardial infarction but also for transient myocardial ischemia, and thrombotic stroke. Figure 13.1 also traces out the significant role of circadian factors implicated in the pathophysiology of these heart events (see the first five rows of Fig. 13.1), which are further discussed in the pathophysiology section (which follows). The same circadian pattern of a morning peak in ventricular tachyarrhythmias has been reported (Mallavarapu et al., 1995). The firing patterns of implantable cardioverter-defribrillators of 390 patients who sustained 2,692 episodes of ventricular tachycardia, or ventricular fibrillation were reviewed. The peak incidence occurred between 10 and 11 am, with a nadir between 2 and 3 am. Not only did more events happen in this window, but also “first shocks” were more likely to fail for these morning patients, and greater energy was required for termination of the morning tachyarrhythmias than to those applied at other times.
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Principal oscillator
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Fig. 13.1 Circadian clocks and pathophysiology of cardiovascular disease (Reprinted by permission from Macmillan Publishers Ltd: Hastings MH, Reddy AB & Maywood ES, 2003, p. 658)
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Implications for Management of Cardiac Patients The broader question for all involved in CR is whether the accumulating evidence is strong enough to propose new guidelines for management of cardiac patients? While sleep is often taken as a comorbid feature of anxiety or depression, recent studies have shown that treatment targeting depression or anxiety does not always resolve sleep disturbance. Manber demonstrated that treatment of depression alone in patients with both depressed mood and disturbed sleep is not effective: adding treatment that targets the sleep disturbance is necessary for improved clinical outcomes (Manber et al., 2008). While the AHA position paper (Somers et al., 2008) advocated for routine sleep screening, this was only for SA. Recent studies have shown that chronically misaligned sleep (shift work and insomnia) is not benign for heart health. The just released Canadian Guidelines (3rd ed) (see Table 13.1) concluded that broader screening for all sleep disorders, including a routine brief sleep assessment, is advised for all cardiac patients. It is anticipated that sleep guidelines covering sleep apnea and sleep disturbances will soon appear in other jurisdictions. Two clinical examples will be described later in this report to illustrate how these guidelines can be implimented to facilitate actual patients in their recovery from MI. As well, there will be a full discussion of how to screen for sleep apnea. The case illustration of the comorbidity of insomnia and depression will illustrate how treatment of insomnia (together with maintaining an active exercise program) can significantly reduce depression and help with return to work.
Pathophysiology Living on the earth has meant that all living creatures have had to adjust to the 24-h ebb and flow, of day followed by night. This circadian rhythm of light and dark provides the background context for survival and activity for all living organisms.
Table 13.1 Guidelines for managing sleep problems from the Canadian Guidelines All cardiac rehabilitation patients should undergo screening for potential sleep disorders (requisite) Cardiac rehabilitation patients with a potential sleep disorder should undergo screening for sleep apnea with a validated screening instrument such as STOP-BANG (requisite) All Cardiac Rehab programs should implement a brief comprehensive sleep assessment that discriminates patients who suffer from clinically significant insomnia that could put them at risk for a future major depressive episode (requisite) Cardiac rehabilitation patients screening positive for sleep disorders should be referred to a centre with expertise in the evaluation and treatment of sleep disorders (discretionary) This table is reproduced with permission from the Canadian Guidelines for Cardiac Rehabilitation and Cardiovascular Disease Prevention: Translating Knowledge into Action, 3rd Edition, 2009. © Canadian Association of Cardiac Rehabilitation (p. 177)
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Physiological research in the last two decades has uncovered the mechanism of an internal, cellular “genetic clock” that is embedded in every cell in the body and works to regulate how every physiological system responds to the environment. Having access to this cellular circadian rhythm provides every organ with an internal sense of what time it is “out there” and is hugely adaptive in programming activity and rest. This internalized clock helps to (1) time awakening, (2) maintain energy levels across the day, and (3) shut down organ systems to rest again at night. An excellent review of the basic physiology of this internal circadian system in humans is available in the Sleep Research Society’s Basics of Sleep Guide (Scheer & Shea, 2009). One organ in the body that never gets a total rest is the heart. From before birth, until one’s dying breath, the heart muscle continues to contract and release, beat after beat, to provide oxygen and food for life. The beat of the heart sustains life in every one of our 50 trillion cells. So, how does the heart “rest”? Heart health requires the capacity to respond to changing load levels across activities and situations. Any “mechanism” that can assist in improving the responsiveness of the heart to predictable load cycles will provide a huge competitive advantage to the organism. Every cell has “cellular clock genes” (see rows 3 and 4 in Fig. 13.1) that allow the organism to anticipate changes in load demand before they occur (Scheer & Shea, 2009; Young, 2009). That allows each organ system the opportunity to synchronize its biological activity with the background of 24-h activity cycles of the whole organism. The cellular clock genes have the potential of helping to sustain a healthier heart: but only when organ systems are synchronized with each other and with the environment. In the last section, evidence was provided indicating that short inadequate sleep is related to increased CHD and mortality. Advances in basic sleep science provide an understanding of how the cell’s genetic clock lays the foundation for other biological systems, such as the cardiovascular system. When the rhythm of these processes becomes desynchronized due to persisting misalignments between activity-rest cycles of organ systems, heart health suffers and increases the risk for CHD and death.
Cellular Clock Genes and the SCN In humans, every cell in the body has its own internal clock to track time, organ systems have peripheral (or regional) clocks, and the entire circadian system has a central co-coordinator; the circadian system is a multilevel system that is organized hierarchically. The superchiasmatic nucleus (SCN), also called “the master clock,” coordinates the activity-rest cycles of all organ systems in the body (Ko & Takahashi, 2006). This process begins with the SCN sending output signals via the autonomic nervous system and the endocrine pathways through the pineal gland, to regulate all the body’s organ systems. The SCN, in turn, receives input from light sensors to maintain the organism’s synchronization with the outer world (see top row Fig. 13.1).
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Circadian Rhythms in the Cardiovascular System The cardiovascular system also has profound circadian rhythms that impact heart health (see row two in Fig. 13.1). While recurring rhythms in lab animals have been observed for many years, regular rhythms of clock genes within the human heart have just been documented (Leibetseder et al., 2009). These authors reported that the circadian amplitudes of the mRNA clock genes in heart tissue were more distinct than those found in any other human tissue so far investigated. However, comparison of rhythms between clinical groups (normal, CAD, and cardiomyopathy) has not shown any differences in the amplitudes of these rhythms between groups. The cycles of the clock genes in turn activate other basic cardiovascular physiological functions, as a cascade of protein syntheses and other psychophysiological reactions (see row five in Fig. 13.1). Among these are heartbeat frequency, arterial blood pressure, renal plasma flow, urine production, and intestinal peristaltic motility (Schibler, 2006); ultimately, these cascades summate to shape global behaviors like feeding and sleep–wake patterns. These clock genes regulate many signaling cascades, but this section will limit itself to cardiovascular functions.
The SCN Drives Heart Functions The anatomical and functional picture of how heart functions are controlled has evolved significantly across the past 10 years and now clearly implicates circadian rhythms as control mechanisms for cardiovascular output (Scheer, Kalsbeek, & Buijs, 2003). The mechanisms for how the SCN exerts this control were recently discovered. In a series of experiments with rats, in which the SCN was lesioned, Scheer found that the SCN affected heart function through a multisynaptic pathway from the SCN. Using a staining technique, Scheer demonstrated that the SCN sends a signal directly to the heart, by way of the paraventricular nucleus (PVN) in the hypothalamus (Scheer, Ter Horst, van Der Vliet, & Buijs, 2001) (row 1 control over row 2, Fig. 13.1). Using this neuronal pathway, the SCN both inhibits heart activity through the parasympathetic system at night as well as stimulates it through activation of the sympathetic system during the day. In fact, similar multisynaptic pathways have been found to originate in the SCN and to innervate other organ systems, suggesting that the SCN orchestrates a range of organ systems via autonomic routes. The SCN influences the body regionally via this system of multisynaptic autonomic pathways. The resulting system of pathways (not all fully understood yet) provides the backbone of a common rhythmic source for many regional end-organ systems to synchronize with. Each day the SCN drives sympathetic activity, which results in the daily peak in release of cortisol through the night, which begins to increase body temperature, and finally awakens the individual from sleep. Sympathetic activity supports sustained activity throughout the day, and the sun setting triggers melatonin release which slows metabolism, activates the parasympathetic system,
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and slows activity to allow sleep onset and the deep sleep stages that support anabolic renewal of the heart. One of the component outputs of this cascade is basal heart rate (BHR). BHR has an endogenous circadian rhythm of about 6.5 bpm, meaning that at night, BHR is lower by 6.5 beats from daytime levels. At night, the nocturnal rest phase is driven by the SCN entirely through modulation of parasympathetic cardiac outflow; it is not influenced by sympathetic outflow, prior locomotor activity levels, or sleep– wake patterns. The SCN has other ways of impacting BHR, for example, to prepare the heart for the day. When humans are exposed to light at night, this light increases both BHR and cortisol levels. But it only works when light is introduced in the middle of the night, or early in the morning (end of night) – not if it is introduced later, during the day. The early morning increase in BHR by light exposure was found to be mediated by sympathetic cardiac outflow. To summarize, the SCN has direct connections with the heart and uses both the parasympathetic and the sympathetic nervous systems to regulate heart activity (see rows 1 and 2 in Fig. 3.1). When the rat SCN is lesioned, the BHR is flat throughout the 24-h period and stays at a level midway between the usual maximal and minimum levels. Why? Because the SCN is off-line, BHR rate is determined by deep brain signals. There is no parasympathetic outflow at night to slow BHR, and there is no sympathetic outflow during the day to increase BHR. So, it remains stuck in the middle of the range.
Disentangling Circadian Rhythms from Sleep–Wake Activity Patterns While it has long been recognized that the incidence of adverse cardiac events peaks at around 10 am (see row six in Fig. 13.1), it has not been clear whether this is due to the behavioral shift (from sleep to waking) or due to underlying physiological circadian rhythms (heart rate, blood platelet aggregability, etc.). Steven Shea and his colleagues at Harvard Medical School have been involved in an ongoing series of studies to disentangle these issues. In the “everyday life context,” our behavioral sleep–wake cycle overlaps completely with the underlying physiological circadian cycle being generated by our SCN. However, the underlying SCN and other entrained physiological cycles cannot shift (or be “entrained”) by more than an hour a day. So, when normal subjects are put on a “28-hour day” schedule (each activity “day” extended to 17 h 40 min, and each sleep period to 10 h 20 min), the sleep–wake pattern shifts into a 28-h cycle, while the underlying physiological cycles in the SCN and the physiology it coordinates (body temperature, hormone expression, etc.) remain locked in a 24-h cycle. As a result, the physiological cycles are disengaged from the behavioral cycles. This “forced desynchrony” protocol is used to record continuous physiological data, for as long as needed. Data is then analyzed by aggregating it into “bins”: either 28-h cycles (sleep–wake behavior rhythms) or 24-h cycles (circadian rhythms). If the variables studied demonstrate more concordance with the behavioral cycle, these functions are described as governed by behavioral, sleep–wake rhythms; but,
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if they continue to cycle with a 24-h period, they are described as exhibiting true circadian rhythmicity (driven by the circadian system, not patterns of behavior like awakening or feeding, etc).
Blood Pressure (BP) Scheer demonstrated an independent endogenous circadian rhythm to BP with the peak occurring at about 9 pm, just before melatonin is released (Scheer et al., 2010). Melatonin slows down the entire metabolic system to prepare it for the rest period. Scheer had subjects do a standardized exercise protocol throughout the forced desynchrony period. Heart and autonomic systems responded differentially, depending on the circadian phase of adrenal, sympathetic and vagal cardiac activity, and systolic blood pressure. These results are of great interest to cardiac rehab professionals, as they include standardized administration of an exercise task at different times throughout the circadian cycle.
Vasculature From the early discovery that there was circadian variation of both the vagally mediated baroreflex and the sympathetically mediated reflex to orthostasis (Hossmann, Fitzgerald, & Dollery, 1980), researchers and clinicians have come to understand there is an intricate interplay between circadian rhythms, the vasculature, and the stress system (see rows one and two in Fig. 13.1). There are profound circadian rhythms present in vasoactive responses (including eNOS activity), endothelial functioning, angiogenesis, and thrombotic risk (see recent reviews for a full discussion [Paschos & FitzGerald, 2010; Rudic, 2009]).
Heart Rate Variability (HRV) HRV is taken as a measure of heart health. Among HF patients, HRV is a predictor of sudden cardiac death (La Rovere et al., 2003). In a study reported in 2004, Hu, Ivanov, and their colleagues demonstrated that heartbeat dynamics exhibited a significant circadian variation (Hu et al., 2004). Specifically, heart rate plateaued in the evening, with a maximum before 9 pm and a minimum at 5 am. HRV showed a significant circadian rhythm with increasing variability across the night of sleep. Hu noted that the DFAa (a coefficient that is statistically derived from HRV dynamics) is more predictive of cardiac events than HRV itself (Hu et al., 2004). DFAa exhibits its best (lowest) values in the middle of the sleep period (a = 0.8 at 2 am) when parasympathetic outflow is greatest and its worst values by early morning (a = 1.2 at 10 am) when sympathetic outflow peaks. The authors concluded that endogenous circadian-mediated influences on cardiac control (and not behavioral sleep stage shifts alone) likely play the key role in the early morning pattern of cardiac deaths observed (see row six Fig. 13.1).
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Adrenal Hormones The same group recently clarified how complex these processes are – and how they might combine to account for cardiovascular risk (Scheer et al., 2010). They demonstrated that BP is impacted by the morning surge in autonomic stimulation of the adrenal gland, evident in surges of plasma epinephrine and norepinephrine. While this factor alone could not account the distribution of heart attacks reported by Muller (row 6, Fig. 13.1), the combination of rapid increase in epinephrine released at daybreak, with vagal withdrawal in parasympathetic outflow in the morning, together, did yield a simple conceptual model of two key cardiac circadian factors (row 5, Fig. 13.1) that predicted the observed peaks and troughs in MIs across the 24-hour day (row 6). Their proposal of a ‘sympathovagal reactivity’ hypothesis to highlight the importance of the interaction between sympathetic and parasympathetic outflows provides specific and testable circadian targets for behavioral treatment interventions in human studies. These insights guided the behavioral treatment interventions proposed by the current author, and will be presented in the last part of this chapter.
Circadian Rhythms Drive Diurnal Activity in Stress Systems The Autonomic System and the HPA Axis All the components of the stress system are wired into and controlled by the circadian system. The daily function of the stress system is to activate the organism for behavior throughout the day. Psychologists typically focus on the ancillary function, which is as the “emergency” function, or backup system for self-protective action. The emergency function provides an added surge of response in dramatic threat situations. While psychologists are used to thinking of stress as synonymous with the “emergency” function, this is clearly not consistent with the emerging picture of its more important diurnal role. In normal daily routines, epinephrine, cortisol, glucose, insulin, and melatonin levels exhibit circadian rhythms to provide the body with sustained energy throughout the day. All of these individual cycling hormones contribute to orderly recurrent cycles that promote activity-rest; or become desynchronized and undermine health. The stress system is engaged daily to activate and to deactivate the organism. Meerlo and colleagues (Meerlo, Sgoifo, & Suchecki, 2008) have pointed out that sleep deprivation is stressful, in part because it disrupts the regular predictable patterns of stress hormones. Among the more important findings from animal studies is that the longer that sleep is disrupted, the more significant the alteration in HPA axis functions; across time, sleep restriction gradually decreases the sensitivity of stress regulation by CRH and serotonin receptors. Martino and colleagues have demonstrated that sustained disruption of the normal 24-h sleep–wake rhythm caused altered gene cycling in the SCN in mice, with concomitant downregulation of key cardiac functions (genes in the hypertrophic
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pathways) (Martino et al., 2007). Phenotypic rescue from this pathological state was defined as reversal or attenuation of abnormal pathological gene states and was only observed to occur when the normal external day–night rhythm was restored. The authors concluded that these results demonstrated the importance of diurnal rhythms as vital determinants in heart disease, with disrupted rhythms contributing to the progression of organ dysfunction. Most importantly, Martino was able to show that resynchronization of sleep–wake rhythms restored the pathological heart physiology to normal; that is, that restoration of normal sleep effectively treated heart disease (Martino et al., 2007). Resynchronization of sleep–wake rhythms for human heart patients has not been tested. This possibility could easily be tested through a systematic behavioral intervention program that would simultaneously target effective resynchronization of circadian physiology, as well as diurnal behaviors (including sleep–wake patterns and energy expenditure). The elements of such an approach are discussed this later in chapter. While more human studies are needed, it is clear that chronic sleep deprivation alone causes changes in the brain which likely affect neuroendocrine reactivity and stress sensitivity. This impacts the individual’s competence in handling the “emergency” stressors that challenge him or her and begins a vicious cycle of worse sleep, more stress, daytime fatigue, still worse sleep, etc. The result is desynchronized hormonal and sleep–wake systems and the elimination of the buffer system that manages “emergency” stressors. Finally, evidence from animal models has demonstrated that restoration of normal sleep-wake cycling restored heart dysfunction as well.
Summary of Relationships Between Sleep and Traditional Risk Factors Human research has demonstrated that disturbed sleep impacts likelihood of cardiovascular events. The cause of these events is more evident from experimental animal studies, which has highlighted the impact of circadian rhythm disruptions, which significantly impact traditional risk factors such as dyslipidemia (Young, 2009), hypertension (Hermida, 2007), as well as obesity (Green, Takahashi, & Bass, 2008) and diabetes (Scheer, Hilton, Mantzoros, & Shea, 2009; Shea, Hilton, Orlova, Ayers, & Mantzoros, 2005). Sole and Martino argued the full extent of the role of circadian misalignment for clinical outcomes of cardiac patients is only just beginning to be understood, and now needs to be assessed with human studies that target investigated of the role of circadian factors in heart disease (Sole & Martino, 2009).
Behavioral Sleep Medicine The field of behavioral sleep medicine has evolved from two fields of research: health psychology (behavioral medicine) and sleep disorders medicine (Stepanski & Perlis, 2000). Each has developed a knowledge base to allow the assessment of clinical problems, as well as intervention techniques and strategies to address those disturbances.
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Behavioral sleep medicine aims to assist clinicians in understanding the psychological (cognitive and behavioral) factors that contribute to the development and/or maintenance of sleep disorders and to develop behavioral interventions targeted to effective management of sleep disorders among specific patient populations. In the final sections of this chapter, we will outline how application of these clinical skills can improve sleep disturbances among cardiac patients.
General Clinical Skills to Manage Sleep Disturbances Among Cardiac Patients The balance of this chapter will focus on managing the two most common sleep problems undermining the progress of CR patients: assessment and management of SA and chronic insomnia.
Diagnosis of Sleep Problems Clinical skill in treatment generally rests on clinical skill in diagnosis. Without a proper diagnosis, treatment response is haphazard. There are a broad range of diagnostic possibilities for serious sleep disturbances (including primary sleep disorders like sleep apnea, primary insomnia, narcolepsy, and periodic limb movements), as well as a range of medical conditions, like thyroid problems, and psychiatric conditions like depression. Every clinician working with cardiac sleep problems is urged to familiarize themselves with the American Academy of Sleep Medicine’s, 2005 International Classification of Sleep Disorders, 2nd ed (ICSD-2). The user-friendly Case Book of Sleep Medicine (2008) highlights 70 cases in six different clusters of sleep disturbances, including insomnia, sleep-related breathing disorders, circadian rhythm disorders, hypersomnias and others, and is an excellent reference to develop experience with sleep problems. While insomnia is best diagnosed from a thorough clinical interview and history of the patient’s sleep problems, other primary sleep disorders can only be evaluated in a sleep laboratory. There are many excellent overviews of conducting a thorough investigation of sleep disturbance (C. Morin, 1993; Reitav & Dickstein, 2001; Wilson, 2008). Assessment will include a well-structured clinical interview as well as the completion of 1–2 weeks of sleep logs and completion of selected paper-andpencil tests to evaluate possible precipitating and perpetuating factors. Among the primary sleep disorders most frequently found among cardiac patients are OSA, periodic limb movements, and restless legs syndrome (see Walters & Rye, 2009). Each of the above is characterized by distinctive biomarkers that are readily evident in the sleep laboratory measurements, but would otherwise be “invisible” to the patient. However, detection of the likelihood of the possible existence of such underlying problems is the clinician’s chief task.
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The clinician managing the cardiac patient needs to become increasingly familiar with all of the sleep diagnoses, but initially, the two most important skills are asking direct questions to detect the presence of insomnia and/or SA. While SA can only be diagnosed in the sleep lab, not every patient complaining of a sleep disturbance should be sent to the lab. The clinician has a vital role to prescreen for the features of SA and to cultivate their “index of clinical suspicion” about the presence of SA. Collop (Collop et al., 2007) suggested that the clinician’s first task is to answer the following question: Does this patient have a high pretest probability of moderate to severe SA?
Sleep Apnea (SA) Apnea means the patient stops breathing for at least 10 s, accompanied by an oxygen desaturization of 3–4%. The number of such respiratory events (hypopneas, apneas, and respiratory arousals) are added up and averaged for each hour of sleep. Mild apnea is defined as ³5 such events each hour, moderate SA is ³15, and severe is ³30. The SA can be caused by the brain “forgetting” to make an effort to breathe (called central sleep apnea, or CSA), by a blockage in the back of the throat where the air passageway is soft and easily collapses (called obstructive sleep apnea, or OSA), or by a combination of both, called complex (or mixed) apnea (CA). The frequencies of the three types are about 84% OSA, 1% CSA, and 15% CA (Morgenthaler, Kagramanov, Hanak, & Decker, 2006). The balance of this chapter will focus on management of OSA, as it is the most common presenting apnea.
The First Task for Suspected SA: Improving the Index of Suspicion The sleep disorder that is most lethal to cardiac patients is SA (Marin, Carrizo, Vicente, & Agusti, 2005). There are five paper-and-pencil tests to screen for apnea: the Berlin questionnaire, the American Society of Anesthesiologists Checklist, the Wisconsin sleep questionnaire, the Sleep Apnea Clinical Score (SACS, or Clemens Criteria), and the STOP and STOP-BANG screening measures (Chung et al., 2008a, b). Validation data has been presented in a population of general surgical patients (Chung et al., 2008a), but none of these instruments have been validated within a population of cardiac patients. All of the instruments enquire into three clinical domains, and if two are positive, then the patient is at high risk and should be sent for a sleep evaluation. The three domains are (1) snoring, (2) daytime sleepiness, and (3) hypertension. Rather than rely on paper-and-pencil questionnaires, the present author suggests a brief clinical inquiry into each domain. Loud Snoring Many patients are not aware of their own snoring. Sometimes they will recall waking up gasping for air, but this is inconsistent. Asking the patient if they sleep on their
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back or side, or whether they wake up with a dry mouth (from mouth breathing) or a headache (from nocturnal anoxia) are effective follow-up questions in this domain. Daytime Sleepiness Most patients are well aware of this, but heart failure patients are very poor at reporting daytime sleepiness. Encouraging them to do a behavioral test of their actual sleepiness can be very helpful. Behavioral equivalents might include inquiry into car accidents, or falling asleep watching TV at night. It is also important to ask about strategies used to overcome sleepiness, such as consuming numerous coffees, other sources of caffeine, cigarettes, or sugared snacks. Hypertension Many SA patients have elevated BP and even treatment-resistant HBP. However, there are other medical conditions that could be suggestive of an underlying chronic SA condition including chronic pain (from persistent inflammation), gout, or sleeping in bed in a propped up position. Finally, Bradley has recently documented that a sedentary lifestyle can be just as indicative of risk as obesity: asking about activity levels and ankle swelling in the evening can be clinically suggestive of sleep apnea (Redolfi et al., 2011). Once identified, high likelihood patients should be referred for a sleep lab study at an accredited sleep lab facility, where the testing is conducted by a board-certified sleep medicine specialist. Recently, portable monitoring (PM) systems have become available and represent a credible alternative for the diagnosis of SA for many patients in otherwise underserviced area (Berry, Hill, Thompson, & McLaurin, 2008). While there continues to be great debate about the value of home assessment techniques, the development of new technologies promises to permit many more alternatives for confirmation of clinical hunches. Clinically, however, getting the diagnosis is not as important or as challenging as is the task of helping the patient adapt to and use the treatment every night.
Adoption Challenges Once a sleep test has confirmed SA, the process of adaptation to the positive airway pressure (PAP) device begins. It proceeds through selection of masks and machine, titration of CPAP levels, and is completed when the patient has accommodated to their CPAP machine. For most patients, this process takes up to 90 days. While PAP machines are not the only treatment alternative, they are the most effective for the majority of SA patients, and the first line of treatment to be used. Failure to comply with treatment means the patient does not want to use the equipment at all. Failure to adhere to treatment is defined as the patient not being able to use the equipment for the minimum duration that would allow correction of the airway problem. Successful adherence is typically defined as using the CPAP
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machine for five nights (70% of the week), for 4 h or more a night. This is also termed “the Medicare criteria,” as Medicare only pays for PAP equipment if its use meets this criterion. Using this criterion, one study found that 20% of patients diagnosed with OSA refused CPAP at the outset (no compliance), while another 16% had dropped out by 2 weeks (no adherence), and at 30 months, only 50% of patients were using their CPAP for 3.6 h a night. These dismal results for use of a life-saving therapy have led to many studies on how to improve these marginal adherence rates. Lewis followed 80 consecutive patients diagnosed with OSA (Lewis, Seale, Bartle, Watkins, & Ebden, 2004). They tracked anxiety, depression, problems encountered at the very start of treatment (at the CPAP titration session, at which the optimal pressure level is determined for the patient), and whether they lived alone. The anxiety and depression scores did not predict adherence problems, but the occurrence of problems at the outset of treatment, living alone, and having had a recent life event did. Interestingly, those living alone were less likely to adopt the treatment, as were those who had had a recent life event. The authors noted that patients having life events were likely still coping with those stressors and exhibited more difficulty with PAP adoption. However, the most powerful predictor of poor adherence was asking one simple question right at the outset: Did you encounter any problems on your first night of using the CPAP? Richards wondered whether providing newly diagnosed OSA patients with a structured informational session at the start of treatment would help with adherence (Richards, Bartlett, Wong, Malouff, & Grunstein, 2007). The authors enrolled 100 consecutive patients diagnosed with OSA into a trial of an educational session (ES) compared with treatment as usual (TAU). At 28 days into the treatment, the ES group was using the CPAP for 5.4 h, while the TAU group was using the machine for half that time, or 2.5 h less each night. In total, 88% of the ES group met the 4-h treatment target, compared to only 39% of the TAU group. Stepnowsky followed 528 CPAP users for 5 months: 63% could not meet the 4-h criteria for nightly usage! 21% used CPAP from 4 to 6 h, and only 16% for 6 h or longer (Stepnowsky & Dimsdale, 2002). So, how much is enough? Most in the field would agree the answer is “All night, every night”. Of all the sleep disorders, SA is the simplest diagnosis to confirm, but for many patients, it is the hardest treatment to adhere to. Some patients have trouble finding a mask they are comfortable wearing. Others are mouth breathers at night and cannot get the mask to work for them without very unpleasant “blow-bys” of air. Still others awaken in the night with panic attacks triggered by the terrifying feeling that they are suffocating. These problems can usually be very effectively addressed through two to six treatment sessions to assist patients with the adoption process of accommodating to PAP treatment. There will still be patients who just cannot adapt to the CPAP. In these cases, there are other alternatives that could be very helpful, including dental appliances and oral surgeries. Refer the patient back to the board-certified assessor who tested the patient for a discussion of these alternative treatment choices. The balance of this
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chapter will provide an outline of the eight key issues in helping patients adapt to treatment for SA. Steps in the Intervention Process Education and Resistance to Change Regular use of a PAP is a major lifestyle change for most patients. As with all major lifestyle changes, the first phase of intervention is evaluation of the patient’s motivation to actually use the mask. Many find the equipment bulky and awkward. Some equate it with their heart problems, yet another sign of deteriorating health, or think it unattractive to their mates. Their initial reaction is that they would rather die than use the machine. The clinician’s challenge is to help the patient understand that that is exactly the choice they face. This author emphasizes the increased risks of further heart attack, stroke, and early death (see clinical example below). The patient can be given homework in the first meeting to do a Google search for sleep apnea and come back with a page of information on risks and benefits. The result of this effort is always instructive about the patient’s readiness to participate in a serious dialogue about the need for the PAP. Another excellent resource for work with SA patients is the treatment manual for clinical management of poor adherence to CPAP: motivational enhancement (Aloia, Arnedt, Riggs, Hecht, & Borrelli, 2004). The manual provides a clear outline of interventions given across two 45-min sessions to motivate patients to understand the importance of overcoming barriers to use of PAP. Mobilizing Supports Asking the patient to talk to spouse, family, and friends about the PAP helps to bring potential problems to the surface quickly by identifying unsupportive, uninformed, or critical support persons. Addressing these potential barriers to adoption is critical to long term success. On the other hand, this exercise also helps to identify sources of support and encouragement. Identifying Disease Burden Patients should track their sleep with a sleep log for a baseline period. In particular, it is important to assess energy level across each day, number of naps, sleepiness during meetings, etc. A patient who is asked to observe when they get tired, whether they have to pass on certain activities, etc., is becoming more aware of the actual burden of SA on their daily activities. This is most helpful in preparing the ambivalent patient for action. In the first weeks of treatment, many patients may not be able to keep the mask on for more than an hour or two on most nights. Be encouraging and focus on achievements, but also remind patients that SA kills and makes them sick. Their best efforts are critical for both their physical health as well as their emotional wellbeing.
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When they start to have one or two nights a week of successful adherence (4–6 h use), ask the patient to pay attention to their energy levels that day. While not all of the associated symptoms of SA change quickly, at least one or two will, and it is critical to hone in on the positive signs as they appear. Other symptoms will change later, and some not at all. Often, one early sign of change is that patients do not have to wake up to go to the washroom at night. Once the patient begins to experience at least one real difference in their previous difficulties, the process becomes easier. Identifying Mechanical Challenges Progress can be compromised by other clinical problems. Comfort with the mask, mouth breathing, and anxiety reactions all become serious challenges to adoption if not dealt with quickly. The clinician should take the initiative to ask about problems with use of the machine, comfort with the masks, and problems with mouth breathing. With regard to mask fit, the patient needs to know that there is an optimal degree of tightening of the “head gear” straps; more is not better as overtightening will impair the seal and will cause the mask to leak. Similarly, use of the nasal pillows can cause rhinitis (runny nose). Without proper guidance, all this can become very discouraging to the patient. At this stage, the best referral is to a large volume supplier who often has more options and experience with fitting masks for difficult patient situations. The patient should be encouraged to be actively involved in making these decisions. Panic Attacks and Fear of Suffocation It is common for some patients to wake up in the middle of the night and feel they are suffocating. Upon awakening, the patient may think “This PAP machine is choking me.” This experience can happen because of claustrophobic feelings but can also be triggered by actual objective mask problems causing a feeling of suffocation. Specifically, with a nasal mask, opening the mouth will lead to oral air escape which can give a sense of suffocation. In patients with normal nasal function, this will lead to the patient closing their mouth thus correcting the abnormal air escape. However, in patients with nasal problems or habitual mouth breathing, this may not happen. Such mouth breathers often benefit from changing to a full face mask. Alternatively, because of the larger size of these full face masks (which are more obtrusive and have greater facial coverage), some patients will feel more claustrophobic with a full face mask. In such patients, a trial of nasal irrigation with a mild saline solution prior to bed (like Netipot), or use of a nasal aspirator (like HydraSense), corrects this problem for many patients. When it does not, corrective nasal or sinus surgery can be helpful. Patients have to understand that such surgery does NOT correct their OSA; it will just enable them to use a less obtrusive nasal mask. Additionally, because of various anatomical factors, some patients will need quite high CPAP pressures causing tolerance problems. In such cases, certain pharyngeal operations, such as a UPPP, may not be curative but allow the use of a lower PAP pressure. Similarly, many patients require higher PAP pressures sleeping supine.
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Thus, if the pressures needed are too high, another strategy is to combine an appropriate lower pressure (as determined by the CPAP titration) together with position management to keep the patient off their back. Although psychological factors causing claustrophobia, or a sense of suffocation, are certainly real, one must also be aware of a range of actual CPAP usage and fitting issues which mimic them. Where claustrophobia is the key issue, a brief explanation of what happens during an apneic event can serve to normalize the patient’s feeling and help them to begin to be more accepting of the machine. Accurately discriminating the real cause for the panic reaction is important because these feelings can be very intense and absolutely real to the patient. Ignoring these feelings or focusing on anything else will usually not be credible to the patient. In fact, it is helpful to keep reiterating to the patient throughout the treatment that the CPAP is a life-saving treatment. Repeating the message with slight changes in the emphasis will gradually help the patient understand in a deeper way how critical the CPAP is to their mental and physical health and well-being. Of course, this is done with clinical tact and timing, and humor wherever possible. Finally, in addition to the comorbid presence of anxiety disorders, there can also be the comorbid presence of insomnia together with sleep apnea. In a recent review of studies that evaluated the presence of insomnia symptoms within their cohort of OSA patients, Luyster found that prevalence of insomnia ranged from 39% to 55% depending on criteria used for defining insomnia (Luyster, Buysse, & Strollo, 2010). The authors highlight that the existence of an unidentified comorbid insomnia will likely complicate acceptance of the CPAP treatment and that attention to the potential impact of the insomnia on acceptance of the CPAP therapy is important for long-term management of these patients. For such patients, interventions from the next section of this chapter can be added. Relaxation Training Understanding the dynamics of the panic attacks is not enough to stop the panicky reactions. These are automatic and visceral and can keep occurring for months. To help the patient overcome these anxiety reactions, deep breathing and progressive muscle relaxation can be very useful. As well, an individually tailored “exercise prescription” of walking 5 days a week is helpful in managing anxiety. Most patients take 4–6 weeks to get a reliable sense that they can modulate their own anxiety. When that happens, they will start having confidence in their ability to manage their anxiety and usually begin to report the first nights of using the machine for 6 h or more. The alternative to training the patient to relax is to get a machine with a “ramp up” feature (that gradually increases the air pressure across a 30-min window) or to have the patient take a sleeping pill for a 2-week adjustment period. The sleeping pill will help many patients sleep through the panicky feelings initially. After 2 weeks, the underlying anxiety reaction about suffocation is usually deconditioned if the patient has been using the machine across the entire night. If they have not, it can continue to be a problem, and a longer period with the hypnotic may be needed.
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Cognitive Deficits Another complication that can arise is complaints of cognitive impairment by the patient. This can be secondary to the long-term effects of untreated OSA. Or it can be the onset of dementia that could be related to family risk, smoking, or other risk factors that is only being exacerbated by the OSA. In any case, it is often important to evaluate cognitive competence. The Montreal Cognitive Assessment (MoCA) (Nasreddine et al., 2005) is more sensitive than the mini-mental status test to detect early slippage. It is easy to administer and is made available for clinical, educational, and research purposes without fees. Patients who are in decline should be counseled to be active, get as much bright light as possible during the day, and continue to use the CPAP and other sleep hygiene strategies to optimize their sleep pattern. Recent research has also emphasized the importance of maintaining predictable daily patterns of activity to improve functionality. Tracking “Good Days” Once all forgoing clinical tasks have been completed, review of energy levels on “good sleep” days becomes much more meaningful. The patients are more interested in their results and start to experience more regular success. However, setbacks are typical.
Clinical Example: Sleep Apnea Bob, a 51-year-old married man, had recurrent angina due to a mild MI. He was treated with a stent and sent for CR. Bob was married, had three young children, and was working as an architect. Work was hectic, and work stress was increasing steadily in the past year due to chronic understaffing. Five months after his MI, Bob presented for consultation to the Psychology Service by saying “I am having a hard time accepting this.” He was particularly anxious about his future, having had an MI at a young age. History: Bob had always been healthy and active. Bob said he had experienced “about twenty deaths before age 21”. Most important among these was the death of his mother from cancer when he was 10. Just prior to his MI, his stepmother had died. He did not have diabetes, was not obese, never smoked, only drank socially, and had only seen doctors for annual checkups. His family doctor was concerned about Bob’s snoring and tiredness and had referred him for a sleep test 6 years ago. Bob had gone for four sleep tests from 2004 to 2009. All tests demonstrated severe OSA, but Bob was confused and declined all treatments. The first doctor assessing his apnea had advised him to undergo surgery to remove his soft palate, but this was not acceptable to Bob. A second sleep test indicated he had both OSA and periodic limb movement, but Bob was not clear what treatment he required, if any. The third doctor told him he must use a CPAP machine.
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He went for a machine and was told he was a mouth breather. He chose a full face mask, but still had problems with blow by that he described as “gale force winds.” More difficult was repeatedly awakening with the feeling that he was suffocating. In a panic, he would instinctively take the CPAP off. He said it felt like “someone was putting a pillow over my mouth.” Between his uncertainty about needing the CPAP, mechanical difficulties in using it, and the challenges of managing other ongoing life stresses (hectic family life, death of his stepmother, and work stress), Bob stopped using the CPAP altogether. He thought he may have used his CPAP for 6 months in total across the past 6 years, and not at all before or since his MI in the past year. His sleep pattern indicated poor sleep. Most nights he woke up two to four times. He went to the washroom at least once a night. He usually fell asleep again easily, but on occasion, he was up for hours. He rated his sleep quality as below average most nights. Bob had heart palpitations after his MI and became more anxious about his health. He went to the ER once during the treatment due to worries about his heart and began to focus on his heart’s activity. Formulation: Bob was worried about his heart and moderately anxious but did not meet DSM criteria for any nonsleep diagnosis. He had been diagnosed with OSA for 6 years, but remained untreated due to three main barriers to adopting PAP: (1) no understanding of the mortality risks of not using PAP, (2) significant panic at sleep onset using PAP, and (3) he was a mouth breather. Treatment targeted these three barriers to adoption. Mortality risk was corrected by reviewing Marin’s longitudinal data demonstrating a 33% risk of having either a heart attack or stroke in the next 12 years, with half those patients dying (17% risk of death). This made quite an impact on him. He later said it was the single biggest reason he made the necessary effort to use his CPAP. The second barrier was his panic reaction in the middle of the night. This required a combination of education and relaxation training. He was educated about how the body has activated the stress reaction all night to help him wake up to start breathing again for years. This longstanding pattern put him at the threshold of nightly panic attacks. In addition, the patient was given diaphragmatic breathing exercises to do, which helped him to calm down and reduce sympathetic arousal. The third barrier was the mechanical problems. The patient was advised to contact his supplier again and visit to try out other mask options. He was also advised to call his sleep clinic to schedule a reassessment of his pressure settings. Bob was followed for 3 months to monitor his progress. Within a week, he had started putting the mask on every night. However, it was usually removed within an hour. Bob had little conscious recollection of how this happened initially. With time, he realized he lacked the patience to don the equipment again in the middle of the night. Gradually, Bob had more success: most nights he was able to use the machine for 3 h. He noticed he no longer had to wake up to urinate, but still had no improvement in his daytime energy. He continued with his breathing exercises on a haphazard basis. However, when his breaths per minute were counted, he took only 10 breaths a minute. Most normal breathers take about 10–12 breaths a minute, while patients who take shallow breaths
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and are at risk for hyperventilating and triggering a panic attack take 16–24 breaths per minute. The panicky feeling persisted for about 6 weeks, but gradually subsided. After 2 weeks, he used the CPAP five nights a week. Stuffiness remained a recurrent problem, but on other nights, he was able to keep it on for 2–4 h. After 2 months, he was using the CPAP most nights and typically for 4–6 h. Bob met the Medicare criterion (of using PAP for at least 4 h a night 70% of the week) by week 10. After 3 months of treatment, he was using the CPAP 6 h a night most nights. He was motivated to continue treatment, but did have some setbacks. When he had a head cold, he did not use the machine at all for a week. On recovery, he was eager to start using the PAP machine again. By this time, it was easy to point out to Bob that the nights he used the machine for longer, he typically rated his sleep and his energy level in the morning as better. This helped him understand that this was a long-term process. His usual sleep pattern was sleeping from 11 pm to 6:45 am with only one awakening, usually for a minute or two, and in the morning, he awoke feeling refreshed.
Behavioral Treatment of Insomnia Many of the techniques used in behavioral sleep medicine are well known to health psychologists, for example, use of progressive muscle relaxation, setting agendas for treatment sessions, etc. Others are more unique to the field of sleep disorders, like using sleep hygiene instructions, stimulus control for sleep, and sleep restriction (Hauri, 1991; C. Morin, 1993) or sleep compression (Lichstein, Riedel, Wilson, Lester, & Aguillard, 2001). The choice of individual techniques and strategies will depend on a careful assessment of the patient’s sleep problems. The framework used by most behavioral sleep clinicians to structure the assessment is Spielman’s behavioral model of insomnia (Spielman, Caruso, & Glovinsky, 1987). The clinician applies their understanding of the factors that impact sleep processes negatively and determines the most likely predisposing, precipitating, and perpetuating factors maintaining the sleep disturbance (Reitav & Dickstein, 2001; Wilson, 2008).
Range of Treatment Interventions There are a broad range of clinical interventions that are available for treatment of sleep disorders. Deciding which tools are most effective for which patient is to some degree a clinical skill that develops with experience. In addition, there are challenges that are unique to managing an older population. To be better prepared for handling these issues, the reader is referred to a number of resources to orient them to working with an older population. Based on Morin’s (C. M. Morin, 2004) early work establishing the effectiveness of Cognitive Behavior Therapy for Insomnia (CBTi) with older adults, Lichstein and Morin published a
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monograph on late life insomnia (Lichstein & Morin, 2000). There is also a recent review article (Dzierzewski et al., 2010) that provides both a review of the range of interventions that can be used and a thoughtful evaluation of the clinical issues that come up with treating the older adult.
Resynchronizing Circadian Rhythms for Cardiac Patients A Modified Cognitive Behavioral Treatment Model As early as 2003, the accumulating evidence for circadian oscillators impacting cardiovascular health (and disease outcomes) was mounting. Hastings proposed that targeting sleep disturbances directly presented “new avenues for therapeutic intervention in conditions where disturbance of circadian gene expression is an important cause of morbidity” (Hastings, Reddy, & Maywood, 2003, p. 649). In the past decade, nobody has addressed the question of whether such interventions need to be modified to target the unique challenges of the cardiac patient. The cognitive behavioral therapy model for insomnia (CBTi) has proved itself to be a robust model for treating sleep problems in insomniacs of all ages. The basic principles of the model also work well with high functioning cardiac patients with insomnia, but there is a need for additional modifications for patients with more serious pathology. For example, Luyster et al., (2010) have noted that insomnia and SA frequently cooccur and these more complex clinical challenges require modified, combination therapy. Sleep–Wake Disturbances in Cardiac Patients The two principal matters to consider are as follows: (1) Does treatment of cardiac patients with insomnia differ from patients with uncomplicated insomnia? (2) Do cardiac patients with sleep disturbance differ from patients with other medical conditions? Complicating this question is the fact that “cardiac patients” are a broad spectrum (Dzau et al., 2006a, b), from patients with hypertension, CAD and angina, arrhythmias, and MIs to those with diabetes, heart failure, and kidney disease. For a treatment to be effective with such a broad range of patients, it must be sensitive to the multiple challenges that each patient presents with, as well as easily adaptable, and effective for most patients. For example, HF patients can present with both sleep apnea and insomnia. Assessment of these patients requires simultaneously evaluating fatigue and the source (obstructive, central, or complex) and seriousness (mild, moderate, or severe) of apneas and determining additional causes of sleep disruption. Treatment usually requires the staged introduction of both PAP treatment as well as behavioral interventions to improve sleep. On the basis of the current author’s experiences with treating this population, an adapted version of the standard CBTi model is suggested for cardiac patients with compromised heart functions. Specifically:
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1. More fragile patients who are still in medical recovery and have compromised heart functions (e.g., MIs, heart failure, and transplant patients) need treatment to respect tenuous cardiac functions: this is the safety concern. 2. Treatment may need to target fatigue and daytime sleepiness, by increasing daytime napping and sleep opportunities first, and later focus on night time sleep improvement. 3. Comorbid health challenges often found among cardiac patients (obesity, diabetes, and general medical comorbidities, etc.) may require additional adaptations of the basic CBTi model in some cases. Patients who are likely to require modified procedures are those on the frail end of the cardiovascular spectrum and include heart transplant patients, patients with renal disease, heart failure patients, postsurgical patients with valvular surgery or CABG, and others with compromised heart functions.
Treatment Interventions First Phase: Sleep Recovery The broad spectrum of patients seen in cardiac rehab includes patients recovering from open heart surgery, as well as those with MIs with significant heart damage. This spectrum of more fragile patients is more likely to complain of excessive sleepiness and fatigue, than of disturbed sleep, but these often occur together. As a result, triage and diagnostic evaluation is a more complex process. For example, the disease burden experienced by heart transplant patients increases their drive for sleep. This can be due to the impact of the surgery itself, generalized inflammation, physical deconditioning, age, or the physiological burden of multiple new medications. There are a number of important transitional processes that are part of the recovery process and should be supported in treatment (see Chaps. 5 and 7, this volume). During this phase, the clinician must evaluate sleep, daytime sleepiness, and fatigue. Clinically, the important difference between sleepiness and fatigue is that a daytime nap will relieve sleepiness, but not fatigue. Also important during this stage is supporting the patient in their continuation of their individualized exercise program. Regular physical activity is one of the ingredients that will help build capacity in patients who are struggling (see Chap. 14, this volume). An effective standardized way of assessing the patient’s specific problem is use of a modified form of the maintenance of wakefulness test (Doghramji et al., 1997). A behavioral evaluation of the patient’s sleepiness and fatigue at the beginning of treatment is very helpful in complex cases. It allows a standardized procedure by which to compare patients from different ethnic backgrounds, who may mean very different things when they say they are “sleepy” or “tired.” Based on the results of this test, one can begin to set objectives for the patient in their recovery. It may be helpful to suggest to the patient that their first objective is to get the sleep that their body needs. This assessment will help establish
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whether the patient may need an additional morning rest period, or perhaps two or more may be needed for a given patient. Patients are also involved in deciding on the best times for their rests. However, rests after 3 pm are NOT allowed, except when ill. Second Phase: Resynchronization of Basic Circadian Rhythms The resynchronization phase of the treatment involves education about the impact of circadian rhythms. Patients are taught deep breathing and progressive muscle relaxation skills in order to learn to relax their bodies and activate the parasympathetic system. The basic intervention at this stage is the CBTi protocol described by Perlis (Perlis, Jungquist, Smith, & Donn, 2005). However, strict adherence to using a sleep restriction intervention may not be safe, and there are other effective alternatives. Lichstein has presented an alternative sleep compression model, in which the titration of the sleep restriction window is accomplished gradually across 5 weeks (Lichstein et al., 2001). He found that the intervention was effective with an older adult population, particularly with those with low daytime fatigue ratings. However, patients with high fatigue ratings did better with an approach that taught effective relaxation strategies. With heart patients, the initial emphasis is put on patients taking better care of themselves. Patients are taught diaphragmatic breathing and progressive muscle relaxation to increase their ability to relax and calm themselves. They are advised to practice these skills at least 30 min a day. Anchor times for wake-up are adhered to from the outset, but scheduled naps are allowed. Initially, patients are advised to take three opportunities to rest: at 10 am, noon, and 2 pm. Based on their actual need for sleep during these times, an individualized plan to permit napping during their preferred time(s) is allowed. Across subsequent weeks, the napping window is gradually reduced as nocturnal sleep improves. Other behavioral strategies are incorporated based on the patient’s health and lifestyle. For example, night time snacking is a problem for some patients and will be disruptive to sleep. For these patients, meal distribution across the day is reviewed and recommendations made. Finally, for the few patients who come to the program with a history of relying on sleep medicines, the use of hypnotics is reconsidered as patients develop more confidence and predictability in their sleep–wake cycles.
Clinical Example: Management of Insomnia Alan is a 55-year-old Caucasian IT rep who had nausea and chest pain one morning while working out. At the hospital, he was advised he had a “substantial heart attack” requiring a stent placed into his anterior coronary artery. He led an active lifestyle and was in excellent health. He had no previous cardiac events, was not treated for any risk factors, and had no history of hypertension, smoking, or drinking. His father smoked and had an MI in his 40s.
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Alan had no complications from the stent, but experienced persistent weekly palpitations. A 14-day event monitor logged 27 events that included dizziness; light headedness; tingling in his arms, fingers, and gums; and narrowing vision. One of the 27 was a 15-beat wide ectopy at 150 bpm. Nuclear testing found a severe predominantly fixed perfusion defect involving the midanterior wall, affecting 15% of the myocardium. Alan had no previous problems with depression or anxiety but had been diagnosed with inflammatory arthritis (20 years ago) and psoriasis since age 16. Three months after the MI, he began feeling depressed, so his cardiologist referred him for cardiac rehabilitation and started him on citalopram. After his MI, Alan’s sleep was severely disturbed: sleeping from 1:30 to 5 am, he estimated he was sleeping 3–4 h most nights. Before his heart attack, he slept soundly for 6 h nightly and was never tired; now, his sleep was very fragmented, waking up hourly all night. Trying sleep medicine made him feel lousy the next day. Alan dismissed the sleep problem as “laziness” and never considered that sleep might be important for his recovery. At CR, he attended an educational panel and heard that rest and sleep play a big part in cardiac recovery. He was referred to the Psychology Service. At the consultation appointment, 5 months post event, his chief complaint was feeling irritable and depressed. He lost 23 pounds in 5 months, had no sexual interest, had badly fragmented sleep, felt fatigued easily, and described his memory as “lousy” now. Alan had been on citalopram for 2 weeks when he started CR. Once his CR exercise began, Alan started to feel better. Suspecting he had not been on the citalopram long enough for it to have started to work, he believed that his depression was from the lack of physical exercise, so he stopped the medication. However, he continued to experience significant cardiac symptoms of chest pain, indigestion, tightness between his shoulder blades, dyspnea on exertion, and dizziness during his cool down, and he was asked to slow down all exercising. His exercise prescription had been to walk 40 min a day, which was cut to 1.5 miles in 24 min. Slowing down made him feel more depressed. A few weeks later, he was given the green light to resume normal exercising again. Once he resumed 40 min of exercise again, his depression also improved. Alan felt he had done the right thing by stopping the citalopram; otherwise, he would never have known whether it was the citalopram or the exercising that made him feel better. He felt good about his decision and heartened by his positive response to exercising. The first behavioral intervention in Alan’s treatment was to promote recovery sleep. He was advised to lie down to rest three times each day (at 9 am, 11 am, and 1 pm). Initially seeing this as laziness, he was skeptical about accepting the forced rest windows. He was not happy to lie down, but he understood the goals and was compliant to follow the guidelines, resting every 2 h daily when at home. In the first week, he slept in at least one of the three rest windows every day and napped twice on 4 days. In the second week of active treatment, Alan was already starting to sleep longer at night and only napped on 2 days. Across the next weeks, these forced rest periods were reduced. By the start of the third week, he said he did not need to lie down
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three times. Thereafter, he had scheduled rests at 11 am and 1 pm, but he rarely napped at either time. Alan had one flare-up during the week-end before his forced rests were reduced with stabbing pains in his chest and visited the emergency room. They kept him overnight and did an ECG (which was normal) before sending him home. In subsequent weeks, he never napped more than twice in any given week. Still, it was encouraging to him to see his energy level improve. Despite discontinuing his citalopram, he continued his regular exercise, and his sleep and mood both continued to improve with exercise. As his sleep and energy improved, he was also taught breathing and muscle relaxation techniques. Across the next number of weeks, his arousal symptoms began to gradually improve. He fell asleep faster, which was encouraging. His night time awakenings were still slow to respond to treatment. He was encoura
