Depression and Heart Disease -  - ebook

Depression and Heart Disease ebook

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Opis

Recently, there has been a growing awareness of the multiple interrelationships between depression and various physical diseases. Patients with psychiatric problems, particularly depression, may be more susceptible to cardiovascular disorders. Depression and Heart Disease synthesizes current evidence, including some previously unpublished data, in a concise, easy-to-read format. The authors succinctly describe the epidemiology, pathogenesis (including cytokines and genetics), and risk factors of the comorbidity between Depression and Heart Disease. The book also reviews the best pharmacological and psychotherapeutic approaches for people with this comorbidity.

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Liczba stron: 257




Contents

List of Contributors

Preface

CHAPTER 1: Epidemiology of the Comorbidity between Depression and Heart Disease

DEPRESSION AFTER MYOCARDIAL INFARCTION OR UNSTABLE ANGINA

DEPRESSION AND STABLE CORONARY ARTERY DISEASE

DEPRESSION AND CORONARY ARTERY BYPASS GRAFTING

DEPRESSION AND CORONARY ARTERY DISEASE DEVELOPMENT

DEPRESSION AND CONGESTIVE HEART FAILURE

CONCLUSIONS AND CLINICAL IMPLICATIONS

CHAPTER 2: The Association between Depression and Heart Disease: The Role of Biological Mechanisms

AUTONOMIC NERVOUS SYSTEM DYSREGULATION

BLOOD CLOTTING AND ENDOTHELIAL DYSFUNCTION

INFLAMMATION

NEUROENDOCRINE ABNORMALITIES

CONCLUSIONS

CHAPTER 3: The Association between Depression and Heart Disease: The Role of Genetic Factors

TWIN STUDIES

MDD and CAD

MDD and CAD Risk Factors

GENETIC ASSOCIATION STUDIES

CONCLUDING REMARKS

CHAPTER 4: Behavioural and Psychological Mechanisms Linking Depression and Heart Disease

BEHAVIOURAL MECHANISMS LINKING DEPRESSION AND HEART DISEASE

PSYCHOLOGICAL MECHANISMS LINKING DEPRESSION AND HEART DISEASE

CONCLUSIONS

ACKNOWLEDGEMENTS AND DISCLAIMER

CHAPTER 5: Depression and Cardiovascular Disease: The Safety of Antidepressant Drugs and their Ability to Improve Mood and Reduce Medical Morbidity

THE SAFETY OF ANTIDEPRESSANT DRUGS

THE ABILITY OF ANTIDEPRESSANT DRUGS TO INFLUENCE MEDICAL MORBIDITY AND MORTALITY

IMPLEMENTING TREATMENT OF DEPRESSION IN A MEDICAL SETTING

CONCLUSIONS

ACKNOWLEDGEMENT

CHAPTER 6: Psychotherapies for Depression in People with Heart Disease

COGNITIVE BEHAVIOUR THERAPY

INTERPERSONAL PSYCHOTHERAPY

The CREATE Trial

PROBLEM-SOLVING THERAPY

DIRECTIONS FOR FUTURE RESEARCH

Acknowledgement

Index

World Psychiatric Association titles in the “Depression” series

In recent years, there has been a growing awareness of the multiple interrelationships between depression and various physical diseases. This series of volumes dealing with the comorbidity of depression with diabetes, heart disease and cancer provides an update of currently available evidence on these interrelationships.

Depression and DiabetesEdited by Wayne Katon, Mario Maj and Norman SartoriusISBN: 9780470688380

Depression and Heart DiseaseEdited by Alexander Glassman, Mario Maj and Norman SartoriusISBN: 9780470710579

Depression and CancerEdited by David W. Kissane, Mario Maj and Norman SartoriusISBN: 9780470689660

Related WPA title on depression:

Depressive Disorders, 3eEdited by Helen Herrman, Mario Maj and Norman SartoriusISBN: 9780470987209

For all other WPA titles published by John Wiley & Sons Ltd, please visit the following website pages:

http://eu.wiley.com/WileyCDA/Section/id-305609.xhtml

http://eu.wiley.com/WileyCDA/Section/id-303180.xhtml

This edition first published 2011 © 2011 John Wiley & Sons, Ltd.

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Library of Congress Cataloguing-in-Publication Data

Depression and heart disease / editors, Alexander Glassman, Mario Maj, Norman Sartorius.p. ; cm. Includes bibliographical references and index. ISBN 978-0-470-71057-9 (pbk.)1. Depression, Mental–Complications. 2. Heart–Diseases–Psychological aspects. I. Glassman, Alexander H., 1934- II. Maj, Mario, 1953- III. Sartorius, N. [DNLM: 1. Depressive Disorder–complications. 2. Depressive Disorder–psychology. 3. Cardiovascular Diseases–etiology. 4. Cardiovascular Diseases–psychology. WM 171]RC537.D42746 2011 616.85’27–dc222010027876

List of Contributors

J. Thomas Bigger, Jr. Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA

Robert M. Carney Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA

Eco de Geus Department of Biological Psychology, VU University, Amsterdam, The Netherlands

Mary Kate Elfrey Department of Medicine, Johns Hopkins Bayview Medical Center, Baltimore, MD, USA

Kenneth E. Freedland Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA

Alexander H. Glassman Department of Clinical Psychopharmacology, New York State Psychiatric Institute, New York, NY, USA and Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, NY, USA

Wei Jiang Department of Psychiatry and Behavioral Sciences, Department of Medicine, Duke South Hospital, Durham, NC, USA

Palmiero Monteleone Department of Psychiatry, University of Naples SUN, Naples, Italy

Glen L. Xiong Department of Psychiatry and Behavioral Sciences, Department of Medicine, University of California, Davis, CA, USA

Roy C. Ziegelstein Department of Medicine, Johns Hopkins Bayview Medical Center, Baltimore, MD, USA

Preface

The idea that depression is related to cardiac morbidity and death has been prevalent for hundreds of years. Although intuitively appealing, it has been scientifically difficult to prove. Both the existence of the association and the mechanisms behind the association have proven much more complicated than might have been expected. This book examines the evidence that the association exists, the various mechanisms that might underlie the association and our ability to treat depression in the face of cardiovascular disease.

Drs Jiang and Xiong review in their chapter the epidemiology of the comorbidity between depression and heart disease. Extensive epidemio-logical data is now available, but the interpretation of the data is complicated by the need to control for cardiac risk factors and medications that might be used to treat depression. Cigarette smoking is an example of a cardiac risk factor that is also known to be seen more frequently in depressed patients. From the perspective of depressed patients, it matters little if their risk for cardiac disease comes from cigarette smoking or is directly related to depression. However, this is an important distinction in any scientific understanding of the mechanisms creating the association.

Individuals suffering from depression followed for long periods of time are at excess risk for cardiac morbidity and mortality after controlling for treatment as well as known cardiovascular risk factors. Initially, studies focused on large community samples. This was done in order to avoid confounding with antidepressant medications, which were ubiquitous to samples collected from clinical populations, and because it minimised the possibility that depression was caused by chronic cardiac disease.

Since the 1990s, there has been a shift in interest from long-term studies of medically healthy individuals to the effects of depression in patients with known cardiovascular disease. Much of the interest has centred on the relationship between depression and acute coronary syndromes. The landmark study of Frasure-Smith in 1993 [1] indicated that depression observed in the cardiac intensive care unit predicted a fivefold increase in the risk of cardiac mortality over the next 6 months. Since that time a large number, but not all, studies have replicated this effect of depression. Many studies have controlled for both cardiac risk factors and the severity of the cardiac event and, although the effect size attributable to depression has diminished, the risk in depressed, post-coronary patients seems to exceed the increase in risk usually seen in physically healthy depressed individuals.

The high prevalence of depression, along with a higher risk associated with acute cardiac events, initially made it seem as if it would be relatively easy to study the influence of depression on both cardiac morbidity and mortality. However, a number of factors have conspired to make that task much more difficult than it originally seemed. Medical treatment of patients after an acute coronary syndrome has radically reduced the incidence of adverse cardiac events and, as a consequence of this, the number of depressed patients necessary to see an effect of antidepressant treatment on medical morbidity and mortality has increased. In addition, when studies began in the mid-1990s, the majority of cases of depression after an acute coronary syndrome were untreated. As the awareness of the risk associated with depression increased and information about the safety of selective serotonin reuptake inhibitors (SSRIs) grew, it became harder to find either ethics boards or depressed patients willing to accept placebo treatment. Although the need for a definitive clinical trial testing whether antidepressant treatment would reduce medical complications has been obvious for at least a decade, the cost and practicality of such a trial has grown more and more difficult.

While efforts to mount a definitive clinical trial have stalled, investigators have focused on potential mechanisms that might underlie the association between depression and heart disease. Health behaviours, compliance, platelet reactivity, heart rate variability, endothelial reactivity, sympathetic activity, genetics and inflammation have all been suggested as possible mediators. At this point it would seem very unlikely that any one mediator is responsible for the association. It is likely that the association stems from multiple sources and they are probably not the same in all depressed patients.

Drs Ziegelstein and Elfrey review in their chapter the behavioural and psychological mechanisms linking depression and heart disease, with a special focus on compliance with treatment. Statins, beta-blockers, anti-platelet drugs and calcium channel blockers reduce mortality after an acute coronary syndrome, but only if patients take their medication, and the evidence is that depressed patients are less likely to adhere to medical prescriptions. If treating depression successfully improves compliance, it must to some degree reduce morbidity and mortality. Although improved compliance and other health behaviours are almost certain to contribute to reducing the increased morbidity and mortality associated with depression, they will almost certainly account for only a part of the risk.

As reviewed by Dr Monteleone in his chapter, autonomic nervous system dysregulation, endothelial dysfunctions, platelet abnormalities, neuroendocrine abnormalities, and inflammation have all been suggested as potential biological mechanisms behind the association between depression and heart disease. All have been demonstrated to exist in both conditions. However, to which degree any of these potential mechanisms actually drive the association is unclear. Perhaps the best studied of these mechanisms involves inflammatory markers. Dozens of studies have looked for abnormal inflammatory markers in depressed patients and some markers are almost always found. The observation that alpha-interferon used to treat hepatitis C or malignant melanoma is associated with a marked increase in the onset of major depression makes it clear that increased inflammatory activity can provoke depression. However, it remains unclear whether inflammation associated with depression increases the risk of heart disease or if the degree of inflammation associated with acute heart disease increases the risk for depression. It is certainly possible that the relationship is bidirectional and/or that the inflammation characteristic of each condition is the result of some common genetic vulnerability. In a similar way, low heart rate variability is associated with increased mortality in cardiovascular patients and is also characteristic of more severe depressions and may be the result of some common genetic predisposition. The possible role of genetic factors in contributing to the association between depression and heart disease is reviewed by Dr de Geus in his chapter.

Regardless of the mechanism, a strong association between depression and the risk of cardiovascular morbidity and mortality makes the treatment of depression after an acute coronary syndrome all the more important. This became obvious in 1993 with the publication of FrasureSmith’s landmark paper. However, at that time, there was no evidence that antidepressant drugs were safe in the period immediately after an acute coronary syndrome. There was, in fact, considerable evidence that tricyclic antidepressants were dangerous in patients with cardiac disease. For that reason, the only large treatment trial of depression after an acute coronary syndrome compared psychotherapy with usual care. In that trial, psychotherapy was modestly more effective than usual care in reducing depression, but there was no evidence for any reduction in mortality. There is now a need to establish whether a more practical and efficacious psychotherapy can be developed. The other large trial was never powered to test the effect of antidepressants on medical risk, but was an SSRI safety trial. It was the early 2000s before it became clear that SSRIs were safe in the immediate period after an acute coronary syndrome. Interestingly, although the antidepressant effect was similar across drug and psychotherapy treatments, those patients who received an SSRI appeared to have a reduction in medical morbidity and mortality. Unfortunately, the evidence that SSRIs can reduce morbidity and mortality is suggestive but not definitive. Antidepressant use in the psychotherapy trial was not randomised and the SSRI treatment trial, although suggestive, was grossly underpowered to address the question. Current available evidence concerning pharmacotherapies and psychotherapies for depression in patients with heart disease is reviewed, respectively, by Drs Glassman and Bigger, and by Drs Carney and Freedland in their chapters.

Depression’s importance as a public health problem is due to both its high lifetime prevalence and the significant disability that it causes. World Health Statistics in 2007 [2] revealed that individuals with depression and one other chronic condition had much lower health scores when compared with those who had only a chronic condition. Given that ischaemic heart disease and unipolar major depression are predicted by the World Health Organization to be the leading causes of disability-adjusted life years by 2020 [3], the increased risk associated with this comorbidity causes a dramatic increase in health burden worldwide. In many primary care settings, when patients present with multiple disorders that include depression, this condition often remains undiagnosed. Particularly in acute coronary events, even if it is diagnosed, treatment usually focuses on the coronary disease. The timely diagnosis and treatment of depressive disorders is essential, and understanding the mechanisms underlying the increased morbidity and mortality associated with the comorbidity of depression and heart disease is crucial to a rational treatment.

REFERENCES

1. Frasure-Smith, N., Lesperance, F. and Talajic, M. (1993) Depression following myocardial infarction. Impact on 6-month survival. JAMA, 270, 1819–1825.

2. World Health Organization (2007) World Health Statistics 2007. World Health Organization, Geneva.

3. Mathers, C.D. and Loncar, D. (2006) Projection of global mortality and burden of disease from 2002 to 2030. PLoS Med., 3, 2011–2030.

Alexander GlassmanMario Maj Norman Sartorius

CHAPTER 1

Epidemiology of the Comorbidity between Depression and Heart Disease

Wei Jiang

Department of Psychiatry and Behavioral Sciences, Department of Medicine, Duke South Hospital, Durham, NC, USA

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