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University of California, San Diego, Cardiology 111A Veterans Administration Health Care System, La Jolla, CA 92161, Email: rshabetai@ucsd.edu
An extensive literature attests to the relation between cardiovascular and psychiatric disorders. Most of the earlier studies concerned the impact of such manifestations of mental illness as chronic stress, anxiety, and depression on the clinical course and outcome of ischemic heart disease, including worsening angina, new or recurrent myocardial infarction, and the precipitation or exacerbation of arrhythmias, sometimes even leading to sudden death. The number of patients was small in many of the studies, and in some, anxiety and depression were lumped together. Certain personality types were considered as having a higher risk for heart attack than the general population. In addition to its effects on the manifestations and prognosis, depression is recognized as a risk factor for coronary heart disease ranking equally or above lipodystrophy, smoking, and hypertension by epidemiologists but, unfortunately, not by most cardiologists.
The appreciation that depression exerts unfavorable effects on heart failure came considerably later. Now, however, current editions of cardiology texts and books on heart failure devote space to the impact of mental illness, especially depression and social isolation, on heart failure (1, 2). Here, even more than in the case of ischemic heart disease, the situation is complicated by difficulties in deciding whether to ascribe symptoms like dyspnea, fatigue, insomnia, anorexia, or even palpitation to disease of the heart or of the nervous system (3). Similarly, cachexia may be a manifestation of high circulating levels of cytokines (eg, tumor necrosis factor) or gastrointestinal and hepatic congestion. On the other hand, depression, when severe enough, can result in malnutrition. Acute mental stress, such as mental arithmetic or a stress interview, can induce transient changes in left ventricular systolic and diastolic function (4), and, in susceptible individuals, the hypertensive and tachycardic reactions are impressive. Animals also show significant hemodynamic responses, and although these results are suggestive of chronic mental stress, they cannot be extrapolated to chronic depression.
Until now it was not known whether depression is a risk factor for the development of heart failure, because a prospective trial addressing this issue had not been published. The article by Williams and colleagues in this issue of Psychosomatic Medicine (5) provides convincing evidence that in the case of heart failure, as in the case of ischemic heart disease, we need to consider the possibility that depression should be added to the many conditions that predispose to heart failure. The study has the advantage of being a large prospective study spanning 14 years. After excluding a little more than 300 patients who met the study’s definition of preexisting heart failure, the study population comprised a little more than 1000 men and nearly 1500 women whose average age was 74. The participants were recruited from socially and ethnically diverse inhabitants of private and public housing. Fifty-six of the men and 132 of the women scored higher than 21 on the Center for Epidemiological Studies Depression Scale (CES-D) and were therefore classified as depressed. During follow-up, 188 women and 145 men met the study’s criteria for heart failure. After correcting for known risk factors for heart failure, depression increased the risk of heart failure by 52%, but the increase did not meet statistical significance for the total population of depressed patients (p = .09). When the data for the women were analyzed separately, however, the risk of developing heart failure was almost doubled in the depressed, and the difference was statistically significant (p = .02).
Considering that in both depression and heart failure, increased activity of the renin-angiotensin-aldosterone system and increased sympathetic (but decreased vagal) activity play important roles, and that in both conditions circulating levels of cytokines are elevated, the results of Williams et al.’s study should not come as a complete surprise; it is plausible to ascribe the findings to these and other shared abnormalities in the regulation of the internal milieu. Similarly, sleep disorders are common to depression, heart failure, and cerebrovascular accident. Sleep apnea worsens heart failure and appropriate therapy improves it (6, 7), but heart failure also worsens sleep apnea and appropriate therapy improves it. A similar complex relation seems to operate between depression and heart failure. The protocol of most large heart failure studies includes a quality-of-life instrument such as Minnesota Living With Heart Failure Questionnaire (8), which is used in more than half of American heart failure clinics. Answers to questions relating to mental health issues contribute more to high scores (worse quality of life) than do answers to questions about traditional symptoms of heart failure.
The concept of heart failure continues to evolve. Over the past few decades it was first considered a purely hemodynamic affair, and its treatment was aimed at increasing the force of myocardial contraction, first with cardiac glycosides and later with phosphodiesterase inhibitors. Subsequently vasodilator therapy was introduced (sparing rather than flogging the heart). At first direct vasodilators such as isosorbide and hydralazine were used. Soon afterward angiotensin-converting enzyme (ACE) inhibitors were preferred because they are more effective in prolonging survival and are much easier to use. Cough is an important side effect of the ACE inhibitors, but cough does not complicate the use of angiotensin-1 blockers. Furthermore, recent data suggest that the direct blockers are more effective than ACE inhibitors in achieving prolonged attenuation of circulating and tissue levels of angiotensin-2. Paradoxically, a major heart failure trial indicated that although directly acting vasodilators are more powerful than ACE inhibitors, the latter are superior in prolonging survival. The explanation of this paradox is that angiotensin-1 is a powerful myocardial growth factor and is thus responsible for cardiac remodeling, which is a critically important determinant of ventricular dilation and heart failure after any myocardial insult. ß-Blockers are now standard in the treatment of heart failure, and treatments with cytokine inhibitors and endothelin blockers are in clinical trial. We are now moving to the molecular paradigm of heart failure. Similar considerations doubtless apply to neurology.
The pathophysiology of heart failure is evolving in complexity, and the pace of this evolution will quicken as details of the underlying molecular changes are clarified. It is clear that further research on the interactions between mental and cardiac health is needed at the clinical, biochemical, and molecular levels if we are to understand the interactions of these two illnesses. In the meantime, the need for increased communication between psychiatrists and heart failure specialists is evident. Teams responsible for cardiac transplantation or adult congenital heart disease now routinely include a psychiatrist. Heart failure programs should emulate them. Increasing subspecialization is a well-known phenomenon, but molecular biology crosses the traditional frontiers of medicine, providing the hope that neuroscientists and cardiac researchers may discover how depression and heart failure are linked.
REFERENCES
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  Depression: A Risk Factor for Onset of Heart Failure in the Elderly? Journal Watch Psychiatry, March 6, 2002; 2002(306): 2 - 2. [Full Text]
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