I. Pathophysiologic Mechanisms
II. Drug Management
DEPRESSION IS COMMON IN PATIENTS WITH coronary artery disease and is believed to confer an increased cardiac risk on healthy individuals and on patients with known coronary artery disease. It is stated by some that the degree of risk with major depression appears to be comparable to that observed with other known risk factors and is largely independent of them. Nonetheless, this association needs careful documentation to ascertain what is fact and what is fiction. A few studies indicate that after a heart attack significant depressive features are found in approximately 33% of patients, and major depression is observed in about 15% of these individuals. Other studies indicate symptoms of depression and anxiety after myocardial infarction with rates ranging from 17–37%. Symptoms often persist over the ensuing months and adversely affect the patient’s quality of life, but there is no documentation of increased cardiac mortality. The risk of depression is twice as high in women compared with men. Further studies are required because of the variable reports.
1. Depressed mood was observed to be a significant pre¬dictor of subsequent fatal and nonfatal heart attacks in a prospective study of 2832 healthy adults.

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• II. DRUG MANAGEMENT
  Recent studies indicate that selective serotonin reuptake inhibitors (SSRIs) constitute a major advance in the management of depressed patients with heart disease. Randomized controlled trials are required to document their beneficial effects over a 5- to 7-year period. The antidepressant heart attack randomized trial (SADHART) studied 370 patients with acute MI or unstable angina and major depressive disorder. After a two-week placebo run, patients were randomized to receive sertraline (Zoloft), 50 mg daily or placebo for 24 weeks. Approxi¬mately 33% of these patients had previous episodes of depression. Results indicated that sertraline was effective in treating patients with more severe, recurrent episodes of depression. This drug did not cause adverse cardiac effects, for example, changes in left ventricular ejection fraction or other cardiac measurements. The incidence of the cardio¬vascular events was less frequent in this group, and 22.4% versus 14.5% in the placebo group. This difference did not reach statistical significance, but it is reassuring that no adverse cardiac effects were observed and depression was significantly ameliorated. This was a short-term study and trials to observe whether these agents reduce cardiac mortality long-term are necessary.
• BIBLIOGRAPHY
  Blumenthal, J. A., Lett, H. S., Babyak, M. A. et al. Depression as a risk