2. Over a 15-year observation in 2573 adults, however, depression was not associated with increased risk of coronary events.
3. In a study by Lesperance et al., a total of 896 post myocardial infarction (MI) patients were administered the Beck Depression Inventory during admission and at one year. The severity of depression symptoms during admission was directly linked to the five-year mortality. The greater the depression the higher the five-year mortality. Even though the one-year scores were also linked to five-year cardiac mortality, most of the impact was explained by baseline scores. The authors concluded that the severity of depression symptoms during admission rather than the changes in depres¬sion symptoms at one year was more closely linked to long-term survival.
4. Lane et al. indicated that ‘‘the balance of evidence and argument suggests that it is right for one to be skeptical about a causal link between mood, whether anxiety or depression, after MI and subsequent cardiac events and mortality.’’
5. In a study by Gottlieb et al., 48% of patients with heart failure scored as depressed.
I. PATHOPHYSIOLOGIC MECHANISMS
Autonomic arousal with hyperactivity of the hypothala-mic–adrenocortical and sympathoadrenal axis is provoked by depression. This axis increases corticosteroids and results from this hyperactivity are believed to stimulate the atherosclerotic process that leads to obstruction of coronary arteries. This stimulates the process and increases blood cholesterol and free fatty acids. Norepinephrine secretion is increased and catecholamine surge may cause an increase in blood pressure. Depressed cardiac patients have been shown to have diminished heart rate vari¬ability caused by a relative increase in sympathetic tone. This increases the risk for serious and sometimes life-threatening abnormal heart rhythms. Small blood particles such as platelets and coagulation factors are activated by serotonin and this may contribute to the increased risk of MI.

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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