Depression is a potential new risk factor for coronary artery disease (CAD), similar to obesity and lack of exercise. There is emerging evidence to suggest that although depression may not cause CAD, treating depression would be prudent in such patients.

The prevalence of major depression is high in hospitalized CAD patients. There is good data to suggest that major depression is at least 3 times as common in these patients as in the general community for hospitalized patients. This is true in a variety of populations, including myocardial infarction, unstable angina, congestive heart failure and post-intervention patients.

Interestingly, minor depression is also about 3 times as common in hospitalized CAD patients. This means that about one third of these patients show some degree of depression during hospitalization.

It is difficult to predict which CAD patients will exhibit depression. However, it is more common in women, younger patients, individuals with poor social support and patients with more severe CAD.

Researchers do not know exactly what causes depression. It is likely that a combination of genetics, unhealthy lifestyles and previous stresses create physiologic susceptibility. Then, stressful life events or chronic stress can interact with this susceptibility. This causes neuroendocrine disturbances that result in depression.

It is possible that there is a link between the causes of depression and CAD. There is no causal link. However, the neuroendocrine disturbances of depression may have an impact on the platelet changes, inflammation and autonomic nervous system disturbances that contribute to atherosclerosis.

Dr. Frasure-Smith and colleagues have studied the psychosocial aspects of acute coronary syndromes. They have looked at 896 post-myocardial infarction patients and 430 patients with unstable angina who all received usual care (31% women).

The investigators found that depression had a marked impact on 1-year prognosis, even after adjusting for other major cardiac risks. The impact was most pronounced in the first 6 months, then decreased somewhat.

They also found a dose-response relationship. Patients with worse depression had a worse prognosis. This suggests there may be no safe level of depressive symptoms for CAD.

This is not the only study to suggest a dose-response relationship between depression and CAD outcomes. A 1996 study in the American Journal of Cardiology looked at depression severity in 1,250 catheterization patients. More deaths occurred in patients with moderate/severe depression compared with patients who had mild depression. Adjusting for other cardiac risks, the investigators found that long-term risk of mortality was significantly higher in patients who were depressed.

Consistent results emerged from a more recent study of older patients. A 2001 study in the Archives of General Psychiatry looked at patients age 55 to 85 years with a history of angina, myocardial infarction or congestive heart failure.

There are no prospective studies yet to demonstrate whether treating depression can alter CAD prognosis. However, Dr. Frasure-Smith believes that there is enough evidence to justify additional trials. That evidence should compel physicians to consider depression as a risk factor in patients with established CAD.