Depression boosts blood-vessel disease.

Mild to moderate depression may substantially increase the impact of several known contributors to a blood-vessel disease that can lead to a hear attack or stroke, according to findings released last week at a meeting of the American Heart Association in Memphis.

"Treating depression, even in cases without severe impairment, may be important in both the prevention and treatment of cardiovascular disease," contends epidemiologist George A. Kaplan of the California Department of Health Services in Berkeley.

Kaplan and his co-workers -- including scientists at the University of Kuopio, Finland -- studied 1,225 Finnish men, age 42 to 60, taking part in a larger, ongoing investigation of risk factors for heart disease. The men live in eastern Finland, an area known for high rates of heart and blood-vessel disease.

The researchers looked at the link between depression and atherosclerosis, a disease in which cholesterol-filled plaques collect in arteries. Ultrasound tests indicated that each man suffered from some degree of atherosclerosis in the carotid artery, which carries blood to the brain through its two tributaries in the neck. Thickening of the carotid reflects plaque buildup, which increases the likelihood of stroke. The condition of the carotid artery often mirrors that of the coronary arteries, which cannot be viewed with ultrasound, Kaplan says.

Participants also completed the Minnesota Multiphasic Personality Inventory (MMPI), which includes a scale for depression. Kaplan's group divided the sample into approximately equal numbers of "depressed" and "nondepressed" individuals using MMPI scores. Most of the former group suffered mild to moderate symptoms of depression, including general apathy, denial of personal worth and sleep problems.

Depression showed no direct relationship to the extent of carotid atherosclerosis, Kaplan points out. But depression did amplify the link between atherosclerosis and two of its risk factors, cigarette smoking and fibrinogen, a blood-clotting protein that encourages plaque formation.

Depressed men who smoked displayed three times as much plaque buildup in the carotid as nondepressed men who smoked, with years of smoking and cigarettes smoked per day held constant. Depressed men with elevated fibrinogen levels suffered nearly four times as much carotid atherosclerosis as nondepressed men with the same levels of the protein.

Twice as much plaque formation occurred among depressed ment with increased blood levels of LDL cholesterol (the "bad" cholesterol), compared with nondepressed men with the same LDL levels. Kaplan calls this a "marginally significant" finding.

Since living with poor health caused by heart and blood-vessel disease may produce depression, the researchers separately examined 695 men in the sample with no prior diagnosis or treatment for such problems. Depression exerted comparable effects on the three risk factors.

"These findings provide one more reason for physicians to pay close attention to depression in patients with hear disease," comments Robert Anda, a physician and epidemiologist at the Centers for Disease Control in Atlanta. "[Severe] depression may have an even stronger effect on risk factors for atherosclerosis." However, Anda considers the implications of the new data speculative until additional studies confirm the results.

Kaplan's team plans to follow the Finnish men, tracking the course of their depression and atherosclerosis. For now, however, the findings suggest that depression accentuates the influence of risk factors for the disease through biological pathways that remain unknown, Kaplan says. Blood platelets contain receptors for some chemical messengers in the central nervous system, such as epinephrine and serotonin, which may increase with depression, he points out.

"But we don't know if blood platelets are more activated in depressed people," Anda notes. "Speculation is wide open on physiological mechanisms at work here."