Low Heart Rate Variability In Depressed Patients Contributes To High Mortality After Heart Attack

They say treatments to alleviate symptoms of depression and correct defects in heart rate variability will offer the best hope for improved survival in depressed patients with coronary heart disease.

The researchers studied 311 depressed heart patients who participated in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study and compared them to 367 non-depressed heart patients. They followed patients for about two-and-a-half years.

"Depressed patients were nearly three times as likely to die during the study period as comparable, non-depressed heart patients," says Robert M. Carney, Ph.D., principal investigator and professor of psychiatry. "We also found that lower heart rate variability was responsible for a sizeable portion of that risk."

To monitor heart rate variability, patients wore portable heart monitors for 24 hours after their heart attack. Heart rate variability measures how the heart adjusts to varying levels of demand. In people with low heart rate variability, the heart doesn't make adjustments as quickly as needed.

"We have known for some time that depression increases the risk of death from heart disease, but we didn't know why depressed patients were more likely to die and whether heart rate variability had anything to do with the risk," Carney says. "This study shows it does account for at least a portion of the increased risk."

Carney says understanding that low heart rate variability plays a role makes it important to identify treatments that improve both depression and heart rate variability. He's currently involved in a study that will provide antidepressant drugs and omega-3 fatty acids to depressed heart patients.

Omega-3 fatty acids are found in some types of fish oil and are known to improve several risk factors for heart disease. Unlike the standard omega-3 supplements found in health food stores, Carney and colleagues are using a special formula that they hope will affect both depression and cardiac risk factors.

"Omega-3 is an essential fatty acid, which means we have to get it from the diet," Carney says. "We know it improves a variety of cardiac risk factors, and studies have suggested it also might improve heart rate variability. There's even some indication that our special formulation of omega-3 might be helpful for depression, so we're very excited about its potential to help heart patients with depression."

Carney will follow depressed heart patients for 12 weeks. All will receive antidepressant drugs. Half will get omega-3 supplements, and the other half will receive a sugar pill instead of omega-3.

"We think omega-3 might make cells a little more receptive to antidepressant medications," Carney says. "If that's the case, those medications might have a greater impact, both in improving depression and in reducing risk of future cardiac problems."

Interestingly, the study found that the risk of death increased over time. Depressed heart patients tended to be at greater risk more than 12 months after their heart attacks.

"Cardiologists do a very good job keeping people alive and getting them back on their feet after a heart attack," Carney says. "But in the months after a heart attack, people aren't followed as closely, and many stop taking some of their medications regularly. That's when depression seems to have its most negative effect."

While part of depression's negative effect involves decreased heart rate variability, Carney says it may have other effects, too. So in addition to looking at omega-3 fatty acids to treat depression and heart rate variability, he says it also will be important for researchers to identify other mechanisms through which depression increases the risk of death in the months after a heart attack.

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Carney RM, Blumenthal JA, Freedland KE, Stein PK, Howells WB, Berkman LF, Watkins LL, Czajkowski SM, Hayano J, Domitrovich PP, Jaffe AS. Low heart rate variability and the effect of depression on post-myocardial infarction mortality. Archives of Internal Medicine, vol.165; pp. 1486-1491, July 11, 2005.

This research was funded by a grant from the National Heart, Lung and Blood Institute of the National Institutes of Health.