Infections Can Predict Heart Disease Death

But cause-and-effect relationship is not certain

Edward Edelson

Edward Edelson

Updated on June 27, 2007

MONDAY, Jan. 7, 2002 (HealthDayNews) -- The number of bacteria and viruses that people with heart disease have been exposed to can predict their risk of death, German researchers say.

"We showed a significant association between the number of infections to which a patient has been exposed, and the extent of atherosclerosis in the arteries in the heart, neck and legs. The risk for death was increased by the number of infectious agents, especially in people with advanced artery disease," doctors at Johannes Gutenberg University in Mainz write. They report the finding in tomorrow's issue of Circulation: Journal of the American Heart Association.

Atherosclerosis, sometimes called "hardening of the arteries," is a process in which fatty particles accumulate within blood vessel walls, gradually blocking blood flow. One key component of the condition is inflammation, and there is a theory that the inflammation could be triggered by exposure to infectious agents.

While they say the new finding is of great interest, American experts warn against assuming there is a cause-and-effect relationship between infections and coronary risk.

Instead, says Dr. Sidney Smith, chief science officer of the American Heart Association (AHA), "we need more evidence before we can draw broad conclusions about the role of various infectious agents in atherosclerosis."

And in an editorial accompanying the journal article, Dr. Paul Ridker, director of the Center for Cardiovascular Disease Prevention at Brigham and Women's Hospital in Boston, cautions that the "investigators must be careful not to confuse association with causation."

In the study, the German physicians ran tests for eight disease-causing agents, four viruses and four bacteria on 572 patients who came to the hospital with symptoms of heart disease. Those patients were followed for more than three years.

There was a strong relationship between the number of infections and the risk of death. The death rate was 3.1 percent for patients testing positive for three agents, 9.8 percent for patients testing positive for four or five agents, and 15 percent for those testing positive for six to eight agents.

The common thread uniting infection and heart disease risk is inflammation, say Ridker and Smith.

Ridker cites a study he did that found healthy people with high levels of inflammatory cells were more likely to develop heart disease.

"Our results suggest that inflammation seems to be a fundamental issue," he writes.

"This study is one more link in the chain of evidence associating inflammation with atherosclerosis," Smith says. "But it is important to clarify that we are not at the point where we are able to identify a specific virus or microorganism as a cause of atherosclerosis."

The inflammation theory does have clinical implications, Ridker says. There is some evidence that the protection that aspirin and the cholesterol-lowering statin drugs give is due in part to the fact that they reduce inflammation, he says.

However, the underlying cause of the inflammatory response in heart disease is unclear, he adds. "It appears that both inherited and environmental exposures play major roles," he writes.

And caution is needed because the German study only included people with known heart disease, he says.

"Cross-sectional studies cannot eliminate the possibility that the infection came after the heart disease and not before, or that people with known or suspected artery disease are in poorer health and more prone to infection in general," he says.

What To Do

The AHA has more information about atherosclerosis and inflammation and heart disease.

The Associated Press has this story about studies that link inflammation and heart disease.

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