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(Circulation. 2002;106:e9003.)
© 2002 American Heart Association, Inc.

Cardiovascular News

Ruth SoRelle, MPH

Circulation Newswriter

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The Missing Link Between Infection and Coronary Artery Disease

According to a study in this week’s issue of Circulation (Circulation. 2002;106:184–190), pathogen burden, rather than the type of organism involved, is more likely to be associated with endothelial dysfunction and the severity of coronary artery disease.

Researchers and physicians from the National Heart, Lung, and Blood Institute at the National Institutes of Health, the Cardiovascular Research Institute, and Medstar Research Institute at Washington Hospital Center in Washington, DC, led by Abhiram Prasad, MD, MRCP, assessed the endothelial function of 218 patients undergoing angiography with the use of intracoronary acetylcholine and endothelium independent function with sodium nitroprusside and adenosine. -Globulin antibody titers to cytomegalovirus, Chlamydia pneumoniae, Helicobacter pylori, hepatitis A virus, and herpes simplex-1 virus were also measured. Pathogen burden was defined as the number of positive antibodies.

They found that pathogen burden is an independent risk factor for:

the presence of coronary artery disease

the severity of coronary artery disease

coronary vascular endothelial dysfunction

Patients with 4 or 5 previous infections had a 4.1-fold higher risk of coronary artery disease than those patients with 1 previous infection.

"There was a progressive decline in the dilator response to ACE (acetylcholine) as pathogen burden increased, providing a mechanistic explanation of how infections might predispose to atherogenesis by causing endothelial dysfunction," the authors wrote.

"Importantly, we found that the pathogen burden predicted the presence and severity of CAD more strongly than any single pathogen," they noted in their article. "It is likely that despite major differences in the . . . [Full Text of this Article]