Chronic infection may explain why some smokers prematurely develop the artery-clogging process that causes most heart attacks and strokes, while other smokers remain free of arterial plaque buildup until they are older.

Current and ex-smokers who had common chronic infections such as bronchitis, ulcers, urinary tract infections and even gum disease were more than three times as likely to develop early atherosclerosis than people without such infections. Early atherosclerosis was defined as new plaques in previously normal arteries.

Infection also promoted artery disease in people exposed to secondhand smoke.

"This study provides the first epidemiological evidence that the atherosclerotic effects of smoking are mediated in part by chronic infectious illnesses in smokers," says lead researcher Stefan Kiechl, M.D., professor of neurology at Austria's Innsbruck University Hospital.

Previous research has shown that smoking is linked to respiratory infections, gum infections and chronic ulcer infections. The study by Austrian, Italian and British researchers considered how smoking and exposure to secondhand smoke influences the development of arterial plaques, and the effects of smoking cessation, in patients with and without evidence of chronic infection.

"Active and passive smoking represents one of the most severe risks for atherosclerosis," Kiechl notes. "Smokers are at significantly higher risk of developing severe early atherosclerosis, but we found the risk falls to that of nonsmokers soon after they quit, unless there is a history of chronic infection."

Researchers used ultrasound scans to examine changes in the carotid arteries (the main vessels supplying blood to
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Contact: Carole Bullock
carole.bullock@heart.org
214-706-1279
American Heart Association
5-Sep-2002