Smokers' infections increase risk of early atherosclerosis

September 05, 2002

DALLAS, Sept. 6 - Cigarette smoking turns the entire body into a breeding ground for infection, which may allow artery-clogging plaque to take hold, according to a study reported in the September issue of Stroke: Journal of the American Heart Association.

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 the brain) of 826 men and women ages 40 to 79. The participants were part of the Bruneck Study, a prospective, population-based survey in Bruneck, Italy, designed to identify factors contributing to atherosclerosis.

Over the five-year study period, 332 men and women developed new carotid plaques.

The risk of developing atherosclerosis was closely associated with the number of years and quantity of cigarettes smoked (pack years), regardless of gender, but chronic infection also had a role in plaque development, notes Kiechl.

"Remarkably, in both analyses, increased risk of atherosclerosis was observed only in smokers and ex-smokers with clinical signs of chronic infection. The risk burden in people without evidence of infection did not differ from that in nonsmokers."

Nonsmokers with chronic infection had 1.8 times the risk of premature atherosclerosis as nonsmokers free of infection. Among former smokers with infection, the risk was 1.9 times higher, while current smokers with infection had 2.9 times the risk for premature atherosclerosis as infection-free nonsmokers.

In ex-smokers with chronic infection, the risk of early atherosclerosis remained elevated even 10 years after they quit, while ex-smokers without infection showed a gradual decrease in risk over time, Kiechl says.

"We found that the ongoing risk after quitting is probably the result of chronic infections that develop during the active smoking period, especially respiratory infections, such as smokers bronchitis or chronic obstructive pulmonary disease," he says.

The group of passive smokers with chronic infection in the study also faced an increased risk of early artery disease. Researchers hypothesize that secondhand smoke renders individuals susceptible to respiratory infection and that infection increases the risk of artery disease.

Smokers should be made aware of the findings and should be advised to seek treatment for their chronic infections, he adds.
-end-
Co-authors are Philipp Werner, M.D.; Werner Poewe, M.D.; Johann Willeit, M.D.; Georg Egger, M.D.; Friedrich Oberhollenzer, M.D.; Manuel Mayr; and Qingbo Xu, M.D., Ph.D.

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