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,
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Contact: Carole Bullock
carole.bullock@heart.org
214-706-1279
American Heart Association
5-Sep-2002