DALLAS, Aug. 18 -- The strongest link yet between a chronic lung infection and heart disease has been found in a study of Alaska natives, researchers report in today's Circulation: Journal of the American Heart Association.
Other studies have reported finding the bacteria Chlamydia pneumoniae (C. pneumoniae) in atherosclerotic plaques -- the fatty deposits that build up in the walls of blood vessels and lead to heart attacks and strokes. However, the researchers say the new study is the first to show that the individuals were infected with the bacteria before heart disease was diagnosed.
Researchers studied samples of plaques obtained during autopsies of 60 Alaska natives, all of whom died from accidents. They also measured stored blood samples drawn seven months to 26 years earlier for disease screening programs. Adequate amounts of blood for testing were available for 56 of the individuals.
Scientists tested for the bacteria infection by measuring antibodies -- cells the body produces to defend against disease -- to C. pneumoniae.
The team identified the bacteria in coronary artery plaques from 22 (37 percent) of the Alaska natives who were studied. The organism was found in 39 percent of the early-stage plaques and in 35 percent of the more advanced deposits.
The study found that those who had severe infection were nearly 10 times more likely to have the bacteria identified in their blood vessels when they died than people with little or no evidence of earlier infection.
"The major finding of the report is the evidence of prior infection with Chlamydia pneumoniae. It provides strong evidence in linking this bacteria with atherosclerosis," says the study's lead author, Michael Davidson, M.D., M.P.H., a post-doctoral fellow at the Johns Hopkins University School of Hygiene and Public Health in Baltimore.
To prove scientifically that an event or substance causes a disease, it has to be present before the disease, not just when the disease develops, explains Davidson. "In this situation, we know that the infection occurred before we found the bacteria in the plaques."
The researchers note that this study does not confirm that the bacteria actually causes atherosclerosis, but it does provide more substantial evidence on how the bacteria and the disease could be related. The researchers say they were the first to show the bacterial infection occurred before evidence of the organism was found in the coronary arteries, which bring blood to the heart.
Another key finding is that people with the highest level of infection with the bacteria may have been at the greatest risk of developing a chronic infection within heart tissues, showing early as well as advanced disease.
Davidson's team, which included researchers from the University of Washington, Louisiana State University, and the Alaska Division of Public Health, studied Alaska natives who had a lower risk of heart disease than the general population. Individuals studied included 47 Eskimos, five Aleuts and eight Indians.
All individuals (45 males and 15 females) died between February 1989 and December 1992. Their ages at death ranged from 15 to 57 years.
Davidson and his colleagues also found the bacteria associated with macrophage foam cells -- an abnormal form of a common immune-system cell that has been linked to the early formation of plaque deposits -- in over three fourths of the plaque specimens. These cells and bacteria were found in many of the specimens with the earliest stage of atherosclerosis in which only the lining of the blood vessel thickens. "Compared to heart specimens without the bacteria, we found a very high correlation of foam cells in the tissues with C. pneumoniae," says Davidson.
C. pneumoniae causes about 10 percent of the pneumonia cases in adults. It is related to the microorganism that causes the sexually transmitted disease commonly called chlamydia, but C. pneumoniae is spread when an infected person coughs -- not by sexual contact.
The researchers are continuing their studies in other populations to determine how the infection can be screened for and treated to prevent the development of heart disease.
Co-authors of the paper are Cho-Chou Kuo, M.D., Ph.D.; John P. Middaugh, M.D.; Lee Ann Campbell; San-Pin Wang, M.D., D.Sc.; William P. Newman III, M.D.; John C. Finley, M.D.; and J. Thomas Grayston, M.D.
The above post is reprinted from materials provided by American Heart Association. Note: Materials may be edited for content and length.
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