Exposure to Chlamydia pneumoniae is extremely common, and its incidence increases with age. C pneumoniae infection is strongly associated with coronary artery disease, as well as with atherosclerosis of the carotid artery, aorta, and peripheral arteries. This association has been shown in seroepidemiologic studies and by direct detection of the organism in atherosclerotic lesions by immunohistochemistry, polymerase chain reaction, electron microscopy, and tissue culture. Animal models of atherosclerosis have been used to study the role of C pneumoniae in the initiation and progression of atherosclerotic disease. The association of this organism with cardiovascular complications has inspired many human trials of antibiotics for the secondary prevention of atherosclerosis. C pneumoniae can infect several types of cells, including circulating macrophages, arterial smooth muscle cells, and vascular endothelial cells, causing the secretion of proinflammatory cytokines and procoagulants by endothelial cells and foam cell formation by infected macrophages. This report reviews the role of C pneumoniae in atherogenesis in light of recent, large antibiotic treatment trials, animal studies, and in vitro studies. The role of Chlamydia heat shock protein as a potential mediator of this harmful effect is also reviewed.
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