Background: Established risk factors account for no more than 50% of coronary artery disease cases; therefore, the search continues for other modifiable risk factors. In recent years, there has been renewed interest in the infectious theory of atherosclerosis. Chlamydia pneumoniae has been implicated as a potential cause of atherosclerotic disease.
Objective: This review discusses possible mechanisms of C pneumoniae involvement in atherosclerosis, summarizes the case-control studies and antibiotic trials completed, and identifies remaining questions about future therapy.
Methods: Published data were identified by a MEDLINE search of the English-language literature from 1966 through 2001 using the terms Chlamydia, atherosclerosis, and coronary artery disease. Relevant conference presentations and book chapters were also included.
Results: C pneumoniae antibodies are found in approximately 50% of middle-aged adults world-wide. These antibodies have been detected in atherosclerotic tissue by various methods, including microimmunofluorescence, and several studies have linked high antibody titers with increased risk of cardiovascular events. A few possible mechanisms for this perceived increase in risk have been proposed, such as induction of atheroma through damage to the endothelium, expression of procoagulant factor leading to thrombus formation, and production of cytokines resulting in increased inflammatory response. Results of animal studies suggest that early antibiotic treatment may reduce cardiovascular risk, but the first human studies have not produced conclusive results.
Conclusions: Although a connection has been suggested, the precise mechanism by which C pneumoniae affects atherosclerosis has not yet been identified. Large-scale trials are needed to determine whether eradication of C pneumoniae reduces the incidence of cardiovascular events in humans.