Evidence continues to accumulate to support a role for Chlamydia pneumoniae in the pathogenesis of atherosclerosis, and in particular, coronary heart disease. In an analysis of 18 seroepidemiological studies, individuals with high-liter antibodies to Chlamydia pneumoniae have at least a twofold or larger odds ratio for coronary heart disease compared with seronegative individuals. In addition, viable Chlamydia pneumoniae has been cultured directly from atherosclerotic tissue, and has been demonstrated by polymerase chain reaction, immunocytochemistry, and electron microscopy in nearly 50% of atheromatous lesions, but in only 5% of control samples. Chlamydia pneumoniae has been shown to infect and reproduce in vitro in human smooth muscle cells, coronary artery endothelial cells, and macrophages, and has been shown to induce procoagulant activity and platelet adhesion factors known to contribute to the pathogenesis of atherosclerosis. Furthermore, Chlamydia pneumoniae has been identified in atherosclerotic tissue in two experimental animal models. Finally, two pilot antibiotic trials of post-myocardial infarction patients receiving antibiotics effective against Chlamydia pneumoniae have demonstrated a fivefold reduction in cardiovascular events compared with those patients receiving placebo. Although a causal effect has not been proved, the relationship between Chlamydia pneumoniae and atherosclerosis continues to grow and to stimulate more definitive Studies.