Endovascular presence of viable Chlamydia pneumoniae is a common phenomenon in coronary artery disease

Objectives. We sought to examine coronary arteries for the presence of viable bacteria of the fastidious species Chlamydia pneumoniae. Background. The respiratory pathogen C. pneumoniae has been implicated in the pathogenesis of coronary artery disease (CAD). Previous studies have demonstrated an antichlamydial seroresponse to be a cardiovascular risk factor and coronary atheromata to contain chlamydial components in varying proportions. Endovascular demonstration of replicating bacteria is required to provide evidence for an infectious component in CAD and a rationale to discuss antimicrobial therapy. Methods. Myocardial revascularization was performed in 70 patients. Atherosclerotic lesions from 53 coronary endarterectomy and 17 restenotic bypass samples were cultured and subjected to nested polymerase chain reaction (PCR) for C. pneumoniae. Antichlamydial immunoglobulin G (IgG), IgA and IgM was examined by microimmunofluorescence. Results. Viable C. pneumoniae was recovered from 11 (16%) of 70 atheromata, and chlamydial deoxyribonucleic acid (DNA) was detected in 21 (30%) of 70 atheromata; 17 nonatherosclerotic control samples were PCR-negative (p < 0.01). Fifteen (28%) of 53 endarterectomy and 6 (35%) of 17 bypass samples were PCR-positive. DNA sequencing of six different PCR products did not reveal differences between coronary isolates and respiratory reference strains, suggesting that common respiratory strains gain access to the systemic circulation. Serologic results did not correlate with direct detection results and did not identify individual endovascular infection. Conclusions. A significant proportion of atherosclerotic coronary arteries harbor viable C. pneumoniae. This finding supports the hypothesis of a chlamydial contribution to atherogenesis. Whether chlamydiae initiate atherosclerotic injury, facilitate its progression or colonize atheromata is unknown. However, the endovascular presence of viable bacteria justifies a controlled clinical investigation of antimicrobial treatment benefit in the therapy and prevention of CAD. (C) 1998 by the American College of Cardiology.