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. Backg round. The respiratory pathogen C. pneumoniae has been implicated in t he pathogenesis of coronary artery disease (CAD). Previous studies hav e demonstrated an antichlamydial seroresponse to be a cardiovascular r isk factor and coronary atheromata to contain chlamydial components in varying proportions. Endovascular demonstration of replicating bacter ia 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 lesion s from 53 coronary endarterectomy and 17 restenotic bypass samples wer e 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 wa s recovered from 11 (16%) of 70 atheromata, and chlamydial deoxyribonu cleic acid (DNA) was detected in 21 (30%) of 70 atheromata; 17 nonathe rosclerotic control samples were PCR-negative (p < 0.01). Fifteen (28% ) of 53 endarterectomy and 6 (35%) of 17 bypass samples were PCR-posit ive. DNA sequencing of six different PCR products did not reveal diffe rences between coronary isolates and respiratory reference strains, su ggesting that common respiratory strains gain access to the systemic c irculation. Serologic results did not correlate with direct detection results and did not identify individual endovascular infection. Conclu sions. A significant proportion of atherosclerotic coronary arteries h arbor viable C. pneumoniae. This finding supports the hypothesis of a chlamydial contribution to atherogenesis. Whether chlamydiae initiate atherosclerotic injury, facilitate its progression or colonize atherom ata is unknown. However, the endovascular presence of viable bacteria justifies a controlled clinical investigation of antimicrobial treatme nt benefit in the therapy and prevention of CAD. (C) 1998 by the Ameri can College of Cardiology.