| pubmed-article:9646099 | pubmed:abstractText | The obligate intracellular bacterium Chlamydia pneumoniae has recently been implicated in the pathogenesis of atherosclerosis. Serological response to Chlamydia pneumoniae statistically indicates an increased risk of coronary artery disease and myocardial infarction. This surprising relation is corroborated by the presence of chlamydial structures and even viable Chlamydia pneumoniae in atherosclerotic plaques. These findings have already resulted in initial studies on the potential benefit of antimicrobial therapy in coronary heart disease. However, experimental proof of an etiological role of Chlamydia pneumoniae in arteriosclerosis has not yet been accomplished since a well established animal model and a system of genetic recombination are not yet available. In addition, clinical evaluation of patients is complicated by the lack of a useful parameter to indicate the risk of endovascular infection. Whether chlamydiae initiate atherosclerotic injury. facilitate progression of existing plaques, or merely colonize the lesions is therefore not known. Chlamydial contribution to the development of atherosclerosis is a fascinating hypothesis that may initiate a radical change of clinical practice for one of the leading causes of death. At the current state of scientific knowledge, however, an experimental antichlamydial treatment in coronary heart disease may only be justified in well controlled clinical trials. | lld:pubmed |
