The obligat intracellular bacterium Chlamydia pneumoniae has recently
been implicated in the pathogenesis of atherosclerosis. Serological re
sponse to Chlamydia pneumoniae statistically indicates an increased ri
sk of coronary artery disease and myocardial infarction. This surprisi
ng relation is corroborated by the presence of chlamydial structures a
nd even viable Chlamydia pneumoniae in atherosclerotic plaques. These
findings have already resulted in initial studies on the potential ben
efit of antimicrobial therapy in coronary heart. disease. However, exp
erimental proof of an etiological role of Chlamydia pneumoniae in arte
riosclerosis has not yet been accomplished since a well established an
imal model and a system of genetic recombination are not vet available
. In addition, clinical evaluation of patients is complicated by the l
ack of a useful parameter to indicate the risk of endovascular infecti
on. Whether chlamydiae initiate atherosclerotic injury, facilitate pro
gression of existing plaques. or merely colonize the lesions is theref
ore not known. Chlamydial contribution to the development of atheroscl
erosis is a fascinating hypothesis that may initiate a radical change
of clinical practice for one of the leading causes of death. At the cu
rrent slate of scientific knowledge, however, an experimental antichla
mydial treatment in coronary heart disease may only be justified in we
ll controlled clinical trials.