Several studies have demonstrated an association Chlamydia pneumoniae with
coronary artery disease, suggesting that infection with C. pneumoniae incre
ases the risk for coronary artery disease by factor 2 or more. Since athero
sclerosis is considered to be a chronic inflammatory process, these data wo
uld fit into the response-to-injury hypothesis of atherosclerosis rather th
an representing a completely novel concept. Several pathomechanisms as incr
eased cytokine synthesis, proliferative and proaggregatory effects could tr
ansmit the effects of chronic C. pneumoniae infection. Animal models and fi
rst clinical trials using antibiotic therapy seem to support an etiological
role of C. pneumoniae in coronary artery disease. In this paper the curren
t knowledge of the role of C. pneumoniae in coronary artery disease is revi
ewed and possible pathomechanisms are discussed.