Evidence continues to accumulate to support a role for Chlamydia pneum
oniae in the pathogenesis of atherosclerosis, and in particular, coron
ary heart disease. In an analysis of 18 seroepidemiological studies, i
ndividuals with high-titer antibodies to Chlamydia pneumoniae have at
least a twofold or larger odds ratio for coronary heart disease compar
ed with seronegative individuals. In addition, viable Chlamydia pneumo
niae has been cultured directly from atherosclerotic tissue, and has b
een demonstrated by polymerase chain reaction, immunocytochemistry, an
d electron microscopy in nearly 50% of atheromatous lesions, but in on
ly 5% of control samples. Chlamydia pneumoniae has been shown to infec
t and reproduce in vitro in human smooth muscle cells, coronary artery
endothelial cells, and macrophages, and has been shown to induce proc
oagulant activity and platelet adhesion factors known to contribute to
the pathogenesis of atherosclerosis. Furthermore, Chlamydia pneumonia
e has been identified in atherosclerotic tissue in two experimental an
imal models. Finally, two pilot antibiotic trials of post-myocardial i
nfarction patients receiving antibiotics effective against Chlamydia p
neumoniae have demonstrated a fivefold reduction in cardiovascular eve
nts compared with those patients receiving placebo. Although a causal
effect has not been proved, the relationship between Chlamydia pneumon
iae and atherosclerosis continues to grow and to stimulate more defini
tive studies. (C) 1998 Lippincott-Raven Publishers.