New insights into atherosclerosis, the most common disease affecting corona
ry arteries, may change therapeutic strategies from largely symptomatic to
causal. Atherosclerotic plaques contain a lipid-related, immune-mediated in
flammation, with release of secretory products capable of changing plaque m
orphology. Plaques prone to complications contain large numbers of inflamma
tory cells; stable plaques contain little inflammation. Similarly, atherect
omy specimens from patients with coronary syndromes revealed more inflammat
ory cells in unstable than in stable patients. These observations, and the
fact that acute coronary syndromes are associated with increased blood leve
ls of inflammatory markers, have renewed interest in the possible relations
hip between infection and atherogenesis. Of all potential candidate antigen
s, Chlamydia pneumoniae presently is considered the most likely because a s
ubstantial number of patients with unstable syndromes contain C. pneumoniae
-reactive T cells, both in blood and within the atherosclerotic plaque, sug
gesting enhancement of intraplaque inflammation.