An inflammatory basis to atherosclerosis is now accepted. It remains plausible (but unproven) that common infectious agents may contribute to the inflammatory signal, and hence the development (and/or progression of atherosclerosis and its clinical sequelae. Of the candidate microorganisms implicated, Chlamydia pneumoniae has emerged as the most likely pathogen to have a casual role. Evidence for this is based on sero-epidemiological, pathological and laboratory-based evidence, in addition to early animal models and small-scale antibiotic studies. A past decade of research has now culminated in prospective antibiotic intervention trials in coronary heart disease to be conducted. The results of these studies should help to finally determine whether infection with C. pneumoniae is a pathogenetic factor in atherosclerosis, and whether antibiotic therapy has a role in the secondary prevention of coronary heart disease.