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Evidence is accumulating to suggest that Chlamydia pneumoniae may have a role in the development and/or progression of atherosclerotic-related disorders, in particular coronary heart disease (CHD). The evidence for C. pneumoniae as a potential causative agent is largely based on the findings of (1) seroepidemiological studies, (2) examination of atheromatous plaque specimens, (3) in vitro experiments and animal models and, recently, (4) preliminary anti-chlamydial antibiotic intervention studies. This chapter aims at focusing on the potential, and intriguing, role of antimicrobial therapy in the secondary prevention of CHD. The findings of the preliminary pilot studies are reviewed, as are the aims and controversies surrounding large-scale, prospective intervention trials, now in progress.

In 1908 Sir William Osier first proposed a causative role of infection in the pathogenesis of atherosclerosis [1]. The view that infectious processes may contribute to cardiovascular diseases did not gain wide support, as autopsy and epidemiological studies shifted the attention towards other mechanisms, some of which have now become established risk factors. In recent years, however, it has become apparent that recognised risk factors for coronary heart disease (CHD) do not fully explain the diversity of this disease, or why risk factor modifications have not reduced its incidence as much as has been predicted. Recent observations have prompted research into other potential and hitherto unrecognised influences in the causation of atherogenesis. Amongst these, chronic infection by Gram-negative bacteria and herpesviridae have been shown to have a major role. Current evidence indicates that chronic Chlamydia pneumoniae infection may play a causal role in atherogenesis.