Is there an infective aetiology to atherosclerosis?

Conventional cardiovascular risk factors fail to completely explain the observed variations in the prevalence and severity of coronary heart disease (CHD). Common chronic infections may have an aetiological role in the development of atherosclerosis and CHD, either independently or by interacting with traditional atherogenic risk factors. The evidence for Chlamydia pneumoniae as a potential causative agent is strongest, and is based on findings of numerous sero-epidemiological studies, examination of atheromatous plaque specimens, in vitro animal models and, recently, pilot antichlamydial antibiotic intervention trials. However, the complete natural history of C. pneumoniae, its mechanisms of damage in atherosclerotic disease, and the temporal sequence of infection and CHD remain unclear. Confirmation of true causality for the link between C. pneumoniae and CHD could come after the results of large-scale prospective antibiotic trials, which are to be conducted over the next few years. A proven association could have important implications for public health worldwide, potentially leading to novel and relatively inexpensive therapeutic measures in the secondary prevention of CHD--broad-spectrum antibiotics.