Pathogenesis of atherosclerosis: a possible relation to infection

Abstract

Atherosclerosis is the main underlying cause of coronary heart disease, which in turn is the most common cause of death in the industrialized world. An acute event in coronary heart disease is typically precipitated by thrombosis occurring at the site of atherosclerotic plaque disruption. Atherosclerotic plaques consist of a fibrous cap overlying a lipid-rich core. Many cell types are involved in their formation, including platelets, endothelial cells, activated monocytes, macrophages derived from monocytes and smooth muscle cells. The currently accepted hypothesis is that atherosclerosis develops as a response to injury and that it is primarily a chronic inflammatory condition. The endothelium plays an important role in regulating vascular blood flow and it is now apparent that endothelial dysfunction is an important contributor to the pathogenesis of atherosclerosis. There is growing evidence that infection may be a risk factor for atherosclerosis and myocardial infarction. Numerous studies have reported associations between human coronary heart disease (CHD) and bacterial and viral infections. At present, interest is focused on the potential aetiological role of C. pneumoniae which has been repeatedly identified, using various diagnostic techniques, in atherosclerotic lesions. There is also increasing seroepidemiological evidence of the association between C. pneumoniae and CHD. The role of this organism in atherosclerosis may be analogous to that of chronic C. trachomatis infection in trachoma.