The mechanisms by which infectious agents may contribute to atherosclerosis and its clinical manifestations.

Three infectious agents have recently gained considerable interest as potential pathogens in atherosclerosis and in its clinical manifestations: herpes simplex virus, cytomegalovirus, and Chlamydia pneumoniae. Chronic and often asymptomatic infections with these agents occur widely in the general population. These pathogens may affect atherosclerosis either directly or indirectly. Direct effects on vascular wall cells might include cell lysis, transformation, lipid accumulation, proinflammatory changes, and augmentation of procoagulant activity. Indirect systemic effects may involve induction of acute-phase proteins, establishment of a prothrombotic state, hemodynamic stress caused by tachycardia, increased cardiac output, or a regional inflammatory activation in response to systemic endotoxemia and cytokinemia. The effects of microbial infection, usually in combination with other risk factors (for example, smoking, hyperlipidemia, family history), might promote atherogenesis and eventually trigger acute coronary events.