Microbes have been proposed as inciting agents of tissue injury and inflammation, both of which underlie the pathogenesis of atherosclerosis. Viruses, including the herpes simplex virus and cytomegalovirus, as well as bacteria such as Chlamydia pneumoniae, have been implicated in the process. In vitro, these agents promote a proinflammatory and a procoagulant phenotype in vascular cells. Viruses augment cell accumulation through alterations of apoptosis. Infectious agents may play a role in pathogenesis of atherosclerosis by triggering an autoimmune response due to microbial molecular mimicry. It is unlikely that a single agent is the sole cause or modulator of this heterogeneous disease. Contradictory epidemiological studies may be reconciled with a new construct suggesting that multiple pathogens infecting an individual in aggregate may promote an inflammatory and procoagulant environment that underlies the pathogenesis of atherosclerosis.
- Myocardial infarction