Possible mechanisms of C-reactive protein mediated acute myocardial infarction.

Myocardial infarction is a relevant cardiovascular event worldwide for morbidity and mortality. It has been theorized that acute myocardial infarctions (AMIs) and other acute coronary events that are precipitated by atherosclerosis are due to arterial blockage from fat deposits. It is now known, however, that atherosclerosis involves more than just lipids. Inflammation has also been studied extensively to play a substantial role in myocardial infarction. There have been debates and conflicting reports over the past few years about the value of assessing levels of C-reactive protein and other biomarkers of inflammation for the prediction of cardiovascular events. Several studies have shown that CRP is not only an inflammatory marker, but also involved in the pathogenesis of myocardial infarction. Studies have linked atherogenesis and rupture of atherosclerotic lesion to endothelial dysfunction. CRP directly inhibits endothelial cell nitric oxide (NO) production via destabilizing endothelial NO synthase (eNOS). Decreased NO release causes CRP mediated inhibition of angiogenesis, stimulating endothelial cell apoptosis. CRP can also activate the complement system through the classical pathway. Complement activation plays an important role in mediating monocyte and neutrophil recruitment in an injured myocardium and may therefore lead to increase in infarct size. This article discusses the possible roles of CRP in complement activation, endothelial dysfunction and its impact on the development of myocardial infarction. We also reviewed the possible therapeutic approaches to myocardial infarction.