The Effect Of Atorvastatin On Serum Level Of Matrix Metalloprotease-2 (MMP-2) And Tissue Inhibitors Of Matrix Metalloproteinase-2 (TIMP-2) In Patients With Acute Coronary Syndrome

Background and Objective:Rupture of plaques with thrombosis is considered to be the main reason of acute coronary syndrome (ACS) such as unstable angina (UA) and acute myocardial infarction (AMI). The main components of fibrous cap is extracellular matrix (ECM), and the contents, intensity and thickness of ECM play the very important role in preventing rupture of plaque. Disruption of plaques is easy to occur at sites of thinningof the fibrous cap of the lesion particularly; such rupture leads to hemorrhage into the plaque, thereby resulting in a prothrombotic response followed by rapid occlusion of the artery. The accumulation of macrophage-derived foam cells in vulnerable shoulder regions of atherosclerotic plaques correlates with increased local release of Matrix metalloproteinases (MMPs) and weak fibrous cap tissue and result in plaques rupture. MMPs are a family of zinc-dependent enzymes that play an important role in pathologic state in acute coronary syndrome. Tissue inhibitors of metalloproteinases (TIMPs) are endogenous inhibitors that regulate the activities of MMPs. Recent clinical trials have shown repeatedly that lipid lowering using inhibitors of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase can reduce coronary events and mortality rates. Some trials suggest that statins have beneficial effects independent of lipid lowering, such as decreased macrophage number or activity, anti-inflammation, improvement of endothelial function and so on. The main...