Atorvastatin on vascular endothelial function in patients with ACS and the impact of inflammatory cytokines.docVIP

 PAGE \* MERGEFORMAT 4 Atorvastatin on vascular endothelial function in patients with ACS and the impact of inflammatory cytokines [Keywords:] asymmetric dimethylarginine atorvastatin in acute coronary syndrome Acute coronary syndrome (ACS) is due to the unstable coronary artery plaque rupture, resulting in acute thrombosis caused by acute cardiac ischemia syndrome, including unstable angina and acute non-ST-lift High-myocardial infarction, acute ST-segment elevation myocardial infarction and cardiac ischemic death. Studies have shown that, ACS, 60% to 70% of patients with only mild or moderate coronary stenosis, while the endothelial dysfunction, local inflammatory activity as well as lipid-rich plaque rupture, leading to coronary thrombosis, is caused by the pathological mechanism of ACS. Therefore, endothelial dysfunction, atherosclerosis is not only the early signs of atherosclerosis and is involved in the development of the entire process. 1 ADMA and Vascular Endothelial Function The basic factors that determine endothelial function is the synthesis and secretion by endothelial cells in the production of nitric oxide, degradation and the adjustment process. Nitric oxide is by the endothelial nitric oxide synthase in the catalysis of L-arginine generated citrulline released at the same time, it by activating guanylate cyclase to increase intracellular cyclic guanosine monophosphate, maintain vasodilation , inhibit platelet activation, adhesion and aggregation against endothelium-derived vasoconstrictor substances, and inhibit LDL oxidation, inhibit monocyte adhesion, reduce oxygen free radical production and smooth muscle cell proliferation, in order to protect the normal endothelial function, inhibit arterial the occurrence of atherosclerosis. In recent years, studies have shown that: endothelial nitric oxide synthase inhibitor of endogenous - asymmetric dimethylarginine (asymmetric dimethylarginine, ADMA) as an endothelium-dependent vasodilatatio