非ST段抬高性急性冠状动脉综合征2009(Non-st segment elevation acute coronary syndrome 2009).doc

非ST段抬高性急性冠状动脉综合征2009(Non-st segment elevation acute coronary syndrome 2009).doc

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非ST段抬高性急性冠状动脉综合征2009(Non-st segment elevation acute coronary syndrome 2009)

非ST段抬高性急性冠状动脉综合征2009(Non-st segment elevation acute coronary syndrome 2009) The author of guangdong provincial peoples hospital: jin lijun Non-st-segment elevation acute coronary syndromes (nste-acs) include unstable angina (UAP) and non-st-segment elevation myocardial infarction (NSTEMI), formerly known as non-q Wave myocardial infarction (NQMI), is caused by unstable atherosclerotic plaque, incomplete related artery occlusive thrombosis of platelet on white blood clots, type is different from st-elevation acute coronary syndrome (STE - ACS) in coronary artery occlusive red thrombus. Therefore, the treatment strategy of NSTE - ACS is very different from that of ste-acs. Epidemiology and pathophysiology In the United States, more than 1.4 million people are hospitalized for [1] every year, 70 percent of whom are diagnosed with UAP and NSTEMI, and 30 percent of patients with st-elevation myocardial infarction (STEMI). From a global register, the semiannual survival rate of patients with nste-acs increased from 1999 to 2006. Reduce the number of death from coronary heart disease in the United States each year about half is benefit from the control of risk factors: such as lowering serum cholesterol, effective control of blood pressure, smoking, much more is to benefit from treatment improvement [2, 3]. In addition, the mortality of patients with lower thanks to the specificity of cardiac troponin testing, making clinical more sensitive to myocardial necrosis (which in turn can identify a smaller range of NSTEMIs), now troponin as a biomarker of the specificity of the diagnosis of myocardial necrosis. In the past more than a year of time, pathophysiology research allows us to had a deeper understanding of coronary plaque rupture, for the vast majority of the ACS event provides the basis of pathophysiology [4]. As we can better understand the biological behavior of coronary artery plaque, hope will enable us to better identify vulnerable lesions and find out the more ef

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