大庆油田总医院 温尚煜课程.ppt

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53岁,男性 心前区疼痛4小时入院 高血压,吸烟 心电图: Ⅱ, Ⅲ, aVF ST-段抬高 欣维宁静点 用Diver吸栓导管吸栓 继续吸栓 吸栓,冠脉内异搏定,欣维宁 最终结果 谢谢! 多取出,少放入——林延龄,CISC﹠CCC2010 Slide * Myocardial infarction: Thrombosis superimposed upon atherosclerosis Myocardial infarction is an acute event that occurs when a thrombus or clot suddenly reduces blood flow through a coronary artery. The underlying cause of myocardial infarction is coronary atherosclerosis, a chronic inflammatory disease process that usually begins in late childhood and adolescence. Atherosclerotic plaque forms over time in the coronary arteries – Plaque consists of soft atheroma (or lipid pool), an infiltration of white blood cells that engulf the lipids and forms foam cells, and a fibrous cap. Plaques gradually narrow the arteries supplying the heart muscle. If the narrowing is greater than 50% it may restrict blood flow to the heart muscle sufficiently that the individual experiences chest pain (angina) when under physical or emotional stress. Myocardial infarction consists of a chain of events. It usually begins when the surface of an atheromatous plaque in the coronary arteries ruptures, as a result of shear stress from flowing blood, inflammation of the plaque, or other factors (such as flexion or tension of the fibrous cap). Such factors may cause endothelial cells covering the plaque to become injured and thinned, and to rupture. This exposes the subendothelial adhesion molecules, triggering local platelet aggregation and activation, and formation of a thrombus on the ruptured plaque. * May be useful in STEMI patients with short ischemic times and large clot burdens Figure 2. Myocardial Reperfusion Data on Angiography and Electrocardiography, According to Treatment Group. The percentages of patients are shown according to myocardial blush grade on the angiogram (Panel A) and the degree of resolution of ST-segment elevation (Panel B) and persistent ST-segment deviation (Panel C) on the electrocardiogram. PCI d

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