冠心病的基础及临床医学院讲课课件详解.pptVIP

* Unstable plaques are characterized by a large lipid core and thin fibrous cap. Inflammatory cells and activated macrophages are believed to be involved in destabilizing the plaque and the fibrous cap. * Platelets play a central role in the development of thrombi and subsequent ischemic events. The process of platelet-mediated thrombus formation involves adhesion, activation, and aggregation. Within seconds of injury, platelets adhere to collagen fibrils through glycoprotein (GP) Ia/IIa receptors. An adhesive glycoprotein, von Willebrand factor (vWF) allows platelets to stay attached to the subendothelial vessel wall (via GP Ib) despite high shear forces. Following adhesion, platelets are activated to secrete a variety of agonists including thrombin, serotonin, adenosine diphosphate (ADP), and thromboxane A2 (TXA2). These agonists, which further augment the platelet activation process, bind to specific receptor sites on the platelets to activate the GP IIb/IIIa receptor complex, the final common pathway to platelet aggregation. Once activated, the GP IIb/IIIa receptor undergoes a conformational change that enables it to bind with fibrinogen.[1,2] Handin RI. Bleeding and thrombosis. In: Fauci AS, Braunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine. Vol 1. 14th ed. New York, NY: McGraw-Hill; 1998:339-345. Schafer AI. Antiplatelet therapy. Am J Med. 1996;101:199-209. * A cross-section of a coronary artery demonstrating the vulnerable plaque, with its large lipid core and thin fibrous cap * *Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age 70 years, systolic blood pressure 120 mmHg, sinus tachycardia 110 or heart rate 60, increased time since onset of symptoms of STEMI. * STEMI的即时处理 卧床、监护、氧气补充 抗血小板治疗：即可给予阿司匹林300mg ，继之100-300mg qd维持；氯吡格雷300mg，继之75mg qd维持 硝酸酯类药物：对急性心梗无明确治疗作用，但可排除由冠脉痉挛引起的胸痛和ST段抬高，在再灌注治疗前可含服或静脉使用硝酸甘油。对急性心梗合并高血压、急性左心衰竭有治疗