[临床医学]急性冠脉综合症.ppt

ACS治疗原则 开通血管并保持通畅 预防血栓再次形成 稳定心脏电与机械力功能 基本措施 抗凝、抗血小板、抗缺血及溶栓等 他汀类药物、介入治疗 既往无心绞痛 无持续性胸痛 未曾使用抗缺血药 ECG正常或无变化 心肌酶阴性 年轻患者 新发/加重心绞痛 静息痛或持续性痛(20分钟) 无ST段变化 心肌酶阴性 静息痛/持续性痛 心梗后心绞痛 已积极抗缺血治疗 ST段有动态变化 心肌酶阳性 高龄患者 无ST段抬高型ACS的危险分层 低危 中危 高危 无ST段持续抬高 中危 高危 低危 阿斯匹林或与GPⅡb/Ⅲa拮抗剂合用 肝素、β受体阻滞剂、硝酸酯类、他汀类 钙通道阻滞剂？、 ACEI？ 内科治疗 门诊危险分层 反复缺血发作 危险性分层试验（运动负荷试验、灌注显像、心功能测定等） 阳性 阴性 内科治疗 冠脉造影 血管重建 胸痛≤12h 胸痛≥12h ST段持续抬高 直接PCI 溶栓 择期冠脉造影 PCI或者CABG 抗凝、抗血小板 抗缺血、他汀 ACEI？ 展 望 在我国尽早在三级医院建立胸痛中心 并制定相关ACS诊治规范 临床前诊断出不稳定斑块并干预 一级预防  Thank you for your time ! * The mechanism of action of clopidogrel is similar to that of ticlopidine but different from that of aspirin.[1] Both clopidogrel and ticlopidine require biotransformation for their pharmacologic activity. Clopidogrel is a potent, noncompetitive inhibitor of ADP-induced platelet aggregation. Clopidogrel inhibits the binding of ADP to platelet membrane receptors. The effect of clopidogrel on ADP binding is irreversible[2] and lasts for the duration of platelet life, about 7 to 10 days. The inhibition is also specific and does not significantly affect cyclooxygenase or arachidonic acid metabolism.[1] Both low- and high-affinity ADP receptors are present on platelets, and the active metabolite of clopidogrel binds to the low-affinity receptors.[1] ADP binding to this site is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen. Fibrinogen links different platelets together to form the platelet aggregate.[3] Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding with fibrinogen.[3] Aspirin inhibits the cyclooxygenase enzyme, preventing the production of prostaglandin and thromboxane A2 (TXA2) from arachidonic acid.[3] TXA2 activates the GP IIb/IIIa binding site on the platelet, allowing fibrinogen to bind. Aspirin also exerts its effects on other parts of the body system.[3] Paradoxically, aspirin blocks synthesis of prostacyclin by e