PCI患者围术期的抗血小板治疗1.pptVIP

* 血小板不仅参与了动脉粥样硬化的发生与发展，更重要的是，血小板活化与动脉粥样硬化血栓形成密切相关。如图所示。 国际权威指南都明确推荐抗血小板治疗是ACS二级预防的基本措施。 * 这是稳定斑块和部稳定斑块的示意图。不稳定斑块的纤维帽非常薄，在血液剪切力的作用下纤维帽的肩部特别容易破损，造成斑块破裂形成血栓，导致患者再发缺血性血管事件。 Atherosclerotic plaque has 2 main components: a soft, lipid-rich core and a hard, collagen-rich fibrous cap. In stable plaques, a thick fibrous cap may represent 70% of plaque volume. It stabilizes the plaque and prevents it from undergoing rupture. In contrast, unstable plaque has a thin fibrous cap and is at greater risk for rupture. In unstable plaque, the lipid-rich core may represent the majority of the plaque volume. The core is rich in extracellular lipids, which are formed by trapping blood-derived lipids, notably low-density lipoprotein, or by lipid-filled macrophages, known as foam cells. The plaque destabilizes due to inflammation by foam cells and other inflammatory mediators that make the plaque more vulnerable to rupture. This commonly occurs at the junction of the plaque and the less diseased vessel wall. As a result, the lipid core may be exposed to flowing blood leading to platelet-mediated thrombus formation. Falk reviewed the work of other investigators regarding the severity of stenosis and its association with the risk of MI. Results showed that 86% of MIs resulted from lesions that were 70% stenosed. Most experts prior to Falk thought that patients had heart attacks because of blockages that increased in size until they blocked the blood vessel and caused a heart attack.1 Based on the findings of Falk, we now know the primary cause of a heart attack is the rupture of unstable plaques that are 70% stenosed and are clinically silent. Approximately 200 patients from 4 studies were studied to generate these results, which have been confirmed in other studies.1 References 1 Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657-671. 2 Libby P. Molecular bases of the acute coronary syndromes. Circulation. 1995;91:2844-2850. * 尽管NSTEMI的院内死亡率低于STEMI， 但远期预后（1年）