ST段抬高型心肌梗死罪魁祸首病变PCI后另一冠状动脉斑块立即破裂

Oğuz Kılıç, S. Yılmaz
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引用次数: 0

摘要

st段抬高型心肌梗死(STEMI)通常是单冠状动脉血栓形成的结果。急性期多发冠状动脉血栓的发生率很低。多支冠状动脉血栓形成的病因尚不清楚。观察性研究表明,血栓形成背后的斑块不稳定并不仅仅是局部血管原因造成的。这些病理生理过程,如炎症、交感神经活动和儿茶酚胺的排放,在整个冠状动脉网络中起作用,导致多个斑块不稳定。1,2我们认为多发冠状动脉闭塞病变的发病机制可能与心肌梗死急性期多发动脉粥样硬化斑块破裂有关。在我们的病例中,由于前路STEMI,第一次经皮冠状动脉介入治疗是在左前降支进行的。在随访的第二个小时,下STEMI发生,经皮冠状动脉介入治疗边缘肌。
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Immediate Rupture of Another Coronary Plaque After PCI of the Culprit Lesion in ST Segment Elevation Myocardial Infarction
ST-segment elevation myocardial infarction (STEMI) is usually the result of thrombosis in the single coronary artery. The incidence of multiple coronary artery thrombosis in acute phase is very low. The etiology of multivessel coronary thrombosis is still unclear. Observational studies have shown that plaque instability underlying thrombosis is not due to local vascular causes alone. These pathophysiological processes such as inflammation, sympathic activity and catecholamines discharge act across the entire coronary network and cause multiple plaque instability.1,2 We think that the pathogenesis of multiple coronary occlusive lesions may be explained by multiple atherosclerotic plaque rupture during the acute phase of myocardial infarction. In our case, the first percutaneous coronary intervention was performed on the left anterior descending artery due to anterior STEMI. At the second hour of follow-up, inferior STEMI developed and percutaneous coronary intervention was performed on optus marginalis.
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