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Thrombus Aspiration Therapy and Coronary Thrombus Components in Patients with Acute ST-Elevation Myocardial Infarction

机译:急性ST段抬高型心肌梗死患者的血栓抽吸疗法和冠状动脉血栓成分

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Inflammation and oxidative stress play key roles in atherosclerotic plaque instability, and plaque rupture/erosion and subsequent thrombus formation constitute the principal mechanisms of total vessel occlusion and acute ST-elevation myocardial infarction (STEMI). Plaque disruption triggers the formation of initial platelet aggregates that grow in association with an increase in fibrin formation, leading to persistent coronary flow obstruction and blood coagulation. The fibrin network may trap large numbers of erythrocytes and inflammatory cells to form an erythrocyte-rich thrombus. In fact, previous clinical studies have shown that not only platelet-rich white thrombi, but also erythrocyte-rich red thrombi can be visualized using angioscopy in patients with acute coronary syndrome. Recently, the development of thrombus aspiration and distal protection devices has significantly improved the clinical outcomes of percutaneous intervention in STEMI patients and has enabled the evaluation of antemortem coronary artery thrombi. This is important because previous autopsy studies were unable to differentiate coronary thrombi responsible for myocardial ischemia from postmortem clots. Using frozen samples of aspirated thrombi and specific monoclonal antibodies, we investigated the cellular components of thrombi (platelets, erythrocytes, fibrin and inflammatory cells, such as myeloperoxidase-positive cells) and pathologically evaluated the relationships between erythrocyte-rich thrombi and inflammation, oxidative stress and clinical outcomes in STEMI patients. Therefore, this review article focuses on the efficacy of thrombus aspiration therapy and the components of aspirated intracoronary thrombi in STEMI patients and presents the results of recent studies regarding the relationship between the composition of aspirated intracoronary thrombi and clinical outcomes.
机译:炎症和氧化应激在动脉粥样硬化斑块不稳定性中起关键作用,并且斑块破裂/侵蚀和随后的血栓形成是总血管闭塞和急性ST抬高型心肌梗塞(STEMI)的主要机制。斑块破裂触发了初始血小板聚集体的形成,该聚集体随着血纤蛋白形成的增加而增长,导致持续性冠状动脉血流阻塞和血液凝固。纤维蛋白网络可捕获大量的红细胞和炎性细胞,形成富含红细胞的血栓。实际上,以前的临床研究表明,在急性冠状动脉综合征患者中,不仅可以使用血小板丰富的白色血栓,而且可以使用血管造影的方式来查看富含红细胞的红色血栓。近来,血栓抽吸和远端保护装置的开发显着改善了STEMI患者经皮介入治疗的临床效果,并能够评估死前冠状动脉血栓。这一点很重要,因为以前的尸检研究无法区分死后血栓和引起心肌缺血的冠状动脉血栓。使用吸入的血栓和特异性单克隆抗体的冷冻样品,我们研究了血栓的细胞成分(血小板,红细胞,纤维蛋白和炎性细胞,例如髓过氧化物酶阳性细胞),并通过病理学评估了富血红素血栓与炎症,氧化应激之间的关系。和STEMI患者的临床结局。因此,这篇综述文章着重于STEMI患者的血栓抽吸疗法和冠状动脉内血栓抽吸的成分,并介绍了有关冠状动脉内血栓抽吸物的成分与临床结局之间关系的最新研究结果。

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