Department of Cardiology, Osaka City General Hospital, Osaka 534-0021, Japan.
J Atheroscler Thromb. 2013;20(6):524-37. doi: 10.5551/jat.17608. Epub 2013 Apr 30.
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.
炎症和氧化应激在动脉粥样硬化斑块不稳定中起关键作用,斑块破裂/侵蚀以及随后的血栓形成构成了血管完全闭塞和急性 ST 段抬高型心肌梗死(STEMI)的主要机制。斑块破裂触发初始血小板聚集的形成,这些聚集物与纤维蛋白形成的增加相关,导致持续的冠状动脉血流阻塞和血液凝结。纤维蛋白网络可能会捕获大量红细胞和炎症细胞,形成富含红细胞的血栓。事实上,以前的临床研究表明,在急性冠状动脉综合征患者中,血管内镜不仅可以观察到富含血小板的白色血栓,还可以观察到富含红细胞的红色血栓。最近,血栓抽吸和远端保护装置的发展显著改善了 STEMI 患者经皮介入治疗的临床结果,并能够评估生前冠状动脉血栓。这一点很重要,因为以前的尸检研究无法区分导致心肌缺血的冠状动脉血栓与死后血栓。通过对抽吸血栓的冷冻样本和特定的单克隆抗体进行研究,我们研究了血栓的细胞成分(血小板、红细胞、纤维蛋白和炎症细胞,如髓过氧化物酶阳性细胞),并从病理学上评估了富含红细胞的血栓与炎症、氧化应激和 STEMI 患者临床结局之间的关系。因此,本文重点讨论了血栓抽吸治疗的疗效以及 STEMI 患者抽吸冠状动脉内血栓的成分,并介绍了最近关于抽吸冠状动脉内血栓成分与临床结局之间关系的研究结果。