Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany.
Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany.
Hamostaseologie. 2023 Apr;43(2):110-121. doi: 10.1055/a-1739-9351. Epub 2022 Jul 29.
Coronary artery disease, including myocardial infarction (MI), remains a leading cause of global mortality. Rapid reperfusion therapy is key to the improvement of patient outcome but contributes substantially to the final cardiac damage. This phenomenon is called "ischemia/reperfusion injury (IRI)." The underlying mechanisms of IRI are complex and not fully understood. Contributing cellular and molecular mechanisms involve the formation of microthrombi, alterations in ion concentrations, pH shifts, dysregulation of osmolality, and, importantly, inflammation. Beyond their known action as drivers of the development of coronary plaques leading to MI, platelets have been identified as important mediators in myocardial IRI. Circulating platelets are activated by the IRI-provoked damages in the vascular endothelium. This leads to platelet adherence to the reperfused endothelium, aggregation, and the formation of microthrombi. Furthermore, activated platelets release vasoconstrictive substances, act via surface molecules, and enhance leukocyte infiltration into post-IR tissue, that is, via platelet-leukocyte complexes. A better understanding of platelet contributions to myocardial IRI, including their interaction with other lesion-associated cells, is necessary to develop effective treatment strategies to prevent IRI and further improve the condition of the reperfused myocardium. In this review, we briefly summarize platelet properties that modulate IRI. We also describe the beneficial impacts of antiplatelet agents as well as their mechanisms of action in IRI beyond classic effects.
冠状动脉疾病，包括心肌梗死（MI），仍然是全球死亡的主要原因。快速再灌注治疗是改善患者预后的关键，但会对最终的心脏损伤产生重大影响。这种现象称为“缺血/再灌注损伤（IRI）”。IRI 的潜在机制很复杂，尚未完全了解。促成的细胞和分子机制包括微血栓的形成、离子浓度的改变、pH 值变化、渗透压失调，以及重要的炎症。除了已知的作为导致心肌梗死的冠状动脉斑块发展的驱动因素外，血小板也被确定为心肌 IRI 的重要介质。循环血小板被 IRI 引起的血管内皮损伤激活。这导致血小板黏附在再灌注的内皮上，聚集并形成微血栓。此外，激活的血小板释放血管收缩物质，通过表面分子发挥作用，并增强白细胞浸润到再灌注后的组织中，即通过血小板-白细胞复合物。为了开发有效的治疗策略来预防 IRI 并进一步改善再灌注心肌的状况，有必要更好地了解血小板对心肌 IRI 的贡献，包括它们与其他病变相关细胞的相互作用。在这篇综述中，我们简要总结了调节 IRI 的血小板特性。我们还描述了抗血小板药物的有益影响及其在 IRI 中的作用机制，超出了经典作用。
