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替格瑞洛对急性心肌梗死患者心肌细胞保护作用的研究现状及进展
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Abstract:
急性心肌梗死(AMI)是由于冠状动脉血供急剧减少或中断,使相应心肌因持久性缺血而发生局部坏死。该病具有极高的发病率和死亡率,严重威胁着患者的健康状况。即使AMI患者及时接受介入治疗,心肌细胞的损伤和死亡仍然存在,这对患者的预后造成了显著影响。替格瑞洛是一种新型的P2Y12受体拮抗剂,其通过可逆、非竞争性地结合血小板表面的P2Y12受体,有效地抑制了血小板的活性。近年来的研究表明,替格瑞洛不仅能够通过抑制血小板聚集来改善冠状动脉的血流,还可以通过多种途径直接或间接地保护心肌细胞,因此成为了研究的焦点。本研究旨在结合近期国内外发表的相关研究,对替格瑞洛在急性心肌梗死患者心肌细胞保护作用方面的研究现状及进展进行综述。
Acute myocardial infarction (AMI) is caused by a rapid reduction or interruption of coronary artery blood supply, leading to local necrosis of the corresponding myocardium due to persistent ischemia. The disease has a very high incidence rate and mortality, which seriously threatens the health of patients. Even if AMI patients receive timely intervention treatment, myocardial cell damage and death still exist, which has a significant impact on the prognosis of patients. Ticagrelor is a novel P2Y12 receptor antagonist that effectively inhibits platelet activity by reversibly and non-competitively binding to the P2Y12 receptor on the surface of platelets. Recent studies have shown that ticagrelor not only improves coronary artery blood flow by inhibiting platelet aggregation, but also directly or indirectly protects myocardial cells through various pathways, making it a focus of research. This study aims to review the current status and progress of research on the cardiomyocyte protective effects of ticagrelor in patients with acute myocardial infarction, based on recent studies published both domestically and internationally.
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