微血管阻塞和心肌内出血在再灌注性心脏损伤中的作用。临床数据分析。
The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data.
作者信息
Ryabov Vyacheslav V, Vyshlov Evgenii V, Maslov Leonid N, Naryzhnaya Natalia V, Mukhomedzyanov Alexandr V, Boshchenko Alla A, Derkachev Ivan A, Kurbatov Boris K, Krylatov Andrey V, Gombozhapova Aleksandra E, Dil Stanislav V, Samoylova Julia O, Fu Feng, Pei Jian-Ming, Sufianova Galina Z, Diez Emiliano R
机构信息
Department of Emergency Cardiology and Laboratory of Experimental Cardiology, Cardiology Research Institute, branch of the Federal State Budgetary Scientific Institution "Tomsk National Research Medical Center of the Russian Academy of Sciences", 634012 Tomsk, Russia.
Department of Physiology and Pathophysiology, National Key Discipline of Cell Biology, School of Basic Medicine, Fourth Military Medical University, 710032 Xi'an, Shaanxi, China.
出版信息
Rev Cardiovasc Med. 2024 Mar 14;25(3):105. doi: 10.31083/j.rcm2503105. eCollection 2024 Mar.
Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41-50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn't been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type channel blockers result in the long-term improvement of coronary blood flow in patients with MVO.
冠状动脉微血管阻塞（MVO）会促使急性心肌梗死（AMI）和经皮冠状动脉介入治疗（PCI）患者的死亡率及主要不良心脏事件增加。在41%-50%的ST段抬高型心肌梗死和PCI患者中可观察到心肌内出血（IMH）。IMH的发生伴有炎症。有证据表明微血栓不参与MVO的发展。MVO的出现与梗死面积、心脏缺血持续时间及心肌水肿有关。然而，尚无确凿证据表明心肌水肿在MVO的发展中起重要作用。有证据表明血小板、炎症、超负荷、神经肽Y和内皮素-1可能参与MVO的发病机制。在AMI和PCI患者中，内皮细胞损伤在MVO形成中的作用仍不清楚。MVO患者的一氧化氮生成是否减少尚不清楚。仅获得了关于炎症参与MVO发展的间接证据。活性氧（ROS）在MVO发病机制中的作用尚未研究。坏死性凋亡和炎性小体在AMI和PCI患者MVO发病机制中的作用也未研究。血栓素A2、血管加压素、血管紧张素II和前列环素平衡在MVO形成中的意义目前尚不清楚。关于冠状动脉痉挛在MVO发展中作用的确凿证据尚未确立。此前尚未对AMI和PCI患者的神经肽Y、内皮素-1水平与MVO大小进行相关性分析。肾上腺素是否会加重心肌细胞的再灌注坏死尚不清楚。双联抗血小板治疗可提高PCI预防MVO的疗效。肾上腺素或L型钙通道阻滞剂是否能使MVO患者的冠状动脉血流得到长期改善尚不清楚。
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