Intra-myocardial hemorrhage and cardiac microvascular injury in ischemia/reperfusion. A systematic review of current evidences

IF 3 3区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS

Current Problems in Cardiology Pub Date : 2024-11-05 DOI:10.1016/j.cpcardiol.2024.102918

Konstantin V. Zavadovsky MD, PhD, DrSc , Vyacheslav V. Ryabov MD, PhD, DrSc , Evgeny V. Vyshlov MD, PhD, DrSc , Olga V. Mochula MD, PhD , Maria Sirotina MD , Artur Kan MD , Alexander V. Mukhomedzyanov MD, PhD , Ivan A. Derkachev MD , Nikita S. Voronkov MD, PhD , Andrey V. Mochula MD, PhD , Alexandra S. Maksimova MD, PhD , Leonid N. Maslov MD, PhD, DrSc

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Abstract

The in-hospital mortality rate in acute myocardial infarction (AMI) remains high despite the undoubted achievements in treatment of this disease achieved in the last 40 years. The dangerous complications of AMI remain cardiac microvascular injury (CMI) and intramyocardial hemorrhage (IMH). IMH is a widespread pathology that occurs in 42 – 57% of patients with ST-segment elevation myocardial infarction and percutaneous coronary intervention. IMH is associated with larger infarct size and contractile dysfunction. IMH is accompanied by inflammation. The appearance of IMH is depending on the duration of ischemia and requires reperfusion of the heart. IMH is accompanied by contractile dysfunction and adverse remodeling of the heart. The most likely cause of IMH is CMI. Pretreatment with ATL-146e, melatonin, tanshinone IIA, relaxin, empagliflozin, dapagliflozin, and astragaloside IV can mitigate I/R-induced CMI. CMI is accompanied by an increase in the myocardial and plasma proinflammatory cytokine levels and also the downregulation of tight junction proteins in cardiac vascular endothelial cells. However, there is no convincing evidence that proinflammatory cytokines trigger CMI. An increase in the proinflammatory cytokine levels and CMI could be two independent processes.

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缺血/再灌注时的心肌内出血和心脏微血管损伤。当前证据的系统回顾。

尽管在过去 40 年中，急性心肌梗死（AMI）的治疗取得了毋庸置疑的成就，但其院内死亡率仍然居高不下。急性心肌梗死的危险并发症仍然是心脏微血管损伤（CMI）和心肌内出血（IMH）。心肌内出血是一种广泛的病理现象，在 ST 段抬高型心肌梗死和经皮冠状动脉介入治疗的患者中，42% 到 57% 都会发生心肌内出血。IMH 与梗死面积增大和收缩功能障碍有关。IMH 还伴有炎症。IMH 的出现取决于缺血时间的长短，需要对心脏进行再灌注。IMH 伴有收缩功能障碍和心脏的不良重塑。导致 IMH 的最可能原因是 CMI。使用 ATL-146e、褪黑素、丹参酮 IIA、松弛素、empagliflozin、dapagliflozin 和黄芪甲苷 IV 进行预处理可减轻 I/R 诱导的 CMI。CMI 伴随着心肌和血浆中促炎细胞因子水平的升高，以及心脏血管内皮细胞中紧密连接蛋白的下调。然而，没有令人信服的证据表明促炎细胞因子会引发 CMI。促炎细胞因子水平的升高和 CMI 可能是两个独立的过程。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Current Problems in Cardiology 医学-心血管系统

CiteScore

4.80

自引率

2.40%

发文量

392

审稿时长

6 days

期刊介绍： Under the editorial leadership of noted cardiologist Dr. Hector O. Ventura, Current Problems in Cardiology provides focused, comprehensive coverage of important clinical topics in cardiology. Each monthly issues, addresses a selected clinical problem or condition, including pathophysiology, invasive and noninvasive diagnosis, drug therapy, surgical management, and rehabilitation; or explores the clinical applications of a diagnostic modality or a particular category of drugs. Critical commentary from the distinguished editorial board accompanies each monograph, providing readers with additional insights. An extensive bibliography in each issue saves hours of library research.