Leonid N Maslov, Natalia V Naryzhnaya, Sergey V Popov, Alexandr V Mukhomedzyanov, Ivan A Derkachev, Boris K Kurbatov, Andrey V Krylatov, Feng Fu, Jianming Pei, Vyacheslav V Ryabov, Evgenii V Vyshlov, Svetlana V Gusakova, Alla A Boshchenko, Akpay Sarybaev
{"title":"A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena.","authors":"Leonid N Maslov, Natalia V Naryzhnaya, Sergey V Popov, Alexandr V Mukhomedzyanov, Ivan A Derkachev, Boris K Kurbatov, Andrey V Krylatov, Feng Fu, Jianming Pei, Vyacheslav V Ryabov, Evgenii V Vyshlov, Svetlana V Gusakova, Alla A Boshchenko, Akpay Sarybaev","doi":"10.7555/JBR.37.20230021","DOIUrl":null,"url":null,"abstract":"<p><p>The analysis of experimental data demonstrates that platelets and neutrophils are involved in the no-reflow phenomenon, also known as microvascular obstruction (MVO). However, studies performed in the isolated perfused hearts subjected to ischemia/reperfusion (I/R) do not suggest the involvement of microembolization and microthrombi in this phenomenon. The intracoronary administration of alteplase has been found to have no effect on the occurrence of MVO in patients with acute myocardial infarction. Consequently, the major events preceding the appearance of MVO in coronary arteries are independent of microthrombi, platelets, and neutrophils. Endothelial cells appear to be the target where ischemia can disrupt the endothelium-dependent vasodilation of coronary arteries. However, reperfusion triggers more pronounced damage, possibly mediated by pyroptosis. MVO and intra-myocardial hemorrhage contribute to the adverse post-infarction myocardial remodeling. Therefore, pharmacological agents used to treat MVO should prevent endothelial injury and induce relaxation of smooth muscles. Ischemic conditioning protocols have been shown to prevent MVO, with L-type Ca <sup>2+</sup> channel blockers appearing the most effective in treating MVO.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"37 4","pages":"281-302"},"PeriodicalIF":2.2000,"publicationDate":"2023-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10387746/pdf/","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomedical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.7555/JBR.37.20230021","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 1
Abstract
The analysis of experimental data demonstrates that platelets and neutrophils are involved in the no-reflow phenomenon, also known as microvascular obstruction (MVO). However, studies performed in the isolated perfused hearts subjected to ischemia/reperfusion (I/R) do not suggest the involvement of microembolization and microthrombi in this phenomenon. The intracoronary administration of alteplase has been found to have no effect on the occurrence of MVO in patients with acute myocardial infarction. Consequently, the major events preceding the appearance of MVO in coronary arteries are independent of microthrombi, platelets, and neutrophils. Endothelial cells appear to be the target where ischemia can disrupt the endothelium-dependent vasodilation of coronary arteries. However, reperfusion triggers more pronounced damage, possibly mediated by pyroptosis. MVO and intra-myocardial hemorrhage contribute to the adverse post-infarction myocardial remodeling. Therefore, pharmacological agents used to treat MVO should prevent endothelial injury and induce relaxation of smooth muscles. Ischemic conditioning protocols have been shown to prevent MVO, with L-type Ca 2+ channel blockers appearing the most effective in treating MVO.
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