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CC BY-NC-ND 4.0 · Hamostaseologie 2023; 43(02): 110-121
DOI: 10.1055/a-1739-9351
Review Article

Platelets in Myocardial Ischemia/Reperfusion Injury

Nancy Schanze
1   Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany
2   Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany
,
Muataz Ali Hamad
1   Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany
3   Spemann Graduate School of Biology and Medicine (SGBM), University of Freiburg, Freiburg, Germany
4   Faculty of Biology, University of Freiburg, Freiburg, Germany
,
Thomas Georg Nührenberg
5   Department of Cardiology and Angiology II, Heart Center, University of Freiburg, Freiburg, Germany
6   Institute for Experimental and Clinical Pharmacology and Toxicology, University of Freiburg, Freiburg, Germany
,
Christoph Bode
1   Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany
,
Daniel Duerschmied
1   Department of Cardiology and Angiology I, Heart Center, University of Freiburg, Freiburg, Germany
2   Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Germany
7   European Center for AngioScience (ECAS) and German Center for Cardiovascular Research (DZHK) partner site Heidelberg/Mannheim, Mannheim, Germany
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Abstract

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.

Keywords

myocardial infarction - ischemia reperfusion injury - platelets - reperfusion - ischemia


Publication History

Received: 15 June 2021

Accepted: 13 January 2022

Article published online:
29 July 2022

© 2022. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

Georg Thieme Verlag KG
Rüdigerstraße 14, 70469 Stuttgart, Germany

 

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