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      Myocardial ischaemia–reperfusion injury and cardioprotection in perspective

      Nature Reviews Cardiology
      Springer Science and Business Media LLC

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          Abstract

          <p class="first" id="d37382553e53">Despite the increasing use and success of interventional coronary reperfusion strategies, morbidity and mortality from acute myocardial infarction are still substantial. Myocardial infarct size is a major determinant of prognosis in these patients. Therefore, cardioprotective strategies aim to reduce infarct size. However, a perplexing gap exists between the many preclinical studies reporting infarct size reduction with mechanical and pharmacological interventions and the poor translation into better clinical outcomes in patients. This Review revisits the pathophysiology of myocardial ischaemia-reperfusion injury, including the role of autophagy and forms of cell death such as necrosis, apoptosis, necroptosis and pyroptosis. Other cellular compartments in addition to cardiomyocytes are addressed, notably the coronary microcirculation. Preclinical and clinical research developments in mechanical and pharmacological approaches to induce cardioprotection, and their signal transduction pathways, are discussed. Additive cardioprotective interventions are advocated. For clinical translation into treatments for patients with acute myocardial infarction, who typically are of advanced age, have comorbidities and are receiving several medications, not only infarct size reduction but also attenuation of coronary microvascular obstruction, as well as longer-term targets including infarct repair and reverse remodelling, must be considered to improve patient outcomes. Future clinical trials must focus on patients who really need adjunct cardioprotection, that is, those with severe haemodynamic alterations. </p>

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          Author and article information

          Journal
          Nature Reviews Cardiology
          Nat Rev Cardiol
          Springer Science and Business Media LLC
          1759-5002
          1759-5010
          July 3 2020
          Article
          10.1038/s41569-020-0403-y
          32620851
          9b135c6f-9206-456d-a3d0-3b3f2375c4c0
          © 2020

          http://www.springer.com/tdm

          http://www.springer.com/tdm

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