Reducing myocardial infarct size: myth or reality

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Reducing myocardial infarct size: myth or reality

Derek J. Hausenloy, MD, PhD, FACC, FESC

Derek J. Hausenloy, MD, PhD, FACC, FESC

Cardiovascular and Metabolic Disorders Program, Duke-NUS Graduate Medical School, Singapore, Singapore; National Heart Research Institute Singapore, National Heart Centre Singapore, Singapore 169609, Singapore; The Hatter Cardiovascular Institute, Institute of Cardiovascular Science, University College London, UK; National Institute of Health Research University College London Hospitals Biomedical Research Centre, London, UK

  • This year marks the 30th anniversary of the first report of “ischemic preconditioning,” which after reperfusion is the most powerful endogenous intervention for reducing myocardial infarct (MI) size. The last 3 to 4 decades have witnessed the accumulation of a huge amount of published literature in the research field of “cardioprotection”—a term used here to describe mechanical and pharmacological interventions for reducing MI size. Much of the research has focused on targeting “myocardial reperfusion injury,” which denotes the myocardial injury and cardiomyocyte death that paradoxically occur on reperfusing acutely ischemic myocardium and which has been demonstrated to contribute up to 50% of the final MI size. Despite timely reperfusion by primary percutaneous coronary intervention (PPCI), mortality and morbidity after an acute ST-segment elevation MI (STEMI) remain significant, with 7% death and 22% heart failure at 1-year follow-up. Thus, novel cardioprotective therapies are required to target myocardial reperfusion injury and reduce MI size in order to preserve left ventricular systolic function and prevent the onset of heart failure after STEMI. However, the results of a large number of clinical studies in reperfused STEMI patients have failed to demonstrate reduced MI size and improved clinical outcomes. The reasons for this are multiple and complex and have been discussed extensively in the literature; they can be attributed to problems with the design of both experimental and clinical studies used to test novel cardioprotective therapies.
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