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Myocardial protection: is primary PCI enough?

Nature Clinical Practice Cardiovascular Medicine volume 6, pages 12–13 (2009)Cite this article

Timely and effective myocardial reperfusion using primary percutaneous coronary intervention (PCI) remains the most effective treatment strategy for limiting myocardial infarct size, reducing left ventricular remodeling, preserving left ventricular systolic function and improving clinical outcomes following a ST-segment elevation myocardial infarction (STEMI). Criteria exist for determining the most suitable reperfusion strategy for patients presenting with a STEMI, and are based on the time from onset of symptoms, the presence of risk factors and the medical facilities available. A huge research effort continues in an attempt to further refine the optimum antithrombotic and antiplatelet therapy required to maintain the patency of the infarct-related coronary artery. Despite optimum primary PCI, the mortality and morbidity following a STEMI remains sizable. Clearly, primary PCI alone is not enough to eliminate the risk of future cardiovascular events entirely. Novel cardioprotective strategies are, therefore, required to further improve clinical outcomes in this patient group.

A largely overlooked treatment strategy is to protect the myocardium from the detrimental effects that arise from the process of myocardial reperfusion itself. Somewhat paradoxically, the actual process of restoring coronary blood flow to previously ischemic myocardium can in itself exacerbate the myocardial injury sustained during ischemia—a phenomenon termed 'myocardial reperfusion injury' (reviewed fully elsewhere1). Previous attempts to limit this form of myocardial injury in patients after a STEMI—using pharmacological strategies involving antioxidant therapy, calcium-channel antagonists, anti-inflammatory agents, and sodium–hydrogen exchange inhibitors as adjuncts to primary PCI—have on the whole produced disappointing results. As a result, investigators are now re-examining the current process for translating an experimental cardioprotective strategy into the clinic.1 Potential shortfalls of the current process include the design of clinical studies and the inadequacy of the animal infarct models currently used.2 The clinical relevance of these models has been questioned, as has their failure to take into account the effects of comorbid illnesses such as diabetes mellitus and hypertension, and factors such as age and hypercholesterolemia.

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Authors and Affiliations

  1. DJ Hausenloy is a Senior Clinical Research Fellow, and DM Yellon is Director of the Hatter Cardiovascular Institute, University College London, London, UK.,

    Derek J Hausenloy & Derek M Yellon

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  1. Derek J Hausenloy
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  2. Derek M Yellon
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Correspondence to Derek M Yellon.

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The authors declare no competing financial interests.

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Hausenloy, D., Yellon, D. Myocardial protection: is primary PCI enough?. Nat Rev Cardiol 6, 12–13 (2009). https://doi.org/10.1038/ncpcardio1371

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