Abstract
The most effective treatment for ST-elevation myocardial infarction (MI) is primary percutaneous coronary intervention to achieve early coronary reperfusion.1 Antithrombotic therapy, statins, angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers), and β-blockers have all been shown to favorably modify early and late outcomes after ST-elevation MI and are incorporated into routine practice.2 During prolonged ischemia, lactic acidosis and elevated ATP disrupt key transport mechanisms, leading to intracellular calcium overload, autophagy and apoptosis.3 Primary percutaneous coronary intervention restores coronary reperfusion but is also paradoxically associated with reperfusion injury with the generation of oxygen free radicals and proinflammatory neutrophil infiltrates that can exacerbate apoptosis and cell death.3 Myocardial protection is a concept in which the potential adverse effects of reperfusion injury can be attenuated. The main strategy has been to favorably modify target pathways either through specific agents or by general measures such as remote preconditioning in which cells are exposed to moderate levels of ischemia and enhance their protective pathways.4 In spite of clear biological plausibility and favorable …
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