Published online Mar 26, 2014. doi: 10.4330/wjc.v6.i3.100
Revised: December 17, 2013
Accepted: January 17, 2014
Published online: March 26, 2014
Processing time: 111 Days and 12.4 Hours
In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification of several promising pharmacological (cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proof-of-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease.
Core tip: As therapeutic interventions administered at the time myocardial reperfusion have been proven to reduce infarct size in both experimental and clinical models, the existence of a lethal reperfusion injury and its contribution to ischemic cardiac cell death can no longer be ignored. Patients presenting with an acute ST-segment elevation myocardial infarction will likely benefit from therapy aimed at the timely administration of drugs, most likely via primary percutaneous coronary intervention, for the reduction/prevention of lethal reperfusion injury. This approach will ensure that patients maximally benefit from the myocardial salvage that results from these therapies.