Summary
The most effective therapeutic intervention for reducing infarct size and improving outcomes in patients with acute myocardial infarction is the thrombolytic therapy or percutaneous coronary angioplasty. However, this process itself can generate ischemia-reperfusion injury that can be responsible for up to 50% of the final infarct size. Considering oxidative stress as the main damaging agent in this pathology, it has been postulated that reinforcing antioxidant defenses could improve cardiac function. However, up to date clinical trials based on monotherapies have been consistent in the favorable results. In this review the pathophysiological mechanisms of myocardial injury due to ischemia/reperfusion in patients undergoing percutaneous coronary angioplasty are updated. In addition, new th
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