Abstract

Great strides have been made in the treatment of acute myocardial infarction (MI). Improved outcomes and reduced mortality are largely the result of opening the occluded infarct artery as soon as possible and keeping it open. Early reperfusion consistently reduces myocardial infarct size in both experimental animal models and in patients. Article see p 328 Despite the advances in stenting of the occluded coronary artery and shortening of the door-to-balloon time, 1 month mortality postinfarction still hovers at ≈15%, and post-MI heart failure remains problematic. Therefore, there is still a need to try to further reduce myocardial infarct size in 2013. Initial concepts focused on reducing myocardial infarct size by improving the imbalance between O2/nutrient supply and O2/nutrient demand of the heart (Table). Improving O2 supply by inducing early reperfusion with thrombolytic therapy, then angioplasty, and now stenting has been successful and dual-antiplatelet therapy and possibly the addition of anticoagulant therapy have further improved clinical outcomes, maintained vessel patency, and reduced stent thrombosis. Other techniques to improve O2/nutrient supply such as hyperoxemia and erythropoietin have shown benefit in some but not all studies. Antianginal agents that vasodilate the coronary arteries and may improve coronary flow, such as nitrates and calcium blockers, in general, have failed to reduce myocardial infarct size in clinical trials. View this table: Table. Therapies That May Reduce Infarct Size by Either Improving O2 Supply or Reducing O2 Demand Although restoring O2 supply reduces ischemic cardiac damage resulting from MI, attempts at reducing myocardial infarct size by reducing O2 demand have yielded mixed results. Early clinical studies with β-blockers in the pre-reperfusion era were negative. However, chronic β-blockers post-MI were suggested to reduce fatal ventricular arrhythmias, reduce reinfarction, and limit left ventricle (LV) remodeling and post-MI heart failure and death. …

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