Can Myocardial Infarct Size be Reduced by Mechanically Unloading the Left Ventricle?
Oxygen Supply/Demand Approach to Reducing Infarct Size
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 by keeping it open. Early reperfusion consistently reduces myocardial infarct size in both experimental animal models and in patients.
Despite advances in stenting of the occluded coronary artery and shortening of the "door-to-balloon" time, 1 month mortality post infarction still hovers around 15% and post myocardial infarction 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 1). Improving O2 supply by inducing early reperfusion with thrombolytic therapy, then angioplasty, and now stenting has been successful and dual antiplatelet therapy and possibly addition of anticoagulant therapy has 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.
- Received June 4, 2013.
- Accepted June 7, 2013.