Percutaneous Assist Devices for Infarct Size Reduction

Improving myocyte salvage during acute myocardial infarction (AMI) has proved elusive; the keys to success seem to be the ability to lower oxygen demand of ischemic myocardium and also activate salvage enzyme pathways to take advantage of endogenous cardioprotective mechanisms. Pharmacologic approaches have been largely unsuccessful. A percutaneous left ventricular (LV) assist device could improve myocyte salvage during AMI therapy if it were able to reduce myocardial oxygen demand, wall tension, and LV stroke work substantially.