Promising though not yet proven: emerging strategies to promote myocardial salvage.

Remarkable advances in our ability to achieve early and sustained culprit vessel patency in acute myocardial infarction have been satisfying, but our enthusiasm must be tempered by the knowledge that the overall treatment strategy often leaves an inadequate long term clinical result. Early success of percutaneous therapy as judged at angiography does not ensure recovery of normal left ventricular function, the most important determinant of survival in acute myocardial infarction. That congestive heart failure and death still complicate apparently successful percutaneous procedures underscores the need to develop novel therapies which salvage jeopardized myocardium, limit infarct size and preserve left ventricular function. An ever-increasing body of data demonstrates a multifactorial mechanism of myocyte injury and microvascular collapse and also demonstrates that these injuries seem to have a profound impact on long-term outcomes. Given these findings, microvascular protection during the acute event has become the focus of a variety of emerging technologies. The goal of these mechanical and pharmacologic therapies is the restoration of normal metabolic function at the myocyte level. The acute pathologic mechanisms which contribute to sustained left ventricular dysfunction despite angiographically successful revascularization will be reviewed as will be several strategies being developed to counter these pathologic mechanisms.