Adenosine for myocardial protection in acute myocardial infarction.

Published

Journal Article (Review)

Although reperfusion therapy for acute myocardial infarction is known to reduce infarct size, improve left ventricular function, and reduce mortality, the full potential benefit may be limited by acceleration of damage resulting from reperfusion, or "reperfusion injury." Evidence of a variety of mechanisms of reperfusion injury has led to a wide range of proposed therapeutic interventions, including agents to prevent oxygen free radical damage, inhibit white blood cell function, reduce calcium influx, improve microvascular blood flow, inhibit sympathetic stimulation, and improve energy stores. A multitude of agents have been shown to limit infarct size in animals when administered before or during reperfusion. Unfortunately, most have been disappointing when tested clinically. Adenosine, a theoretically attractive agent for preventing reperfusion injury, has shown promise in small, clinical studies, and appears to be an endogenous substance involved in the protective effect of ischemic preconditioning. When studied in the setting of angioplasty for acute myocardial infarction, adenosine was associated with small infarct size and improved coronary flow. As myocardial preservation with reperfusion during bypass surgery shares pathophysiologic characteristics with the reperfused myocardium in acute infarction, early results of adenosine during bypass surgery presented at this symposium support the concept that adenosine may be beneficial. Two ongoing Phase II trials of adenosine in acute myocardial infarction-one with thrombolysis and one with direct angioplasty-will provide important information about the potential benefits of adenosine in the context of reperfusion.

Full Text

Duke Authors

Cited Authors

  • Granger, CB

Published Date

  • June 19, 1997

Published In

Volume / Issue

  • 79 / 12A

Start / End Page

  • 44 - 48

PubMed ID

  • 9223363

Pubmed Central ID

  • 9223363

International Standard Serial Number (ISSN)

  • 0002-9149

Digital Object Identifier (DOI)

  • 10.1016/s0002-9149(97)00263-4

Language

  • eng

Conference Location

  • United States