Coronary reperfusion for the treatment of acute myocardial infarction: postischemic ventricular dysfunction.
There has been recent interest in treating acute myocardial infarction with coronary reperfusion by fibrinolytic therapy. Experimental studies have shown that myocardial infarct size can be reduced by coronary reperfusion. However, return of cardiac function, high energy phosphate metabolism, and cardiac ultrastructure may be delayed within tissue which is salvaged by coronary reperfusion. This postischemic ventricular dysfunction is transient and has been termed the 'stunned myocardium' phenomenon. Although reperfused infarcts are hemorrhagic, the hemorrhage is confined well within tissue which is already necrotic and does not appear to exacerbate the extent of necrosis. Clinical trials designed to assess the benefits of reperfusion for the therapy of acute myocardial infarction should concentrate on long-term rather than short-term changes in cardiac function.
D000818:Animals; D004285:Dogs; D004562:Electrocardiography; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D006321:Heart / Q000502:physiology; D006352:Heart Ventricles / Q000503:physiopathology*; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure
D005343:Fibrinolytic Agents