Myocardial infarct size. Measurements and predictions.
Because patient prognosis is related in part to infarct size, therapies that could limit infarct size should be beneficial. The development of such therapies has been hampered by the lack of proven techniques to measure infarct size or to assess the effect of therapy in living patients. In addition, the evolution of ischemic cell death in human infarcts is not understood, and therefore the amount of ischemic myocardium that might be salvageable at various times after the onset of myocardial infarction is unknown. Experimental studies have contributed to our understanding of the evolution of acute myocardial infarcts. However, there is a continuing need for experimental and human anatomical studies to validate indirect in vivo techniques of estimating infarct size. In addition, reliable experimental models in which potential therapies can be tested are needed. In dogs, infarct size is predetermined in part by the amount of myocardium at risk and the amount of collateral flow in this risk region. Measuring these parameters should provide a framework within which the effects of therapy on infarct size can be assessed.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D006332:Cardiomegaly / Q000209:etiology; D002470:Cell Survival; D003097:Collateral Circulation; D003331:Coronary Vessels; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D004395:Dye Dilution Technique; D004562:Electrocardiography; D006652:Histological Techniques; D006801:Humans; D007527:Isoenzymes; D008722:Methods; D009203:Myocardial Infarction / Q000150:complications / Q000175:diagnosis / Q000473:pathology* / Q000628:therapy; D009206:Myocardium / Q000378:metabolism; D009211:Myoglobin / Q000097:blood; D010101:Oxygen Consumption; D011379:Prognosis; D012306:Risk; D012770:Shock, Cardiogenic / Q000209:etiology; D013997:Time Factors
D007527:Isoenzymes; D009211:Myoglobin; D003402:Creatine Kinase