Modification of infarct size.
The persistent high mortality from power failure resulting from myocardial infarction has stimulated an intensive search for methods of reducing infarct size, which has been shown to relate directly to the occurrence of power failure. By analyzing the time course of myocardial injury during ischemia, the reversibility of lesions with reperfusion, and the characteristics of reversibly injured tissues along the border zone of ischemic areas, concepts have been formulated regarding the possibility of salvaging marginally injured cells. Measures designed to diminish myocardial oxygen consumption, to increase blood flow or oxygen supply to ischemic areas, to increase substrate availability, or to change the degree of swelling and autolysis of injured cells have all been tested in experimental animals with some success. These methods are just beginning to be tested in the clinical setting, and, if successful, will no doubt usher in a new era in medical therapy for acute myocardial infarction.
D000818:Animals; D001243:Assisted Circulation; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000175:diagnosis / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D005996:Nitroglycerin / Q000627:therapeutic use; D010101:Oxygen Consumption; D011433:Propranolol / Q000627:therapeutic use; D012039:Regional Blood Flow
D011433:Propranolol; D003402:Creatine Kinase; D005996:Nitroglycerin