Management of acute myocardial infarction. Pathophysiological considerations.
Development of improved techniques for assessing infarct size in intact experimental animals and in patients has made it possible to evaluate the effectiveness of selected interventions more objectively. It is becoming increasingly apparent that infarct size is an important determinant of prognosis. Experimentally, infarct size can be modified favorably under specified conditions by interventions designed to reduce myocardial oxygen requirements or increase myocardial energy supply during the early evolution of infarction. Preliminary clinical applications of these concepts have been encouraging. The time seems to be right for carefully controlled clinical investigations to determine whether techniques designed to protect ischemic myocardium will be effective in improving survival and reducing morbidity from acute myocardial infarction. On the basis of available evidence, it seems clear that appropriate management of patients with this disorder should include careful attention to the impact of any therapeutic modality on the heart itself. It does not suffice to treat patients with beta-adrenergic agonists simply because they may elevate systemic arterial blood pressure. Hemodynamics can not be the sole criteria in guiding the physician charged with the responsibility for patient management. Rather, he must consider the potential effects of any contemplated therapeutic modality on myocardial viability as well. The ultimate place if interventions designed to protect ischemic myocardium in the therapeutic armamentarium remains to be determined. However, judicious therapy should be designed to minimize myocardial oxygen requirements and maximize myocardial energy supply as well as to prevent criti  l impairment of peripheral perfusion.
D000208:Acute Disease; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001243:Assisted Circulation; D002302:Cardiac Output; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006339:Heart Rate; D006801:Humans; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D011379:Prognosis; D011433:Propranolol / Q000494:pharmacology
D000255:Adenosine Triphosphate; D011433:Propranolol; D003402:Creatine Kinase