Reduction in myocardial infarct size: prevention of heart cell death.
The course of myocardial necrosis, the clinical syndrome, and methods of treatment are presented. Heart cell death may be prevented by maintaining the balance between myocardial oxygen and energy supply and consumption. New technics of improving this balance by reducing myocardial energy demand, altering metabolism, increasing myocardial substrate supply, and protecting cellular integrity are discussed.
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D001243:Assisted Circulation; D001329:Autolysis / Q000188:drug therapy; D002302:Cardiac Output / Q000187:drug effects; D003326:Coronary Circulation; D004734:Energy Metabolism; D004735:Energy Transfer / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006821:Hyaluronoglucosaminidase / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D010101:Oxygen Consumption; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D014665:Vasodilator Agents / Q000627:therapeutic use
D000305:Adrenal Cortex Hormones; D000319:Adrenergic beta-Antagonists; D007328:Insulin; D014665:Vasodilator Agents; D006821:Hyaluronoglucosaminidase; D005947:Glucose; D011188:Potassium