Early estimation of myocardial damage in conscious dogs and patients with evolving acute myocardial infarction.
To estimate the ultimate extent of myocardial damage during evolving myocardial infarction in conscious dogs and patients, we analyzed early serum creatine phosphokinase (CPK) changes with nonlinear curve-fitting techniques. In experiments with dogs, serial serum CPK changes were fit to a log-normal function by the least squares method; the extent of the completed infarct was calculated by analysis of observed serum CPK changes and verified by measurement of myocardial CPK depletion 24 h after coronary occlusion. Early prediction of myocardial damage was based on projected serum CPK values from best fit curves based on data obtained during the first 5 h after initial elevation of enzyme activity. The correlation between predicted and observed values was close (r > 0.96, n = 11). In 11 additional conscious animals subjected to coronary occlusion, isoproterenol was administered continuously as soon as damage had been estimated from projected serum CPK values. The extent of the completed infarct was assessed by analysis of all serial serum CPK values and verified by analysis of myocardial CPK depletion 24 h after coronary occlusion. In each experiment the calculated completed infarct size exceeded infarct size projected before administration of isoproterenol (average increase = 44+/-10 [SE]%). When similar calculations were applied in experiments with eight dogs treated with propranolol, myocardial salvage was detected in 50% of the animals. In 30 patients with uncomplicated acute myocardial infarction the extent of the completed infarct, measured by analysis of CPK activity in serum samples obtained every 2 h, was compared with damage estimated from CPK values projected by the best fit log-normal curve derived from data obtained during the first 7 h after the initial serum CPK elevation. The estimate of damage based on early data correlated closely with the extent of infarction calculated from all available serial serum CPK values (r = 0.93, n = 30). Thus, the extent of the completed infarct could be estimated accurately during the early evolution of infarction. In patients with spontaneous extension of infarction manifested by chest pain and electrocardiographic changes, the calculated extent of the completed infarct exceeded that predicted. Conversely, salvage of myocardium, after reduction of myocardial oxygen requirements by administration of trimethaphan, was reflected by reduction of the extent of the calculated completed infarct with respect to that predicted from early serum CPK changes.
D000208:Acute Disease; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000473:pathology; D001158:Arteries; D003331:Coronary Vessels; D003402:Creatine Kinase / Q000097:blood*; D004285:Dogs; D006801:Humans; D007545:Isoproterenol / Q000627:therapeutic use; D008433:Mathematics; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D011433:Propranolol / Q000627:therapeutic use; D013997:Time Factors; D014294:Trimethaphan / Q000627:therapeutic use
D014294:Trimethaphan; D011433:Propranolol; D003402:Creatine Kinase; D007545:Isoproterenol