Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality.
Clinical and experimental evidence suggest that sympathoadrenal activation contributes to mortality in patients with ischemic heart disease. To determine the level of sympathoadrenal activation in the very early phase of acute myocardial infarction (AMI) and to determine if location of infarction (anterior versus inferior) was related to sympathoadrenal activation, we studied norepinephrine (NE) and epinephrine (E) within 4 hours after the onset of symptoms and prior to any rise in plasma creatine kinase (CK). Mean (+/- SE) initial (NE = 591 +/- 111 pg/ml and E = 73 +/- 19 pg/ml), peak (NE = 1356 +/- 178 and E +/- 1098 +/- 608) and average (NE = 815  +/- 142 and E = 252 +/- 68) plasma catecholamine concentrations were considerably above normal (NE = 228 +/- 10 and E = 34 +/- 2 pg/ml, n 60) and values were similar for inferior and anterior infarctions. During an 18-month follow-up, three patients died in whom the AMI mean NE and E and peak CK were higher than in the eight late survivors. Thus the three AMI patients with peak EP values greater than 1000 died, whereas the eight AMI patients with peak EP values less than 1000 survived (p less than 0.01). The magnitude of sympathoadrenal activation early in the course of clinical AMI appeared related to the extent of myocardial damage and late mortality.
D000208:Acute Disease; D001794:Blood Pressure; D003402:Creatine Kinase / Q000097:blood; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000401:mortality; D009638:Norepinephrine / Q000097:blood*
D003402:Creatine Kinase; D009638:Norepinephrine; D004837:Epinephrine