title: Stress/catecholamine-induced cardiac necrosis. Reduction by beta 1-selective blockade.
abstract: Catecholamine-induced cardiac necrosis is a well-described phenomenon. Patients with severe head injury are known to be in a marked hyperadrenergic state and can experience cardiac morbidity; this was confirmed in a pilot study. A further study was then undertaken to examine a possible relationship between plasma catecholamine concentration and cardiac morbidity in patients with severe head injury and to assess the effect of intervention with the beta 1-selective agent atenolol. The study involved 114 hemodynamically stable patients with acute head injury who were randomized, double blind, to either placebo or atenolol given intravenously (10 mg every six hours) for three days and then orally (100 mg once a day) for four days. Both groups were equally stressed in terms of raised arterial norepinephrine levels. In patients receiving placebo, but not in those given atenolol, there was a significant (P less than 0.01) positive correlation between arterial level of norepinephrine and plasma level of cardiac-specific isoenzyme CK-MB. Thirty percent of the placebo group, in contrast to 7.4% of the atenolol group (P less than 0.05), had pathologically elevated CK-MB levels (ie, greater than 3% of total CK, a value compatible with acute myocardial infarction). Atenolol appeared to significantly reduce the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis (as determined post mortem). The finding that beta 1-selective blockade significantly inhibits catecholamine-induced necrosis has possible broad clinical implications.
authors.affiliation: ICI Pharmaceuticals PLC, Macclesfield, England.
authors.forename: J M
authors.initials: JM
authors.lastname: Cruickshank
authors.forename: G
authors.initials: G
authors.lastname: Neil-Dwyer
authors.forename: Y
authors.initials: Y
authors.lastname: Hayes
authors.forename: J P
authors.initials: JP
authors.lastname: Degaute
authors.forename: T
authors.initials: T
authors.lastname: Kuurne
authors.forename: J
authors.initials: J
authors.lastname: Kytta
authors.forename: M E
authors.initials: ME
authors.lastname: Carruthers
authors.forename: S
authors.initials: S
authors.lastname: Patel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000517:prevention & control; D001262:Atenolol / Q000627:therapeutic use*; D002648:Child; D002986:Clinical Trials as Topic; D006259:Craniocerebral Trauma / Q000097:blood / Q000150:complications*; D003402:Creatine Kinase / Q000097:blood; D004311:Double-Blind Method; D004562:Electrocardiography; D005260:Female; D006352:Heart Ventricles; D006801:Humans; D007527:Isoenzymes; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D009336:Necrosis; D009638:Norepinephrine / Q000097:blood*; D010865:Pilot Projects; D011897:Random Allocation; D011943:Receptors, Adrenergic, beta / Q000187:drug effects; D013312:Stress, Physiological / Q000097:blood / Q000150:complications*
chemical_list: D007527:Isoenzymes; D011943:Receptors, Adrenergic, beta; D001262:Atenolol; D003402:Creatine Kinase; D009638:Norepinephrine