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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Reduction of stress/catecholamine-induced cardiac necrosis by beta 1-selective blockade.

114 haemodynamically stable patients with acute head injury were randomised, double-blind, to either placebo or atenolol given intravenously (10 mg every 6 h) for 3 days then orally (100 mg daily) for a further 4 days. Both groups were equally stressed as shown by raised arterial noradrenaline levels. In patients receiving placebo, but not in those receiving atenolol, there was a significant (p less than 0.01) positive correlation between arterial noradrenaline and levels of the myocardial isoenzyme of creatine kinase (CKMB). 30% of the placebo group compared with 7.4% of the atenolol group (p less than 0.05) showed CKMB levels greater than 3% of total creatine kinase (compatible with myocardial damage). CKMB levels greater than 6% of total creatine kinase (compatible with acute myocardial infarction) were present in 16.7% of patients receiving placebo but in no patients receiving atenolol (p = 0.053). Atenolol appeared to reduce significantly the likelihood of supraventricular tachycardia and ST-segment and T-wave changes and prevented cardiac necrosis seen at necropsy.[1]


  1. Reduction of stress/catecholamine-induced cardiac necrosis by beta 1-selective blockade. Cruickshank, J.M., Neil-Dwyer, G., Degaute, J.P., Hayes, Y., Kuurne, T., Kytta, J., Vincent, J.L., Carruthers, M.E., Patel, S. Lancet (1987) [Pubmed]
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