What Is Wrong with the Failing Heart?

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Abstract
IN the current issue of the Journal, Bristow et al. report that failing left ventricles obtained from patients undergoing cardiac transplantation had a 50 to 56 per cent reduction in β-adrenergic-receptor density, a 45 per cent reduction in maximal isoproterenol-mediated adenylate cyclase stimulation, and 54 to 73 per cent reduction in maximal isoproterenol-stimulated contraction, as compared with left ventricular tissue from human hearts without known or suspected heart failure. The latter hearts had been donated for transplantation or obtained after natural or accidental death.1 These observations are potentially important. A reduction in the density of the β-adrenergic receptors of . . .