Myocardial Dysfunction in Donor Hearts

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Abstract
Background —Potential cardiac donors show various degrees of myocardial dysfunction, and the most severely affected hearts are unsuitable for transplantation. The cause of this acute heart failure is poorly understood. We investigated whether alterations in calcium-handling proteins, β-adrenoceptor density, or the inhibitory G protein G iα could account for this phenomenon in unused donor hearts (n=4 to 8). We compared these with end-stage failing hearts (n=14 to 16) and nonfailing hearts (n=3 to 12). Methods and Results —Myocardial samples were obtained from unused donor hearts displaying ejection fractions P P P P =0.37) relative to the nonfailing heart group (n=5). G iα activity was increased in samples from unused donor and failing hearts relative to nonfailing hearts ( P Conclusions —Increased activity of the inhibitory G protein G iα is a significant contributory factor for impaired contractility in these acutely failing donor hearts.

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