For first-time, isolated aortic valve replacement, mechanical prostheses should be considered in patients under age 65 years with a life expectancy of at least 10 years. Bioprostheses should be considered in patients over age 65 years or with lung disease (in patients over age 60 years), renal disease, coronary disease, ejection fraction less than 40%, or a life expectancy less than 10 years.

Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. Analysis of the beta-receptor included determination of receptor density and adenylate cyclase activity after stimulation independently at the receptor protein, the G protein, and the adenylate cyclase moiety. Myocardial beta-receptor density did not change after the induction of brain death. A decrease in stimulated adenylate cyclase activity was observed within the first hour after brain death at the level of the beta-receptor, the G protein, and the adenylate cyclase moiety, which suggests the occurrence of rapid desensitization of beta-receptor function. Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.

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Tissue injury by Aspergillus niger infection is associated with the deposition of calcium oxalate crystals. Oxalate is recognized to function as a ligand for numerous metal cations and will react with ferric ion to form a coordination complex. We describe oxalate deposition in the lung of a patient with A. niger infection and quantify surface-complexed Fe3+. Crystals collected from lung tissue demonstrated considerable concentrations of surface iron. In addition, we tested the hypothesis that this surface coordination of Fe3+ by oxalate is associated with increased in vitro oxidant generation. Calcium oxalate crystals (1.0 mg/ml) complexed all available Fe3+ from solutions of ferric chloride to concentrations of as much as 1.0 mM. Oxidant generation in both a chemical and a cellular system, measured as thiobarbituric-acid-reactive products of deoxyribose and chemiluminescence, respectively, increased with coordination of higher concentrations of inorganic iron. We conclude that calcium oxalate associated with A. niger infection complexes iron cations onto the crystalline surfaces and may generate oxidants at the solid-solution interface, which could result in tissue injury.

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