Myocardial function and heart failure

In various rat models of cardiac hypertrophy or heart failure, female mice showed less or later cardiac dysfunction than male mice so that survival and cardiac adaptation were reduced in male animals compared to female animals. Also myocardial expression of the genes for (3-myosin, sarcoplasmic reticulum Ca2+-ATPase and acetylcholinesterase differed between pressure-overloaded male and female rats (Gardner et al. 2002; Hayward et al. 2001; 2002). Only a few animal studies have investigated the effects of testosterone on myocardial function giving contradictory results. Castration of either female or male rats resulted in decreases of heart weight and contractile function (Scheuer etal. 1988) which in both sexes were corrected by isosexual hormone replacement. Application of testosterone to rats also led to increased gene expression of the V1 myosin heavy chain isoenzyme. In rats with experimentally induced myocardial infarction, application of testosterone caused myocardial hypertrophy, improved or worsened ventricular function and increased the rate of acute cardiac rupture (Cavasin etal. 2003; Nahrendorf etal. 2003). After trauma and haemorrhage, male but not female mice were found to have depressed immune and cardiac function, the latter being improved by treatment with an anti-androgen (Remmers et al. 1997; 1998; Wichmann etal. 1997). Together the data indicate that testosterone contributes to gender differences in myocardial function but leave open the question of whether testosterone will exert beneficial or adverse effects in the treatment or prevention of heart failure.

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