Response by Padfield and Krahn to Letter Regarding Article, “Characterization of Myocardial Repolarization Reserve in Adolescent Females With Anorexia Nervosa”

Abstract

In Response:We thank Aparci et al for their interest in our article 1 and for the interesting points they raise. We agree that the pathogenesis of ventricular arrhythmias in anorexia nervosa (AN) is likely to be multifactorial; however, the argument that excess growth hormone (GH) may be responsible for arrhythmogenesis in AN is not particularly convincing. The ability of growth hormone to increase muscle mass is well described, and myocyte hypertrophy is a characteristic finding in acromegaly. The observation of late potentials in acromegaly 2 is consistent with the action of GH on myocyte physiology and a plausible arrhythmogenic effect in this context. In contrast to acromegaly, myocardial muscle mass is characteristically decreased in AN because of malnutrition and hypotrophy. Although GH may be increased in AN, this is as a consequence of GH resistance 3 ; therefore, the biologic action of GH in this context is blunted. The theory that GH is exerting an arrhythmogenic effect in the absence of myocyte hypertrophy seems uncertain, and, indeed, administration of GH has been associated with a reduced susceptibility to arrhythmia in animal models of myocardial infarction, albeit through uncertain mechanisms.4,5 Unfortunately, our study was not specifically designed to address this question, and a carefully designed experiment within a suitable animal model of AN would be required to determine this definitively. DISCLOSURESNone. AFFILIATIONFrom University of British Columbia, Vancouver, BC, Canada.