Acute interruption of treatment with nandrolone decanoate is not sufficient to reverse cardiac autonomic dysfunction and ventricular repolarization disturbances in rats

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Abstract

Anabolic androgenic steroids are a class of synthetic compounds derived from testosterone, eventually used by athletes, to improve physical performance. However, anabolic steroids can also modify normal cardiovascular function. Thus, we investigated cardiac electrophysiological and autonomic abnormalities in rats, through a electrocardiographic variability protocol during and after interruption of administration of nandrolone decanoate (DECA) anabolic steroid. Twenty male Wistar rats (60–70 days old) received DECA (10 mg. kg−1i.m) once a week or vehicle, during eight weeks. Electrocardiogram was recorded in conscious rats by a noninvasive method, and time and domain analysis of heart rate variability as well as electrocardiogram intervals (QTc / QTd) were performed. Body mass was lower in treated rats compared to control after 4th and 8th weeks, but not at the end of 14th week. QTc and QTd were longer in DECA group compared to control on 4th, 8th, 11th, but equal on 14th week. Cardiac autonomic dysfunction (vagal attenuation) was present on DECA group after 4th week and did not normalize after interruption of treatment. The animals of DECA group showed a correlation between attenuated parasympathetic modulation and increased correct QT interval. Our data allow us to conclude that long-term treatment with DECA impairs autonomic cardiac physiology, predisposing to cardiovascular risk and sudden death, and interruption of administration does not recovery the normality immediately.

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