Abstract
Background: Humans and mammals have sex-specific differences in cardiac
electrophysiology, linked to the action of sex hormones in the cardiac
muscle. These hormones can either increase or decrease the expression of
ionic channels modulating the cardiac cycle through genomic and
non-genomic interactions. Methods: Systematic search in PubMed, Medline
and EMBASE including keywords pertaining to testosterone and QT
interval. Included experimental studies, observation studies and case
reports presenting the results of testosterone administration, excess or
deficiency in humans and animals. Results: Testosterone has been shown
to shorten the action potential duration, by enhancing the expression of
K+ channels and downregulating ICaL increasing the repolarization
reserve of the cardiac muscle. This increased repolarization reserve
also protects the heart against the effects of QT prolonging drugs and
arrhythmogenesis. This effect has been observed in both genders and
animals. Conclusions: Testosterone deficient states can promote
arrhythmogenesis. The evidence in this paper may be used to guide
clinical consideration relating to testosterone levels and QT prolonging
states and medications, such as increased clinical surveillance of
patients in testosterone deficient states using ECG.