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.
Key words: testosterone; QT interval; QTc; arrhythmia; sex
hormones