4.1 Effect of testosterone on QT interval
The current literature supports the QTc shortening effect of
testosterone in both men and women through the upregulation of
K+ currents and the suppression of
Ca2+ currents. (Tables 1 and 2 ). QTc
prolongation can also be the result of genetic, congenital and acquired
causes including medications, heart blocks, endocrine abnormalities,
electrolyte abnormalities or CNS injury (Table 3 ). Regardless
of the mechanism, a prolonged QT interval is predictive for
arrhythmogenesis, such as increased PVCs and TdP (1). The findings
encountered in animal models support those in humans, portraying similar
mechanisms of action for testosterone (Table 2 ). This further
supports that testosterone levels are inversely correlated with the QT
interval and that testosterone is protective against arrhythmogenesis
(46,47,69). It is important to note that some studies have found the
opposite result or a negative result when studying testosterone effects
in humans and animal models (37,61,72,73).
Table 3, Drug and non-drug causes of QT prolongation or
increased QT prolongation risk (29,30,34,36,41,42,44,83,120,126,127)