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)