Figure
1. Diagram comparing the cardiac action potential measured by an ECG
(left) and represented by the changes in ionic currents (right - Cardiac
cycle). The QT and the APD, represent the same process (3).Abbreviations: INa – Na+ current, ICaL – L-type Ca2+ current,
IKur – delayed rectifier ultra-rapid K+ current, IKr – delayed
rectifier rapid K+ current, IKs – delayed rectifier slow K+ current,
NCX – Na+/Ca2+ exchanger.
Prolongation of the QTc (specially values greater than 500ms) can result
in life-threatening cardiac events (3). Abnormalities can be caused by
genetic conditions, such as long QT syndrome (LQTS), certain medications
(e.g., certain anti-arrhythmic, antimicrobials and psychotropic drugs –
refer to Table 3 for an extensive list of QT prolonging drugs)
and hormones (3). For instance, according to the literature, low levels
of testosterone result in the inhibition of the expression of
repolarizing currents in the heart and thus, it is one of the main
causes of QT interval prolongation (4) – Figure 2 (4–6).
Thus, the aims of this systematic review are to explore the effects of
testosterone on the length of the QT interval and make a strong case for
the clinical importance of testosterone as a key factor in determining
the patient’s susceptibility to arrhythmogenesis.