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.