Moxifloxacin-induced QT interval prolongation and torsades de pointes: a narrative review

Moxifloxacin is widely used for the treatment of a number of infectious diseases because of its favorable pharmacological profile and high clinical success rate. However, it is often criticized for its higher risk of QTc interval prolongation (QTIP) and torsades de pointes (TdP).

A review of published literature on moxifloxacin-related QTIP and TdP. Readers will be provided with a comprehensive overview of the prevalence, cellular mechanism, risk factors, and magnitude of QTIP of moxifloxacin.

In healthy subjects, moxifloxacin prolongs the QTc interval by 11.5-19.5 ms, it binds at the Tyr652 residue in the S6 pore domain of the human ether a-go-go gene related potassium channel. Considerable QTIP (30-60 ms) have also been reported in some patients, for instance the incidence of QTIP (30-60 ms) in elderly pneumonia patients was 15.5%. Moxifloxacin-induced QTIP may be of little clinical importance in healthy individuals. However, marked QTIP (>60 ms) and TdP have been reported in high-risk patients (patients who have multiple QT prolonging risk factors). Patients must be thoroughly assessed prior to the use of moxifloxacin and high-risk patients must be identified using risk assessment tools to ensure safe use of moxifloxacin and to safeguard patients' health.