An antiarrhythmic approach to hydroxychloroquine-induced QT prolongation
Citation
Yetkin, E., Yalta, K., & Waltenberger, J. (2020). An antiarrhythmic approach to hydroxychloroquine-induced QT prolongation. NETHERLANDS HEART JOURNAL, 28(7–8), 437–438. https://doi.org/10.1007/s12471-020-01464-4Abstract
Derivatives of quinolone, namely quinidine, quinine
and hydroxychloroquine (HCQ, hydroxylated form of
aminoquinone), have been used for decades in the
treatment of different diseases, including malaria,
rheumatological diseases, cardiac arrhythmias and,
most recently, the new coronavirus disease 2019
(COVID-19). Although quinidine is no longer widely
used for the termination and prevention of arrhythmias,
quinine and HCQ are still in common use for
rheumatological diseases and malaria. Their common
side-effects, QT prolongation and a risk of proarrhythmia,
have re-emerged as a result of the widespread
use of HCQ in the treatment of COVID-19. In fact,
they all show the main electrophysiological aspects
of class Ia antiarrhythmic drugs. This antiarrhythmic
effect is mainly characterised by the inhibition of fast
Na channels and to a lesser extent by K-channel inhibition.
However, this class I antiarrhythmic effect is
accompanied by a proarrhythmic effect by prolonging
the QT interval, thereby facilitating the occurrence of
torsades de pointes or ventricular arrhythmias. Therefore,
being a derivative of quinolone, like quinidine,
and manifesting class Ia antiarrhythmic drug effects,
HCQ has been given all the attention regarding the