INTRODUCTION
In adults, a typical QTc duration is more significant than 350 and less
than 450 milliseconds for men and greater than 360 and less than 460
milliseconds for women (1). For every additional ten milliseconds, the
probability of having arrhythmic events increases by around 5%. The
reasons behind QT prolongation can be categorized into two groups:
congenital or acquired (2). The hereditary condition known as long QT
syndrome (LQTS) is caused by genetic abnormalities that impact
particular regulatory proteins or ion-channel subunits. It may manifest
in a variety of ways (3). LQTS alters the electrical activity of the
heart and increases the risk of severe irregular heart arrhythmias that
can potentially be fatal. This syndrome is characterized by a prolonged
QT interval detected on the electrocardiogram (ECG). It can develop
consequences including loss of consciousness, syncope, as well as
ultimately fatal sudden cardiac death (SCD) (4).
Medication-induced LQTS is a frequently detected etiology of acquired
LQTS, and a diverse spectrum of drugs triggers it. Comprehending the
mechanisms that promote drug-induced LQTS is fundamental for identifying
and preventing heart arrhythmias in patients who are prescribed these
drugs. Several medications can inhibit the potassium channels that are
essential for the process of cardiac repolarization. The result can lead
to an elevated likelihood of experiencing heart arrhythmias and prolong
the QT interval.
Medications such as antiarrhythmics, antibiotics, antipsychotics,
antihistamines, and antidepressants are commonly associated with LQTS.
Close monitoring of patients on these medications is necessary to detect
any arrhythmias and symptoms associated with QT prolongation (5,6). The
acquired form of QT prolongation is more frequent than the congenital
form. It is usually caused by structural heart conditions (such as
myocardial infarction, heart failure, and left ventricular hypertrophy)
and also by drugs that prolong the QT interval (7).
Despite this, an extended QT interval can indicate possible causes for
arrhythmias, including an increased incidence of PVCs and Torsade de
pointes (TdP) (8,9). TdP is a type of ventricular tachycardia usually
associated with LQTS. QRS complex is identified by the twisting around
the isoelectric line on the ECG and possesses a risk of deteriorating
into ventricular fibrillation, which can result in death (10). The
prolonging of the QT interval caused by particular medications is
commonly acknowledged as raising the probability of drug-induced TdP.
The potential of developing TdP is related to the severity of QT
prolongation. Indicators such as being female, having abnormal levels of
electrolytes, and bearing a genetic tendency to LQTS are considered risk
factors for TdP (11).
Pharmacological treatment utilizing beta-blockers, potassium channel
blockers, or sodium channel blockers can also be applied to control
arrhythmias and prevent recurrence. The choice of using medication for
drug-induced LQTS or TdP should be cautiously addressed in each
instance, taking into account the potential advantages concerning the
dangers of triggering proarrhythmic consequences (12).