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).