QTverlenging

QTverlenging refers to an elongation of the QT interval on an electrocardiogram (ECG), which reflects delayed repolarization of the ventricles. Since the QT interval varies with heart rate, clinicians often use a corrected QT interval (QTc) to assess risk. Prolonged QTc is associated with an increased risk of torsades de pointes, a potentially life-threatening polymorphic ventricular tachycardia that can lead to fainting, cardiac arrest, or sudden death.

Causes of QTverlenging include drug effects, electrolyte disturbances, and congenital conditions. Drug-induced QT prolongation is common and may result from antiarrhythmics (for example, amiodarone, sotalol, dofetilide, ibutilide), antibiotics (macrolides such as erythromycin and azithromycin; fluoroquinolones such as levofloxacin and moxifloxacin), antipsychotics (ziprasidone, haloperidol), antidepressants (citalopram, escitalopram), antiemetics (ondansetron), antifungals (voriconazole), and others including methadone. Other factors include electrolyte abnormalities such as hypokalemia, hypomagnesemia, and hypocalcemia, bradycardia, ischemia, and congenital long QT syndrome.

Mechanistically, many QTprolonging episodes result from inhibition of cardiac hERG potassium channels (IKr), which delays repolarization and can promote early afterdepolarizations that trigger arrhythmias.

Diagnosis and management focus on recognizing high QTc values and mitigating risk. A QTc above about 450 ms in men and 470–480 ms in women is commonly considered prolonged; values above 500 ms significantly raise torsades risk. Management includes reviewing and possibly discontinuing QT-prolonging drugs, correcting electrolyte disturbances, and, if torsades occurs, administering magnesium sulfate and providing appropriate cardiac support. Prevention emphasizes careful drug selection, dose adjustment, and ECG monitoring in at-risk patients.