Epirubicin-induced QT prolongation, monomorphic ventricular tachycardia, and response to beta blockade in long QT syndrome type 2

Congenital long QT syndrome (LQTS) is a group of cardiac channelopathies that are manifested through changes in repolarization. Patients are at increased risk of malignant ventricular arrhythmia, triggered by early afterdepolarization (EAD).1 The primary treatment consists of beta-blockade.2 The relative efficacy of various beta-blockers is a matter of debate and may vary among the genotypes.3, 4, 5 A survey of experts reported that most considered nonselective beta-blockers to be more effective. However, there is limited high-quality evidence and current guidelines abstain from opinion on this matter.6,7 Key Teaching Points • Treatment of long QT syndrome (LQTS) patients with epirubicin may lead to a marked additional QT prolongation. • Treatment with epirubicin in previously asymptomatic LQTS patients may lead to ventricular arrhythmias. • Nonselective beta-blockers are often considered to be more effective than the selective ones in treatment of LQTS. This view is mainly based on expert opinion. The support in existing studies is weak and current guidelines offer no advice on the matter. • The nonselective beta-blocker propranolol is more effective in suppressing these arrhythmias than the selective beta-blocker metoprolol.