Can QT (QT interval) prolongation cause bradycardia in patients?

QT Prolongation Does Not Cause Bradycardia—Bradycardia Causes QT Prolongation and Triggers Torsades de Pointes

QT prolongation does not cause bradycardia; rather, bradycardia is a well-established risk factor that both prolongs the QT interval and triggers life-threatening torsades de pointes in patients with pre-existing QT prolongation. 1 This is a critical distinction for clinical management, as the relationship flows in the opposite direction from what the question implies.

The Causal Relationship: Bradycardia → QT Prolongation → Torsades de Pointes

Bradycardia directly prolongs the QT interval through fundamental cardiac electrophysiology. 2 When heart rate decreases, ventricular repolarization time increases, mechanically extending the QT interval duration. This creates a dangerous substrate for arrhythmias.

Bradycardia as an Immediate Trigger for Torsades de Pointes

Patients with an already prolonged QT interval are at immediate risk of torsades de pointes when they develop sudden bradycardia or long pauses. 1 The American Heart Association specifically identifies the following high-risk ECG findings in patients with QT prolongation:

• Sudden bradycardia or long pauses (including compensatory pauses after ventricular ectopy) 1
• Enhanced U waves 1
• T wave alternans 1
• Polymorphic ventricular premature beats, couplets, and nonsustained polymorphic ventricular tachycardia 1

Clinical Evidence: The Short-Long-Short Sequence

All episodes of drug-induced torsades de pointes are preceded by a characteristic short-long-short cycle length sequence, where the "long" represents a bradycardic pause. 1 This pattern was documented in Holter monitor recordings of 12 patients who developed drug-induced torsades de pointes, demonstrating that bradycardia is the precipitating event, not the consequence. 1

High-Risk Clinical Scenarios

Patients with New-Onset Bradyarrhythmias

Patients who develop complete heart block or long sinus pauses with sick sinus syndrome are specifically prone to develop torsades de pointes. 1 This includes patients who have undergone AV junction ablation to produce complete heart block for rate control. 1 Monitoring should continue until the bradyarrhythmia resolves or definitive treatment (permanent pacing) is instituted. 1

Drug-Induced Scenarios

The most likely time for torsades de pointes to occur in patients receiving ibutilide for atrial fibrillation is at the time of conversion to sinus rhythm when a pause occurs. 1 This represents a classic example of bradycardia-triggered torsades in the setting of QT-prolonging medication.

Sotalol causes both QT prolongation and bradycardia through its beta-blocking properties, creating a particularly dangerous combination. 1 The guidelines specifically warn about this dual mechanism and list bradycardia as a potential adverse effect alongside QT prolongation. 1

Case Evidence from Clinical Practice

A 2023 case report documented persistent bradycardia with high-grade AV block leading to persistently prolonged QTc that resulted in torsades de pointes. 2 The treatment involved shortening the QTc by increasing the heart rate through pacing to prevent further episodes. 2

In a 2001 case series of 13 patients with drug-induced long QT syndrome, bradyarrhythmia was identified as one of the key predisposing factors for torsades de pointes. 3 Female sex, bradyarrhythmia, and hypokalemia were the three major risk factors identified. 3

A 2025 case report described a patient who developed bradycardia-associated torsades de pointes approximately 66 hours post-cardioversion, requiring temporary overdrive pacing. 4 The QTc normalized with pacing, and no further episodes occurred, demonstrating that correcting the bradycardia resolved the arrhythmic risk. 4

Management Implications

Therapeutic Approach to Bradycardia-Induced Torsades

The conventional therapy for torsades de pointes includes isoproterenol or cardiac pacing to increase heart rate and shorten the QT interval. 5 This therapeutic approach directly addresses bradycardia as the causative mechanism.

Temporary overdrive pacing or IV isoproterenol should be considered for recurrent torsades de pointes, particularly when bradycardia is present. 6 The goal is to increase heart rate above 90-100 bpm to suppress the arrhythmia. 6

Atrial or ventricular pacing is highly effective for recurrent episodes of torsades de pointes (Class IIa recommendation from the American Heart Association). 6 This intervention works by eliminating bradycardia and the associated QT prolongation.

Monitoring Requirements

ECG monitoring should continue until bradyarrhythmia has resolved or definitive treatment (permanent pacing) has been instituted in patients with new-onset bradyarrhythmias and QT prolongation. 1

Common Pitfalls to Avoid

• Do not assume QT prolongation causes bradycardia—the causal relationship is reversed, and misunderstanding this can lead to inappropriate management strategies
• Do not overlook bradycardia as a trigger for torsades de pointes—even modest bradycardia in the setting of QT prolongation creates immediate risk 1
• Do not delay pacing in patients with persistent bradycardia and QT prolongation—this combination requires urgent intervention 2, 4
• Do not use beta-blockers or other rate-slowing agents in patients with QT prolongation—these medications can precipitate torsades by inducing bradycardia 1, 3