Torsades de Pointes in Severe Aortic Stenosis: A Case Report of Nightmare Double-trouble.

Torsades de pointes (TdP) is a polymorphic ventricular tachycardia arising in the setting of repolarization prolongation and is often facilitated by bradycardia-dependent mechanisms. Its management becomes particularly challenging in fixed-output physiology, where rate modulation may conflict with hemodynamic stability. Severe aortic stenosis (AS), especially when accompanied by left ventricular dysfunction, represents such a substrate, requiring a careful balance between electrical stabilization and preservation of forward flow. A 70-year-old woman with symptomatic severe AS and moderate left ventricular dysfunction underwent cardiac computed tomography for preoperative assessment. Immediately following contrast administration, she developed sinus bradycardia, marked QT prolongation (corrected QT, 560 ms), ventricular ectopy characterized by long-short sequences, and recurrent TdP with hemodynamic compromise. Intravenous magnesium and a single bolus dose of amiodarone were administered empirically; however, arrhythmia recurred and QT prolongation persisted. Electrolytes were within normal limits aside from low-normal potassium, which was subsequently corrected. In the setting of bradycardia-dependent TdP and a relative contraindication to aggressive β-blockade in a fixed-output state, semipermanent atrial pacing at 90 bpm was instituted. Rate acceleration suppressed ventricular ectopy and prevented further TdP episodes. Coronary angiography demonstrated no obstructive disease. The patient subsequently underwent urgent surgical aortic valve replacement but developed refractory ventricular fibrillation intraoperatively and could not be resuscitated. This case highlights repolarization vulnerability in structural heart disease, wherein bradycardia-dependent QT prolongation, pharmacologic influences, and procedural stress may converge to precipitate malignant ventricular arrhythmias. Recognition of rate-dependent mechanisms and judicious anti-arrhythmic selection are essential when managing electrical instability in structurally compromised hearts. CLINICAL IMPACT: Torsades de pointes in patients with severe structural heart disease presents a unique therapeutic challenge when fixed-output physiology limits conventional rate and antiarrhythmic strategies. This case highlights an important and potentially underrecognized interaction between severe aortic stenosis, acquired QT prolongation, bradycardia, and procedural stress. The immediate onset after contrast administration suggests a trigger-substrate interaction rather than contrast exposure as an isolated cause. Importantly, recurrent bradycardia-dependent torsades was successfully suppressed by controlled atrial pacing at 90 beats/min, despite the hemodynamic constraints of severe aortic stenosis. The case also underscores the need to distinguish pause-dependent torsades from other forms of polymorphic ventricular tachycardia, particularly because drugs such as amiodarone may worsen repolarization. Recognition of the underlying electrophysiologic mechanism and judicious use of pacing may be critical for stabilizing patients with malignant ventricular arrhythmias in structurally compromised hearts.