Abstract

Adaptive cardiac resynchronization therapy (aCRT) algorithms have improved outcomes via dynamic left ventricular (LV) and biventricular (Bi-V) pacing strategies based on real-time assessments of intrinsic atrioventricular (AV) delays. Few cases have shown potential proarrhythmic effects. NA NA A 42-year-old man with a long history of non-ischemic cardiomyopathy underwent implantation of a prophylactic CRT-defibrillator. In the 24-hour period following implantation, there was progressive QT prolongation (Fig.1) followed by non-sustained torsades de pointes and ultimately 8 episodes of sustained, polymorphic VT. Device interrogation revealed 98.5% LV pacing and 1.4% Bi-V pacing. No additional ventricular arrhythmias were observed after programming changes, including increasing the lower rate limit to 90 bpm, turning off aCRT, and reinstitution of simultaneous Bi-V pacing with short AV intervals. We hypothesize that recurrent non-ischemic polymorphic VT in this case was related to induced alteration in transmyocardial repolarization with LV pacing from an epicardial coronary vein. Accentuation of normal dispersion by altering normal depolarization and thus repolarization sequence may precipitate phase 2 reentry. The termination of VT by turning off aCRT and programming a set Bi-V pacing sequence suggests that alteration of transmural repolarization was the proarrhythmic mechanism. Novel programming algorithms intended to minimize non-physiologic right ventricular pacing and more closely mimic physiologic electro-mechanical biventricular activation carry the potential for ventricular proarrhythmia.

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