Right ventricular lead proarrhythmia: A novel intervention for an under-recognized phenomenon

Figures

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  Figure 1. A: Telemetry strip of ventricular tachycardia (VT) at a rate of 135 beats/min, which occurs immediately after a sequence of right ventricular (RV) pacing. From top to bottom, the leads shown are I, II, III, V5, aVR, aVL, and aVF. B: A 12-lead surface electrocardiogram (ECG) of the clinical ventricular tachycardia during electrophysiology study. Precordial lead placement was not in typical location. C: Telemetry strip of recurrent VT with similar morphology following endocardial ablation, which required antitachycardia pacing. D: A 12-lead ECG following reprogramming of cardiac resynchronization therapy device with RV lead programmed with 55-ms delay after left ventricular pacing, which was the shortest delay that clearly altered the pacing vector.

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  Figure 2. A: Posterior-anterior chest radiograph with cardiac resynchronization therapy device over left chest. B: Lateral chest radiograph with right ventricular lead visualized in the apex. C: Endocardial voltage map (Ensite, St. Jude, Minneapolis, MN) of the left ventricle at standard scar settings (0.5–1.5 mV) demonstrating very large septal anterior and apical scar with areas of preserved voltage in mid-inferior and mid-lateral walls (white dots = ablation lesions).

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  Figure 3. Proposed mechanism of ventricular tachycardia (VT) suppression. Lateral projection of plain chest radiograph demonstrating right ventricular (RV) lead pacing directly into a VT circuit within scar. Offsetting left ventricular pacing prior to RV pacing creates a refractory limb of the circuit, which does not allow for reentry. Inset: Schematic histopathologic representation of scar-based substrate, which can promote reentry.