Verapamil-sensitive fascicular ventricular tachycardia (FVT) has been demonstrated to be a reentrant mechanism using the Purkinje network as a part of its reentrant circuit. Although the papillary muscles (PMs) are implicated in arrhythmogenic structure, reentrant FVT originating from the PMs has not been well defined.Methods and Results—
We studied 13 patients in whom FVT was successfully eliminated by ablation at the posterior PMs (n=8; PPM-FVT) and anterior PMs (n=5; APM-FVT). Although intravenous administration of verapamil (5 mg) terminated ventricular tachycardia (VT) in 6 patients, VT was only slowed in the remaining 7 patients. PPM-FVT exhibited right bundle branch block and superior right axis (extreme right axis) or horizontal axis deviation. APM-FVT exhibited right bundle branch block configuration and right axis deviation with deep S wave in leads I, V5, and V6. VT was reproducibly induced by programmed atrial or ventricular stimulation. His-ventricular interval during VT was shorter than that during sinus rhythm. Ablation at the left posterior or anterior fascicular regions often changed the QRS morphology but did not completely eliminate it. Mid-diastolic Purkinje potentials were recorded during VT around the PMs, where ablation successfully eliminated the tachycardia. All patients have been free from recurrent VT after ablation.Conclusions—
Reentrant circuit of verapamil-sensitive FVT can involve the Purkinje network lying around the PMs. PM-FVT is a distinct entity that is characterized by distinctive electrocardiographic characteristics and less sensitivity to verapamil administration compared with common type FVT. Ablation targeting the mid-diastolic Purkinje potentials around the PMs during tachycardia can be effective in suppressing this arrhythmia.