Site-Specific Arrhythmogenesis in Structurally Normal Heart of Non-Brugada Patients with Ventricular Arrhythmias Originating from Ventricular Outflow Tract
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<B>Background:</B> Ventricular fibrillation (VF) and/or polymorphic ventricular tachycardia (PVT) may be initiated by premature ventricular contractions (PVCs) from right ventricular outflow tract (RVOT). <B>Methods:</B> We evaluated the number and the location of PVCs/VTs foci of the 87 patients (mean age 43 y, 54 females) who underwent radiofrequency ablation (RF) to the RVOT or coronary cusp without structural heart disease or Brugada syndrome. <B>Results:</B> Endocardial mapping showed no scar or low voltage area from RVOT during sinus rhythm. Seventy-five patients had monomorphic PVCs/VTs and exhibited no PVT or VF during both Holter monitors and RF. In 12 patients with PVCs of different morphologies, 9 patients had multiple PVCs originated from only RVOT septal area, and showed no PVT/VF. However, the other 3 patients had PVCs from both RVOT septum and free wall origins, and exhibited PVT and VF. Moreover, PVTs/VFs were triggered by spontaneous PVCs from only free wall foci of RVOT in those 3 patients. <B>Conclusions:</B> PVCs from free wall RVOT origin may induce malignant VT/VF in patients with idiopathic RVOT tachy-arrhythmias from multiple foci of both septal and free wall areas. Site-specific arrhythmogenesis presents in such patients.