BACKGROUND: Despite the success of catheter ablation for treatment of idiopathic ventricular tachycardia (VT), occasional patients have been reported in whom VT could not be ablated from the right or left ventricular endocardium or from the aortic sinus of Valsalva (ASOV). METHODS AND RESULTS: In 12 of 138 patients (9%) with idiopathic VT referred for ablation, an epicardial left ventricular site of origin was identified >10 mm from the ASOV. Coronary venous mapping demonstrated epicardial preceding endocardial activation by >10 ms (41+/-7 versus 15+/-11 ms before QRS onset; P<0.001). VT induction was facilitated by catecholamines and terminated by adenosine. Ablation through the coronary veins or via percutaneous transpericardial catheterization was successful in 9 patients; 2 required direct surgical ablation as a result of anatomic constraints. No ECG pattern was specific for epicardial VT. However, slowed initial precordial QRS activation, as quantified by a novel metric, the maximum deflection index, was more useful. A delayed precordial maximum deflection index > or =0.55 identified epicardial VT remote from the ASOV with a sensitivity of 100% and a specificity of 98.7% relative to all other sites of origin (P<0.001). CONCLUSIONS: Although clinically underrecognized, idiopathic VT may originate from the perivascular sites on the left ventricular epicardium. The mechanism is consistent with triggered activity. It is amenable to ablation by transvenous or transpericardial approaches, although technical challenges remain. Recognition of a prolonged precordial maximum deflection index and early use of transvenous epicardial mapping are critical to avoid protracted and unsuccessful ablation elsewhere in the ventricles.
BACKGROUND: Despite the success of catheter ablation for treatment of idiopathic ventricular tachycardia (VT), occasional patients have been reported in whom VT could not be ablated from the right or left ventricular endocardium or from the aortic sinus of Valsalva (ASOV). METHODS AND RESULTS: In 12 of 138 patients (9%) with idiopathic VT referred for ablation, an epicardial left ventricular site of origin was identified >10 mm from the ASOV. Coronary venous mapping demonstrated epicardial preceding endocardial activation by >10 ms (41+/-7 versus 15+/-11 ms before QRS onset; P<0.001). VT induction was facilitated by catecholamines and terminated by adenosine. Ablation through the coronary veins or via percutaneous transpericardial catheterization was successful in 9 patients; 2 required direct surgical ablation as a result of anatomic constraints. No ECG pattern was specific for epicardial VT. However, slowed initial precordial QRS activation, as quantified by a novel metric, the maximum deflection index, was more useful. A delayed precordial maximum deflection index > or =0.55 identified epicardial VT remote from the ASOV with a sensitivity of 100% and a specificity of 98.7% relative to all other sites of origin (P<0.001). CONCLUSIONS: Although clinically underrecognized, idiopathic VT may originate from the perivascular sites on the left ventricular epicardium. The mechanism is consistent with triggered activity. It is amenable to ablation by transvenous or transpericardial approaches, although technical challenges remain. Recognition of a prolonged precordial maximum deflection index and early use of transvenous epicardial mapping are critical to avoid protracted and unsuccessful ablation elsewhere in the ventricles.
Authors: Apoor S Gami; Amit Noheria; Nirusha Lachman; William D Edwards; Paul A Friedman; Deepak Talreja; Stephen C Hammill; Thomas M Munger; Douglas L Packer; Samuel J Asirvatham Journal: J Interv Card Electrophysiol Date: 2010-12-15 Impact factor: 1.900
Authors: Saman Nazarian; Sergey V Kantsevoy; Menekhem M Zviman; Fredrick A Matsen; Hugh Calkins; Ronald D Berger; Henry R Halperin Journal: Heart Rhythm Date: 2008-05-09 Impact factor: 6.343