Novel ECG predictor of difficult cases of outflow tract ventricular tachycardia: peak deflection index on an inferior lead.
ABSTRACT An ECG predictor of ablation success has not been determined for difficult cases of outflow tract ventricular tachycardia/ventricular premature contractions (OT-VT/VPC).
ECG analysis and radiofrequency catheter ablation (RFCA) were performed in 70 patients with OT-VT/VPC. The peak deflection index (PDI) was determined in the inferior lead presenting the tallest R wave by dividing the time from QRS onset to peak QRS deflection by total QRS duration. In 10 (14%) of the 70 patients, RFCA performed at a septal or epicardial site was unsuccessful (group 1), but was successful in the remaining 60 patients (group 2). Neither activation time (35+/-15 ms vs 40+/-12 ms, P=0.3) nor QRS duration (141+/-19 ms vs 137+/-19 ms, P=0.6) were significantly different between groups 1 and 2. However, PDI was significantly higher in group 1 than in group 2 (0.62+/-0.06 vs 0.55+/-0.06, P=0.002). A PDI >0.6 identified unsuccessful OT-VT/VPC with 80% sensitivity and 90% specificity, and may indicate that the origin of the OT-VT/VPC is deep within the ventricular septum or at an epicardial site.
A PDI >0.6 is more likely to be associated with a higher rate of RFCA failure.
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ABSTRACT: 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). 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). 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.Circulation 04/2006; 113(13):1659-66. · 15.20 Impact Factor
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ABSTRACT: A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced.Circulation Journal 06/2008; 72(5):855-60. · 3.58 Impact Factor
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ABSTRACT: Increasing electrode size allows an increase in radiofrequency lesion depth. The purpose of this study was to examine the roles of added electrode cooling and electrode-tissue interface area in producing deeper lesions. METHODS and In 10 dogs, the thigh muscle was exposed and superfused with heparinized blood. An 8-French catheter with 4- or 8-mm tip electrode was positioned against the muscle with a blood flow of 350 mL/min directed around the electrode. Radiofrequency current was delivered using four methods: (1) electrode perpendicular to the muscle, using variable voltage to maintain the electrode-tissue interface temperature at 60 degrees C; (2) same except the surrounding blood was stationary; (3) perpendicular electrode position, maintaining tissue temperature (3.5-mm depth) at 90 degrees C; and (4) electrode parallel to the muscle, maintaining tissue temperature at 90 degrees C. Electrode-tissue interface temperature, tissue temperature (3.5- and 7.0-mm depths), and lesion size were compared between the 4- and 8-mm electrodes in each method. In Methods 1 and 2, the tissue temperatures and lesion depth were greater with the 8-mm electrode. These differences were smaller without blood flow, suggesting the improved convective cooling of the larger electrode resulted in greater power delivered to the tissue at the same electrode-tissue interface temperature. In Method 3 (same tissue current density), the electrode-tissue interface temperature was significantly lower with the 8-mm electrode. With parallel orientation and same tissue temperature at 3.5-mm depth (Method 4), the tissue temperature at 7.0-mm depth and lesion depth were greater with the 8-mm electrode, suggesting increased conductive heating due to larger volume of resistive heating because of the larger electrode-tissue interface area. With a larger electrode, both increased cooling and increased electrode-tissue interface area increase volume of resistive heating and lesion depth.Journal of Cardiovascular Electrophysiology 02/1998; 9(1):47-54. · 3.48 Impact Factor