Branch Block Ventricular Tachycardia Research Articles

Electrocardiographic findings in patients with arrhythmogenic cardiomyopathy and right bundle branch block ventricular tachycardia.

Little is known about patients with right bundle branch block (RBBB)-ventricular tachycardia (VT) and arrhythmogenic cardiomyopathy (ACM). Our aims were: (i) to describe electrocardiogram (ECG) characteristics of sinus rhythm (SR) and VT; (ii) to correlate SR with RBBB-VT ECGs; and (iii) to compare VT ECGs with electro-anatomic mapping (EAM) data. From the European Survey on ACM, 70 patients with spontaneous RBBB-VT were included. Putative left ventricular (LV) sites of origin (SOOs) were estimated with a VT-axis-derived methodology and confirmed by EAM data when available. Overall, 49 (70%) patients met definite Task Force Criteria. Low QRS voltage predominated in lateral leads (n = 37, 55%), but QRS fragmentation was more frequent in inferior leads (n = 15, 23%). T-wave inversion (TWI) was equally frequent in inferior (n = 28, 42%) and lateral (n = 27, 40%) leads. TWI in inferior leads was associated with reduced LV ejection fraction (LVEF; 46 ± 10 vs. 53 ± 8, P = 0.02). Regarding SOOs, the inferior wall harboured 31 (46%) SOOs, followed by the lateral wall (n = 17, 25%), the anterior wall (n = 15, 22%), and the septum (n = 4, 6%). EAM data were available for 16 patients and showed good concordance with the putative SOOs. In all patients with superior-axis RBBB-VT who underwent endo-epicardial VT activation mapping, VT originated from the LV. In patients with ACM and RBBB-VT, RBBB-VTs originated mainly from the inferior and lateral LV walls. SR depolarization and repolarization abnormalities were frequent and associated with underlying variants.

Right bundle branch block ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy more commonly originates from the right ventricle: Criteria for identifying chamber of origin

Right bundle branch block (RBBB) ventricular tachycardia (VT) morphology is a criterion for left ventricular (LV) involvement in arrhythmogenic right ventricular cardiomyopathy (ARVC). The purpose of this study was to determine the frequency and chamber of origin of RBBB VT in patients with ARVC and VT. We studied 110 consecutive patients with VT who met the diagnostic International Task Force criteria for ARVC and underwent VT mapping/ablation. Patients with ≥1 RBBB VT were identified. Right ventricular (RV) origin of the RBBB VT was determined based on standard mapping criteria and elimination with ablation. Nineteen patients (17%) had 26 RBBB VTs. Eleven of these 19 patients (58%) had 16 RBBB VTs from the RV, and 9 patients (47%) had 10 RBBB VTs originating from the LV, with 1 patient demonstrating both. RBBB VT from RV most commonly (13/16 RBBB VTs) had an early precordial QRS transition (V2 or V3), with superiorly and typically leftward directed frontal plane axis, consistent with exit from dilated RV adjacent to inferior LV septum, whereas all 10 VTs from LV had RBBB morphology with positive R waves to V5 or V6 and rightward axis in 6 VTs characteristic of basal lateral origin. In patients with ARVC and VT presenting for VT ablation, RBBB VT occurs in 17% of cases, with most RBBB VTs (62%) originating from the RV and not indicative of LV origin. Precordial R-wave transition and frontal plane axis can be used to identify the anticipated chamber of origin of RBBB VT.

Characterization of Structural Changes in Arrhythmogenic Right Ventricular Cardiomyopathy With Recurrent Ventricular Tachycardia After Ablation: Insights From Repeat Electroanatomic Voltage Mapping.

Data characterizing structural changes of arrhythmogenic right ventricular (RV) cardiomyopathy are limited. Patients presenting with left bundle branch block ventricular tachycardia in the setting of arrhythmogenic RV cardiomyopathy with procedures separated by at least 9 months were included. Nineteen consecutive patients (84% males; mean age 39±15 years [range, 20-76 years]) were included. All 19 patients underwent 2 detailed sinus rhythm electroanatomic endocardial voltage maps (average 385±177 points per map; range, 93-847 points). Time interval between the initial and repeat ablation procedures was mean 50±37 months (range, 9-162). No significant progression of voltage was observed (bipolar: 38 cm2 [interquartile range (IQR), 25-54] versus 53 cm2 [IQR, 25-65], P=0.09; unipolar: 116 cm2 [IQR, 61-209] versus 159 cm2 [IQR, 73-204], P=0.36) for the entire study group. There was a significant increase in RV volumes (percentage increase, 28%; 206 mL [IQR, 170-253] versus 263 mL [IQR, 204-294], P<0.001) for the entire study population. Larger scars at baseline but not changes over time were associated with a significant increase in RV volume (bipolar: Spearman ρ, 0.6965, P=0.006; unipolar: Spearman ρ, 0.5743, P=0.03). Most patients with progressive RV dilatation (8/14, 57%) had moderate (2 patients) or severe (6 patients) tricuspid regurgitation recorded at either initial or repeat ablation procedure. In patients with arrhythmogenic RV cardiomyopathy presenting with recurrent ventricular tachycardia, >10% increase in RV endocardial surface area of bipolar voltage consistent with scar is uncommon during the intermediate term. Most recurrent ventricular tachycardias are localized to regions of prior defined scar. Voltage indexed scar area at baseline but not changes in scar over time is associated with progressive increase in RV size and is consistent with adverse remodeling but not scar progression. Marked tricuspid regurgitation is frequently present in patients with arrhythmogenic RV cardiomyopathy who have progressive RV dilation.

Serial Reevaluation for ARVD/C Is Indicated in Patients Presenting with Left Bundle Branch Block Ventricular Tachycardia and Minor ECG Abnormalities

Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is based on a set of criteria proposed by the International Task Force (TF) for Cardiomyopathies in 1994. To fulfill these criteria, presence of both electrocardiographic and anatomical abnormalities must be assessed with ECG and imaging techniques, respectively. This may be difficult in patients with early/mild forms of the disease as detectable structural abnormalities may still be absent. We evaluated in which patients presenting with right ventricular tachycardia (VT) serial reevaluation for ARVD/C is indicated. Sixty consecutive patients (41 men, mean age 40+/-15 years) were evaluated by the TF criteria for possible ARVD/C because of presentation with a left bundle branch block (LBBB) VT, representing 1 minor criterion. The presence on the ECG of a T-wave inversion beyond lead V2 (1 minor), right precordial QRS prolongation (1 major), or an epsilon wave (1 major) was assessed together with the visualization of severe regional/global right ventricle dysfunction (1 major) or mild segmental dilatation/regional hypokinesia (1 minor) by standard imaging techniques. Initially, 22 (37%) patients were diagnosed as having ARVD/C. After 47+/-39 (range 6-146) months, 23 initially TF-negative patients were reevaluated because of recurrent symptoms, with 12 (52%) additional patients now meeting the TF criteria. Eleven of these 12 (92%) patients presented initially with ECG abnormalities only, but developed structural abnormalities on imaging at follow-up. ECG abnormalities may precede structural abnormalities warranting serial reevaluation for ARVD/C in initially TF-negative patients presenting with LBBB VT with only ECG abnormalities.

Value of task force criteria in the diagnosis of arrhythmogenic right ventricular dysplasia-cardiomyopathy

Besides autopsy determined findings of a fibro-fatty replacement in the right ventricular myocardium, no assured clinical evidence of arrhythmogenie right ventricular dysplasia-cardiomyopathy (ARVD) exists yet. Criteria for the clinical diagnosis of AVRD were complied in 1994 by members of the ISFC work group and the European Association for Cardiology. These criteria include structural, functional, histological, and electrophysiological abnormalities, which were divided into major and minor criteria. With the successive examination of a collective of 24 patients with a histologically determined diagnosis of ARVD at the Jean Rostand Hospital in Ivry-sur-Seien, France, the value of the complied criteria were checked. Global or segmental dilatation of the right ventricle in the sense of major criteria could be proven in 20 patients (83%) using angiography or electrocardiography. Four patients (16%) exhibited only minor criteria in the radionuclear angioscintigraphy or right ventricular angiography in the form of segmental kinetic disturbances of the right ventricular. In all patients, the typical fibrofatty replacement in the right ventricular myocardium could be histologically determined. T-inversion in the right precordial leads were present in 17 patients (71%). A localized QRS-widening of more than 110ms in V1 to V3 in 8 patients (33%) and an epsilon wave in 6 patients (25%) were observed as major criteria. A late potential analysis using signal averaged ECG was only present in 8 patients with positive results in 4 cases (50%) in the sense of minor criteria. Left bundle branch block ventricular tachycardia, which was classified as a minor criterion, was observed in 23 patients (96%); only one patient died without proven arrhythmia from rapidly progressing heart failure. A previous history of unexpected sudden death in family members as a minor criterion arose in 3 of 19 patients (15%). The complied task force criteria for the diagnosis of AVRD led in all 24 cases to the diagnosis of the disease, whereby the value of a determined histological diagnosis was the gold standard. Without inclusion of histological data, the clinical diagnosis was determined in only 10 cases. The question remains whether with a simple division of findings into major and minor criteria a pure clinical diagnosis is possible.