The QRS frontal plane axis changes during left bundle branch block after transcatheter aortic valve replacement.

BACKGROUND AND AIMS: Left bundle branch block (LBBB) is common after transcatheter aortic valve replacement (TAVR) and associated with a left or normal QRS axis. We aim to assess the QRS frontal plane axis shift changes during LBBB after TAVR and determine if the risk of procedure-related high degree atrioventricular block (AVB) is affected by QRS axis shift changes. METHODS AND RESULTS: In a retrospective single-center study of 720 consecutive patients who underwent TAVR, 141 (19.6%) with normal baseline QRS duration developed a new LBBB after TAVR and constituted the study group. Most patients (59.6%) were females and the mean age of the cohort was 81.2 ± 6 years. RESULTS: As compared with the baseline QRS axis before TAVR, the occurrence of LBBB was associated with a leftward QRS axis shift (by 40 ± 28.3°) in 73% of the study patients and a rightward (by 18.6 ± 19.4°) or no change in QRS axis in 25.6% and 1.4% of the study patients, respectively. A left QRS axis (-30°) was observed in 14.9% and 38.3% of the study patients before and after TAVR, respectively. The group of patients exhibiting a rightward or no QRS axis shift had a greater incidence of high degree AVB than the group of patients exhibiting a leftward QRS axis shift (18.4% vs. 6.8%, p = .056). CONCLUSION: Although post TAVR-LBBB is associated with a leftward QRS axis shift in most patients, a non-negligible proportion of patients (27%) exhibited a rightward or no QRS axis shift. The latter group tend to have a higher risk of developing high degree AVB.

Novel Approaches for the Diagnosis of Concealed Nodo-Ventricular and His-Ventricular Pathways.

BACKGROUND: Confirming the presence and participation of concealed nodo-ventricular (cNV) or concealed His-ventricular (cHV) pathways in tachyarrhythmias is challenging. We describe novel observations to aid in diagnosing cNV or cHV pathways. METHODS: We present 7 cases of cNV and cHV pathway-mediated arrhythmias and focus on several laboratory observations: (1) differential ventricular overdrive pacing (VOD) from the base versus apex, (2) response to His refractory premature ventricular complexes, (3) paradoxical atriohisian response (shorter atriohisian interval during tachycardia than that during sinus rhythm) in long RP tachycardia, and (4) the role of adenosine to aid in the diagnosis. RESULTS: Three cases underwent differential VOD during tachycardia. All demonstrated a shorter postpacing interval minus tachycardia cycle length during basal pacing than apical pacing with one case exhibiting apical VOD results compatible with atrioventricular nodal reentrant tachycardia. Basal VOD was useful for localizing the ventricular connection in a case with cHV pathway. In 3 cases, His refractory premature ventricular complexes reset the tachycardia without conduction to the atrium, which excluded the involvement of an atrioventricular pathway or atrial tachycardia, or atrioventricular nodal reentrant tachycardia alone. One case had His refractory premature ventricular complexes followed by subsequent constant AA interval and then tachycardia termination, suggesting a bystander cNV pathway involvement. Two cNV pathway cases presented with long RP tachycardia had paradoxical atriohisian shortening of >15 ms, suggesting parallel activation of the atrium and the atrioventricular node. Adenosine terminated the tachycardia with retrograde block in 2 cases with cNV pathways but had no response on a cHV pathway. CONCLUSIONS: cNV and cHV pathways mediated tachyarrhythmias can present with variable clinical presentations. We emphasize the important role of differential VOD sites, His refractory premature ventricular complexes that reset or terminate the tachycardia without conduction to the atrium, paradoxical atriohisian response in long RP tachycardia, and the use of adenosine for diagnosing cNV and cHV pathways.

The R-wave amplitude in V1 on baseline electrocardiogram correlates with the occurrence of high-degree atrioventricular block following left bundle branch block after transcatheter aortic valve replacement.

AIMS: Several procedural and electrocardiogram (ECG) parameters have been associated with the occurrence of high-degree atrioventricular block (AVB) requiring permanent pacemaker implantation (PPI) after transcatheter aortic valve replacement (TAVR). We hereunder sought to assess if the baseline R-wave amplitude in V1 ECG lead of patients with normal QRS duration undergoing TAVR is associated with a higher patient's risk for developing high-degree AVB following left bundle branch block (LBBB). METHODS AND RESULTS: In this retrospective single-centre study in 720 consecutive patients who underwent TAVR, 141 (19.6%) patients with normal QRS duration developed a new LBBB after TAVR. The 24 (17%) patients who underwent PPI for reasons other than high-degree AVB were excluded from further analysis. In the remaining 117 study patients, 14 (12%) developed high-degree AVB requiring PPI (Group 1) while the remaining 103 (88%) patients did not (Group 2). There were no significant differences in baseline demographic or procedural characteristics nor in PR interval, QRS duration, and QRS axis between these two groups. The incidence of left anterior hemiblock was higher in Group 1 (3 of 14, 21.4%) than that in Group 2 (9 of 103, 8.7%), but the difference was not statistically significant (P = 0.156). The R-wave amplitude in V1 was smaller in Group 1 than that in Group 2 (0.029 ± 0.04 mV vs. 0.11 ± 0.14 mV, P = 0.0316). In the receiver-operating characteristics analysis, the cutoff for R-wave amplitude pre-TAVR was 0.03 mV, area under the curve = 0.7219 (P = 0.0002). CONCLUSION: The R-wave amplitude in lead V1 during baseline ECG in patients with normal QRS duration may predict the occurrence of high-degree AVB following new LBBB after TAVR.

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

AIMS: 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. METHODS AND RESULTS: 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. CONCLUSIONS: 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.

Red Flags in Syncope: Clues for the Diagnosis of Idiopathic Ventricular Fibrillation.

Idiopathic ventricular fibrillation is responsible for ≈5%-7% of aborted cardiac arrest, mainly striking subjects in their forties. Syncope caused by short-coupled rapid polymorphic ventricular tachycardia is frequently noted in a patient's past history. However, a diagnosis of neurally mediated syncope, the most frequent cause of syncope in the young, is often erroneously made. Clinical clues suggest that syncope has an arrhythmic rather than a neurally mediated origin. In addition, the presence of premature ventricular contractions on an electrocardiogram recorded shortly after a syncopal event has utmost importance in establishing the cause of syncope. Although such extrasystoles are frequently benign, especially when associated with a long coupling interval, they also may suggest a malignant origin when closely coupled to the preceding complex with short coupling intervals (usually <350 ms). These arrhythmias mainly originate from the Purkinje system (usually the right ventricle in men and the left ventricle in women) and favorably respond to quinidine as well as to ablation therapy targeting Purkinje-fibers ectopic activity.

Short-Coupled Idiopathic Ventricular Fibrillation: A Literature Review With Extended Follow-Up.

Idiopathic ventricular fibrillation is responsible for approximately 5%-7% of cases of aborted cardiac arrest. Recent studies have shown that short-coupled ventricular premature complexes are present at the onset of idiopathic ventricular fibrillation in 6.6%-17% of patients. The present review provided information on 86 patients with short-coupled malignant ventricular arrhythmias that were reported as case reports or small patient series during the last 70 years. In 75% of the 81 cases published during the last 40 years, extended information and follow-up (from 2.63 ± 4.5 years to 10.67 ± 7.8 years; P < 0.001, between the original publication to the latest update) could be obtained from the authors. The review shows that short-coupled malignant ventricular arrhythmias occurred almost equally in males and females, at the mean age of 40 years. A tendency for later occurrence of the arrhythmia by 4 years was observed in females. A prior history of syncope was noted in 45.3% of the patients, whereas arrhythmic storm occurred in 42% at presentation. The most common mode of revelation of short-coupled malignant ventricular arrhythmias was syncope (53.5%), followed by aborted cardiac arrest (26.7%) and recurrent arrhythmic event after prior implantable-cardioverter defibrillator implantation for idiopathic ventricular fibrillation (17.4%). For the first time, short-coupled malignant arrhythmias exhibiting "not-so-short" coupling intervals (≥350 milliseconds) were found in a significant proportion of patients (17.4%). During long-term follow-up, quinidine yielded a slightly higher success rate in arrhythmia control than ablation. Larger studies are necessary to assess the best strategy for the management of this potentially lethal arrhythmia.