scholarly journals Left Axis Deviation in Brugada Syndrome: Vectorcardiographic Evaluation during Ajmaline Provocation Testing Reveals Additional Depolarization Abnormalities

2021 ◽  
Vol 22 (2) ◽  
pp. 484
Author(s):  
Martijn H. van der Ree ◽  
Jeroen Vendrik ◽  
Jan A. Kors ◽  
Ahmad S. Amin ◽  
Arthur A. M. Wilde ◽  
...  

Patients with Brugada syndrome (BrS) can show a leftward deviation of the frontal QRS-axis upon provocation with sodium channel blockers. The cause of this axis change is unclear. In this study, we aimed to determine (1) the prevalence of this left axis deviation and (2) to evaluate its cause, using the insights that could be derived from vectorcardiograms. Hence, from a large cohort of patients who underwent ajmaline provocation testing (n = 1430), we selected patients in whom a type-1 BrS-ECG was evoked (n = 345). Depolarization and repolarization parameters were analyzed for reconstructed vectorcardiograms and were compared between patients with and without a >30° leftward axis shift. We found (1) that the prevalence of a left axis deviation during provocation testing was 18% and (2) that this left axis deviation was not explained by terminal conduction slowing in the right ventricular outflow tract (4th QRS-loop quartile: +17 ± 14 ms versus +13 ± 15 ms, nonsignificant) but was associated with a more proximal conduction slowing (1st QRS-loop quartile: +12[8;18] ms versus +8[4;12] ms, p < 0.001 and 3rd QRS-loop quartile: +12 ± 10 ms versus +5 ± 7 ms, p < 0.001). There was no important heterogeneity of the action potential morphology (no difference in the ventricular gradient), but a left axis deviation did result in a discordant repolarization (spatial QRS-T angle: 122[59;147]° versus 44[25;91]°, p < 0.001). Thus, although the development of the type-1 BrS-ECG is characterized by a terminal conduction delay in the right ventricle, BrS-patients with a left axis deviation upon sodium channel blocker provocation have an additional proximal conduction slowing, which is associated with a subsequent discordant repolarization. Whether this has implications for risk stratification is still undetermined.

2008 ◽  
Vol 51 (12) ◽  
pp. 1154-1161 ◽  
Author(s):  
Satoshi Nagase ◽  
Kengo Fukushima Kusano ◽  
Hiroshi Morita ◽  
Nobuhiro Nishii ◽  
Kimikazu Banba ◽  
...  

2021 ◽  
Vol 32 (4) ◽  
pp. 1182-1186
Author(s):  
Tsukasa Kamakura ◽  
Josselin Duchateau ◽  
Frédéric Sacher ◽  
Pierre Jais ◽  
Michel Haïssaguerre ◽  
...  

2021 ◽  
Vol 10 (5) ◽  
pp. 1025
Author(s):  
Nicolò Martini ◽  
Martina Testolina ◽  
Gian Luca Toffanin ◽  
Rocco Arancio ◽  
Luca De Mattia ◽  
...  

The so-called Brugada syndrome (BS), first called precordial early repolarization syndrome (PERS), is characterized by the association of a fascinating electrocardiographic pattern, namely an aspect resembling right bundle branch block with a coved and sometime upsloping ST segment elevation in the precordial leads, and major ventricular arrhythmic events that could rarely lead to sudden death. Its electrogenesis has been related to a conduction delay mostly, but not only, located on the right ventricular outflow tract (RVOT), probably due to a progressive fibrosis of the conduction system. Many tests have been proposed to identify people at risk of sudden death and, among all, ajmaline challenge, thanks to its ability to enhance latent conduction defects, became so popular, even if its role is still controversial as it is neither specific nor sensitive enough to guide further invasive investigations and managements. Interestingly, a type 1 pattern has also been induced in many other cardiac diseases or systemic diseases with a cardiac involvement, such as long QT syndrome (LQTS), arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM) and myotonic dystrophy, without any clear arrhythmic risk profile. Evidence-based studies clearly showed that a positive ajmaline test does not provide any additional information on the risk stratification for major ventricular arrhythmic events on asymptomatic individuals with a non-diagnostic Brugada ECG pattern.


Author(s):  
Pablo E Tauber ◽  
Virginia Mansilla ◽  
Pedro Brugada ◽  
Sara S Sánchez P ◽  
Stella M Honoré ◽  
...  

Background: Radiofrequency ablation (RFA) in Brugada syndrome (BrS) has been performed both endocardially and epicardially. The substrate in BrS is thus unclear. Objectives: To investigate the functional endocardial substrate and its correlation with clinical, electrophysiological and ECG findings in order to guide an endocardial ablation. Methods: Thirteen patients (38.7±12.3 years old) with spontaneous type 1 ECG BrS pattern, inducible VF with programmed ventricular stimulation (PVS) and syncope without prodromes were enrolled. Before to endocardial mapping the patients underwent flecainide testing with the purpose of measuring the greatest ST-segment elevation for to be correlated with the size and location of substrate in the electro-anatomic map. Patients underwent endocardial bipolar and electro-anatomic mapping with the purpose of identify areas of abnormal electrograms (EGMs) as target for RFA and determine the location and size of the substrate. Results: When the greatest ST-segment elevation was in the 3rd intercostal space (ICS), the substrate was located upper in the longitudinal plane of the right ventricular outflow tract (RVOT) and a greatest ST-segment elevation in 4th ICS correspond with a location of substrate in lower region of longitudinal plane of RVOT. A QRS complex widening on its initial and final part, with prolonged transmural and regional depolarization time of RVOT corresponded to the substrate locateded in the anterior-lateral region of RVOT. A QRS complex widening rightwards and only prolonged transmural depolarization time corresponded with a substrate located in the anterior, anterior-septal or septal region of RVOT. RFA of endocardial substrate suppressed the inducibility and ECG BrS pattern during 34.7±15.5 months. After RFA, flecainide testing confirmed elimination of the ECG BrS pattern. Endocardial biopsy showed a correlation between functional and ultrastructural alterations in two patients.


2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Yae Min Park ◽  
Mi Sook Cha ◽  
Hanul Choi ◽  
Woong Chol Kang ◽  
Seung Hwan Han ◽  
...  

A 52-year-old male with Brugada syndrome presented with repeated and appropriate shock from an implantable cardioverter defibrillator (ICD). Catheter ablation for substrate elimination targeting low-voltage, complex, and fractionated electrocardiograms and late potentials in the epicardial right ventricular outflow tract was successfully performed. Brugada phenotype in the right precordial leads from the third intercostal space disappeared in the early stage after catheter ablation and that from the standard fourth intercostal space disappeared later. He remained free from ventricular fibrillation over the next fourteen months. We suggest that this novel ablation strategy is effective in Brugada syndrome patients with ICD, and early response after catheter ablation can be predicted by high precordial leads.


EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
P Carvalho ◽  
C Gravinese ◽  
A Previti ◽  
G P Varalda ◽  
L Montagna

Abstract Background 12 lead-Holter monitoring is commonly used for the assessment  of type 1 Brugada repolarization"s burden. However, data considering the prevalence and morphology of premature ventricular contractions (PVC) in these patients is lacking. Purpose. We investigated the prevalence of PVCs in subjects with Brugada syndrome (BRs) phenotype during 24-hour 12 lead-Holter monitoring (12-L Holter), trying to identify their origin according to morphology.  Methods. From January 2013 to September 2018, a total of 156 patients with type 1 BRs phenotype (spontaneous or drug induced) were screened for PVCs. In these patients we placed the right precordial leads at the second (V1-V2) and the forth (V3-V4) intercostal spaces.  Results. 83 subjects (53%) displayed PVCs. Their mean age was 50 years (range 21-73) and 63 (76%) were male. 14 subjects (17%) had a spontaneous type 1 repolarization whereas 69 (83%) presented a drug induced type 1. One patient had implanted an ICD as secondary prevention after an aborted sudden cardiac death. The others were mostly asymptomatic as only five of them (6%) had history of suspected cardiac syncope. 17 subjects (20%) had performed an electrophysiological study, which resulted positive in 3 cases (4%). The population without PVCs had similar baseline characteristics. In 59 (71%) patients PVCs were monomorphic, in the other 29% we analyzed the prevalent morphology. PVCs were classified according to their morphology as follows (i) left bundle branch block (LBBB)/inferior axis suggesting an origin from the right ventricular outflow tract (RVOT), that was shown in 40 (48%) subjects; (ii) right bundle branch block (RBBB)/left axis suggesting an origin close to the posterior fascicle of the left bundle branch in 36 (43%). The other 7 patients presented several morphologies. According to their number during the 24-hour monitoring, PVCs were arbitrarily classified as follows: (i) 1-59,present in 62 patients (75%); (ii) 60-749, present in 16 patients (19%); (iii) 750-9000, present in 4 patients (5%); (iv) &gt;9000, in only one patient (1%).  Conclusions. In our population of subjects with BRs phenotype the prevalence of PCVs is similar to that of the general population. Their morphologies suggest an origin from the RVOT or close to the posterior fascicle of the left bundle branch.


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