scholarly journals Evaluation of the Mandibular Incisive Canal by Panoramic Radiography and Cone-Beam Computed Tomography

2018 ◽  
pp. 1-13
Author(s):  
Pablo E Tauber ◽  
Virginia Mansilla ◽  
Pedro Brugada ◽  
Sara S Sánchez P ◽  
Stella M Honoré ◽  
...  
Keyword(s):  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Qrs Complex ◽  
Incisive Canal ◽  
St Segment Elevation ◽  
Longitudinal Plane ◽  
St Segment ◽  
Endocardial Mapping ◽  
The Right

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.

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 ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Conduction Delay ◽  
Channel Blockers ◽  
Axis Deviation ◽  
Provocation Testing ◽  
The Right

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.

scholarly journals Role of Provocable Brugada ECG Pattern in The Correct Risk Stratification for Major Arrhythmic Events

2021 ◽  
Vol 10 (5) ◽  
pp. 1025
Author(s):  
Nicolò Martini ◽  
Martina Testolina ◽  
Gian Luca Toffanin ◽  
Rocco Arancio ◽  
Luca De Mattia ◽  
...  
Keyword(s):  
Sudden Death ◽  
Risk Stratification ◽  
Right Ventricular ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Conduction Delay ◽  
St Segment Elevation ◽  
Additional Information ◽  
The Right

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.

scholarly journals Sudden Cause of Cardiac Death—Be Aware of Me: A Case Report and Short Review on Brugada Syndrome

2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Jagadeesh K. Kalavakunta ◽  
Vishwaroop Bantu ◽  
Hemasri Tokala ◽  
Mihas Kodenchery
Keyword(s):  
Brugada Syndrome ◽  
Past History ◽  
Short Review ◽  
Case Presentation ◽  
St Segment Elevation ◽  
First Case ◽  
St Segment ◽  
The Right ◽  
Malignant Arrhythmias

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads.Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias.Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.

scholarly journals Brugada syndrome: Case report

2012 ◽  
Vol 140 (1-2) ◽  
pp. 84-90
Author(s):  
Vesna Bisenic ◽  
Sasa Hinic ◽  
Mirjana Krotin ◽  
Branislav Milovanovic ◽  
Jelena Saric ◽  
...  
Keyword(s):  
Family History ◽  
Sudden Death ◽  
Brugada Syndrome ◽  
Troponin T ◽  
Stable Condition ◽  
St Segment Elevation ◽  
St Segment ◽  
History Of ◽  
The Right

Introduction. Brugada syndrome is an arrhythmogenic disease characterized by coved ST segment elevation and J point elevation of at least 2 mm in at least two of the right precordial ECG leads (V1-3) and ventricular arrhythmias, syncope, and sudden death. Risk stratifications of patients with Brugada electrocardiogram are being strongly debated. Case Outline. A 23-year-old man was admitted to the Coronary Care Unit of the Clinical Centre ?Bezanijska kosa? due to weakness, fatigue and chest discomfort. The patient suffered from fainting and palpitations. There was a family history of paternal sudden death at 36 years. Electrocardiogram showed a coved ST segment elevation of 4 mm in leads V1 and V2, recognised as spontaneous type 1 Brugada pattern. Laboratory investigations revealed normal serum cardiac troponin T and serum potassium, and absence of inflammation signs. Echocardiographic finding was normal, except for a mild enlargement of the right atrium and ventricle. The diagnosis of Brugada syndrome was made by Brugada-type 1 electrocardiogram and the family history of sudden death <45 years. The patient was considered as a high risk, because of pre-syncope and palpitations. He underwent ICD implantation (Medtronic MaximoVR7232Cx) using the standard procedure. After implantation, noninvasive electrophysiology study was done and demonstrated inducible VF that was interrupted with the second 35 J DC shock. The patient was discharged in stable condition with beta-blocker therapy. After a year of pacemaker check-ups, there were no either VT/ VF events or ICD therapy. Conclusion. Clinical presentation is the most important parameter in risk stratification of patients with Brugada electrocardiogram and Brugada syndrome.

scholarly journals Longer Repolarization in the Epicardium at the Right Ventricular Outflow Tract Causes Type 1 Electrocardiogram in Patients With Brugada Syndrome

2008 ◽  
Vol 51 (12) ◽  
pp. 1154-1161 ◽  
Author(s):  
Satoshi Nagase ◽  
Kengo Fukushima Kusano ◽  
Hiroshi Morita ◽  
Nobuhiro Nishii ◽  
Kimikazu Banba ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Brugada Syndrome ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
The Right

scholarly journals Fractionated electrograms with ST-segment elevation recorded from the human right ventricular outflow tract

2017 ◽  
Vol 3 (11) ◽  
pp. 546-550 ◽  
Author(s):  
Edward J. Vigmond ◽  
Igor R. Efimov ◽  
Stacey L. Rentschler ◽  
Ruben Coronel ◽  
Bastiaan J. Boukens
Keyword(s):  
Right Ventricular ◽  
Right Ventricular Outflow Tract ◽  
Ventricular Outflow Tract ◽  
Outflow Tract ◽  
Human Right ◽  
St Segment Elevation ◽  
St Segment ◽  
Fractionated Electrograms
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