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brugada ecg

Raoyrin Chanavirut, Pattarapong Makarawate, Ian A Macdonald, Naruemon Leelayuwat
BACKGROUND: Imbalances of the autonomic nervous (ANS), the cardiovascular system, and ionics might contribute to the manifestation of The Brugada Syndrome (BrS). Thus, this study has aimed to investigate the cardio-respiratory fitness and the responses of the ANS both at rest and during a sub-maximal exercise stress test, in BrS patients and in gender-matched and age-matched healthy sedentary controls. METHODS: Eleven BrS patients and 23 healthy controls were recruited in Khon Kaen, Thailand...
October 2016: Journal of Arrhythmia
Jyh-Ming Jimmy Juang, Minoru Horie
In 1992, the Brugada syndrome (BrS) was recognized as a disease responsible for sudden cardiac death, characterized by a right bundle-branch block with ST segment elevation in the leads V1 and V2. This syndrome is highly associated with sudden cardiac death, especially in young males. BrS is currently diagnosed in patients with ST-segment elevation showing type 1 morphology ≥ 2 mm in ≥1 leads among the right precordial leads V1 or V2 positioned in the 2nd, 3rd, or 4th intercostal space, and occurring either spontaneously or after a provocative drug test by the intravenous administration of Class I antiarrhythmic drugs...
October 2016: Journal of Arrhythmia
Altuğ Ösken, Nizamettin Selçuk Yelgeç, Regayip Zehir, Tuğba Kemaloğlu Öz, Selçuk Yaylacı, Ramazan Akdemir, Hüseyin Gündüz
Drug-induced torsades de pointes (TdP) is a rare but potentially fatal adverse effect of commonly prescribed medications including cardiac and noncardiac drugs. Importantly, many drugs have been reported to cause the characteristic Brugada syndrome-linked electrocardiography (ECG) abnormalities and/or (fatal) ventricular tachyarrhythmias. Chlorpheniramine and propranolol have the arrhythmogenic effects reported previously. A review of literature revealed a large number of case reports of chlorpheniramine or propranolol use resulting in QTc prolongation, TdP, or both...
July 2016: Indian Journal of Pharmacology
Tiffany Healey, Clifford Buckley, Matthew Mollman
BACKGROUND: Brugada syndrome is a genetic disorder that increases an individual's risk for sudden cardiac death and ventricular dysrhythmias that was first described by the Brugada brothers in 1992. Brugada syndrome is characterized by an atypical electrocardiogram pattern that includes a bundle branch block and ST-segment elevation in the precordial leads. CASE REPORT: A 74-year-old man had a cardiac arrest at the time of a low-speed motor vehicle collision. When emergency medical services arrived, the patient was in torsades de pointes...
October 14, 2016: Journal of Emergency Medicine
Maria Cecilia Gonzalez Corcia, Juan Sieira, Andrea Sarkozy, Carlo de Asmundis, Gian-Battista Chierchia, Jaime Hernandez Ojeda, Gudrun Pappaert, Pedro Brugada
AIMS: To investigate the clinical characteristics, prognoses, and presence of risk factors in young patients with Brugada syndrome (BS). METHODS AND RESULTS: A consecutive cohort of 128 young BS patients (≤25 years old at diagnosis) was analysed. Eighty-eight patients (69%) were asymptomatic, whereas 40 (31%) presented with clinical manifestations of BS. Markers of prognosis and risk were identified upon comparison of these two groups. A history of malignant syncope was strong predictors of ventricular arrhythmic events...
October 13, 2016: Europace: European Pacing, Arrhythmias, and Cardiac Electrophysiology
Nathalie Behar, Bertrand Petit, Vincent Probst, Frederic Sacher, Gaelle Kervio, Jacques Mansourati, Paul Bru, Alfredo Hernandez, Philippe Mabo
AIM: Modulation of ST-segment elevation (STE) and tachyarrhythmic events by the autonomic nervous system (ANS) has been reported in patients with Brugada syndrome (BS). This study examined and compared the autonomic characteristics and STE in symptomatic vs. asymptomatic patients with BS. METHODS AND RESULT: We studied 40 symptomatic and 78 asymptomatic patients (mean age = 46.1 ± 13.7 years; 88 men) who underwent 24 h, 12-lead electrocardiograms, and exercise and a head-up tilt tests...
October 13, 2016: Europace: European Pacing, Arrhythmias, and Cardiac Electrophysiology
Ehud Chorin, Dan Hu, Charles Antzelevitch, Aviram Hochstadt, Luiz Belardinelli, David Zeltser, Hector Barajas-Martinez, Uri Rozovski, Raphael Rosso, Arnon Adler, Jesaia Benhorin, Sami Viskin
BACKGROUND: The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow of sodium current during phase 3 of the action potential caused by mutations in the SCN5A gene. Most sodium channel blockers reduce the early (peak) and late components of the sodium current (INa and INaL), but ranolazine preferentially reduces INaL. We, therefore, evaluated the effects of ranolazine in LQT3 caused by the D1790G mutation in SCN5A. METHODS AND RESULTS: We performed an experimental study of ranolazine in TSA201 cells expressing the D1790G mutation...
October 2016: Circulation. Arrhythmia and Electrophysiology
Prabhakar A, Bansal B L, Patel R K, Dwivedi R, Padia G
No abstract text is available yet for this article.
January 2016: Journal of the Association of Physicians of India
Jonas Ghouse, Christian T Have, Morten W Skov, Laura Andreasen, Gustav Ahlberg, Jonas B Nielsen, Tea Skaaby, Søren-Peter Olesen, Niels Grarup, Allan Linneberg, Oluf Pedersen, Henrik Vestergaard, Stig Haunsø, Jesper H Svendsen, Torben Hansen, Jørgen K Kanters, Morten S Olesen
PURPOSE: We investigated whether Brugada syndrome (BrS)-associated variants identified in the general population have an effect on J-point elevation as well as whether carriers of BrS variants were more prone to experience syncope and malignant ventricular arrhythmia and had increased mortality compared with noncarriers. METHODS: All BrS-associated variants were identified using the Human Gene Mutation Database (HGMD). Individuals were randomly selected from a general population study using whole-exome sequencing data (n = 870) and genotype array data (n = 6,161) and screened for BrS-associated variants...
October 6, 2016: Genetics in Medicine: Official Journal of the American College of Medical Genetics
Yashwant Agrawal, Sourabh Aggarwal, Jagadeesh K Kalavakunta, Vishal Gupta
Brugada syndrome (BS), a life-threatening channelopathy associated with reduced inward sodium current due to dysfunctional sodium channels, is characterized by ST-segment elevation with downsloping "coved type" (type 1) or "saddle back" (type 2) pattern in V1-V3 precordial chest leads (1, 2). Brugada phenocopy, a term describing conditions inducing Brugada-like pattern of electrocardiogram (EKG) manifestations in patients without true BS, is an emerging condition (3). We describe a case series of Brugada phenocopy with hyponatremia...
October 2016: Journal of the Saudi Heart Association
Enrique Velázquez-Rodríguez, Horacio Rodríguez-Piña, Alex Pacheco-Bouthillier, Marcelo Paz Jiménez-Cruz
BACKGROUND: Typical diagnostic, coved-type 1, Brugada ECG patterns fluctuate spontaneously over time with a high proportion of non-diagnostic ECG patterns. Insulin modulates ion transport mechanisms and causes hyperpolarization of the resting potential. We report our experience with unmasking J-ST changes in response to a dextrose-insulin test. METHODS: Nine patients, mean age 40.5±19.4years (range: 15-65years), presented initially with a non-diagnostic ECG pattern, which was suggestive of Brugada syndrome (group I)...
August 19, 2016: Journal of Electrocardiology
U Lakshmanadoss, A Mertens, M Gallagher, I Kutinsky, B Williamson
Inherited arrhythmia syndromes are a known, albeit rare, cause of sudden cardiac arrest which may present with characteristic electrocardiogram changes in patients with structurally normal heart. There are a variety of distinct arrhythmogenic syndromes that arise from mutations in voltage gated sodium channels, resulting in either gain or loss of function. We describe a patient with a primary inherited arrhythmia syndrome which presented as sudden cardiac arrest. Further workup revealed that her arrest was due to a combination of Brugada syndrome and Long QT3 syndrome secondary to a deleterious mutation of voltage-gated, sodium channel, type V alpha subunit (SCN5A Thr1709Met)...
March 2016: Indian Pacing and Electrophysiology Journal
Srinivasa Prasad, Narayanan Namboodiri, Anees Thajudheen, Gurbhej Singh, Mukund A Prabhu, S P Abhilash, Krishnakumar Mohanan Nair, Aamir Rashid, V K Ajit Kumar, Jaganmohan A Tharakan
BACKGROUND: Many subjects in community have non-type 1 Brugada pattern ECG with atypical symptoms, relevance of which is not clear. Provocative tests to unmask type 1 Brugada pattern in these patients would help in diagnosing Brugada Syndrome. However sensitivity and specificity of provocating drugs are variable. METHODS: We studied 29 patients referred to our institute with clinical presentation suggestive but not diagnostic of Brugada or with non-Type 1 Brugada pattern ECG...
March 2016: Indian Pacing and Electrophysiology Journal
A L M J van der Knijff-van Dortmont, M Dirckx, J J Duvekot, J W Roos-Hesselink, A Gonzalez Candel, C D van der Marel, G P Scoones, V F R Adriaens, I J J Dons-Sinke
SCN5A gene mutations can lead to ion channel defects which can cause cardiac conduction disturbances. In the presence of specific ECG characteristics, this mutation is called Brugada syndrome. Many drugs are associated with adverse events, making anesthesia in patients with SCN5A gene mutations or Brugada syndrome challenging. In this case report, we describe a pregnant patient with this mutation who received epidural analgesia using low dose ropivacaine and sufentanil during labour.
2016: Case Reports in Anesthesiology
Christian Steinberg, Gareth J Padfield, Jean Champagne, Shubhayan Sanatani, Paul Angaran, Jason G Andrade, Jason D Roberts, Jeffrey S Healey, Vijay S Chauhan, David H Birnie, Mikyla Janzen, Brenda Gerull, George J Klein, Richard Leather, Christopher S Simpson, Colette Seifer, Mario Talajic, Martin Gardner, Andrew D Krahn
BACKGROUND: Unexplained cardiac arrest (UCA) may be explained by inherited arrhythmia syndromes. The Cardiac Arrest Survivors With Preserved Ejection Fraction Registry prospectively assessed first-degree relatives of UCA or sudden unexplained death victims to screen for cardiac abnormalities. METHODS AND RESULTS: Around 398 first-degree family members (186 UCA, 212 sudden unexplained death victims' relatives; mean age, 44±17 years) underwent extensive cardiac workup, including ECG, signal averaged ECG, exercise testing, cardiac imaging, Holter-monitoring, and selective provocative drug testing with epinephrine or procainamide...
September 2016: Circulation. Arrhythmia and Electrophysiology
Juan Sieira, Gregory Dendramis, Pedro Brugada
Brugada syndrome is an inherited disease characterized by an increased risk of sudden cardiac death owing to ventricular arrhythmias in the absence of structural heart disease. Since the first description of the syndrome >20 years ago, considerable advances have been made in our understanding of the underlying mechanisms involved and the strategies to stratify at-risk patients. The development of repolarization-depolarization abnormalities in patients with Brugada syndrome can involve genetic alterations, abnormal neural crest cell migration, improper gap junctional communication, or connexome abnormalities...
September 15, 2016: Nature Reviews. Cardiology
Deniz Akdis, Corinna Brunckhorst, Firat Duru, Ardan M Saguner
This overview gives an update on the molecular mechanisms, clinical manifestations, diagnosis and therapy of arrhythmogenic cardiomyopathy (ACM). ACM is mostly hereditary and associated with mutations in genes encoding proteins of the intercalated disc. Three subtypes have been proposed: the classical right-dominant subtype generally referred to as ARVC/D, biventricular forms with early biventricular involvement and left-dominant subtypes with predominant LV involvement. Typical symptoms include palpitations, arrhythmic (pre)syncope and sudden cardiac arrest due to ventricular arrhythmias, which typically occur in athletes...
August 2016: Arrhythmia & Electrophysiology Review
Xu-Miao Chen, Cheng-Cheng Ji, Yun-Jiu Cheng, Li-Juan Liu, Wei-Qi Zhu, Ying Huang, Wei-Ying Chen, Su-Hua Wu
BACKGROUND: Just as high-risk populations for cardiac arrest exist in patients with Brugada syndrome or long QT syndrome, high-risk and low-risk populations for cardiac arrest also exist in patients with early repolarization pattern (ERP). HYPOTHESIS: Electrocardiographic (ECG) characteristics can aid the risk stratification of patients with ERP. METHODS: Electrocardiographic parameters such as magnitude of J-point elevation and J/R ratio were measured...
September 6, 2016: Clinical Cardiology
Masayasu Komatsu, Jun Takahashi, Koji Fukuda, Yusuke Takagi, Takashi Shiroto, Makoto Nakano, Masateru Kondo, Ryuji Tsuburaya, Kiyotaka Hao, Kensuke Nishimiya, Taro Nihei, Yasuharu Matsumoto, Kenta Ito, Yasuhiko Sakata, Satoshi Miyata, Hiroaki Shimokawa
BACKGROUND: Optimal therapy for patients resuscitated from out-of-hospital cardiac arrest (OHCA) who are not found to have structural heart disease remains to be established, especially regarding the use of implantable cardioverter-defibrillators. Coronary artery spasm (CAS) and lethal ventricular arrhythmias are important causes of OHCA. METHODS AND RESULTS: In 47 consecutive OHCA survivors without structural heart disease who had fully recovered (M/F 44/3, 43±13 years...
September 2016: Circulation. Arrhythmia and Electrophysiology
Isik Turker, Takeru Makiyama, Matteo Vatta, Hideki Itoh, Takeshi Ueyama, Akihiko Shimizu, Tomohiko Ai, Minoru Horie
BACKGROUND: Class IC antiarrhythmic agents may induce acquired forms of Brugada Syndrome. We have identified a novel mutation in SCN5A, the gene that encodes the α-subunit of the human cardiac sodium channel (hNav1.5), in a patient who exhibited Brugada- type ECG changes during pharmacotherapy of atrial arrhythmias. OBJECTIVE: To assess whether the novel mutation p.V1328M can cause drug induced Brugada Syndrome. METHODS: Administration of pilsicainide, a class IC antiarrhythmic agent, caused Brugada- type ST elevation in a 66-year-old Japanese male who presented with paroxysmal atrial fibrillation (PAF), type I atrial flutter and inducible ventricular fibrillation (VF) during electrophysiological study...
2016: PloS One
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