Author
Aviram Hochstadt
Bio: Aviram Hochstadt is an academic researcher from Xiamen University. The author has contributed to research in topics: Brugada syndrome & Odds ratio. The author has an hindex of 7, co-authored 11 publications receiving 261 citations.
Papers
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Tel Aviv University1, French Institute of Health and Medical Research2, Catholic University of Korea3, Tokyo Medical and Dental University4, Vrije Universiteit Brussel5, National Taiwan University6, Beth Israel Deaconess Medical Center7, Sunnybrook Health Sciences Centre8, University of Amsterdam9, University of Barcelona10, Xiamen University11, Paris Diderot University12, University of Turin13, St George's, University of London14, St George’s University Hospitals NHS Foundation Trust15, Université libre de Bruxelles16, Hospital Sant Joan de Déu Barcelona17, Copenhagen University Hospital18, University of Copenhagen19, University of Pavia20, Osaka City University21, Hannover Medical School22, University of Padua23, Lankenau Medical Center24, University of Ulsan25
TL;DR: SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) presents the first analysis on the age distribution of AE in brugada syndrome, suggesting 2 age cutoffs that might be important for decision-making.
Abstract: Background Data on the age at first arrhythmic event (AE) in Brugada syndrome are from limited patient cohorts. The aim of this study is 2-fold: (1) to define the age at first AE in a large cohort of patients with Brugada syndrome, and (2) to assess the influence of the mode of AE documentation, sex, and ethnicity on the age at first AE. Methods and Results A survey of 23 centers from 10 Western and 4 Asian countries gathered data from 678 patients with Brugada syndrome (91.3% men) with first AE documented at time of aborted cardiac arrest (group A, n=426) or after prophylactic implantable cardioverter–defibrillator implantation (group B, n=252). The vast majority (94.2%) of the patients were 16 to 70 years old at the time of AE, whereas pediatric ( 70 years) comprised 4.3% and 1.5%, respectively. Peak AE rate occurred between 38 and 48 years (mean, 41.9±14.8; range, 0.27–84 years). Group A patients were younger than in Group B by a mean of 6.7 years (46.1±13.2 versus 39.4±15.0 years; P P =0.003). Whites and Asians exhibited their AE at the same median age (43 years). Conclusions SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) presents the first analysis on the age distribution of AE in Brugada syndrome, suggesting 2 age cutoffs (16 and 70 years) that might be important for decision-making. It also allows gaining insights on the influence of mode of arrhythmia documentation, patient sex, and ethnic origin on the age at AE.
73 citations
Tel Aviv University1, University of Barcelona2, University of Amsterdam3, Université libre de Bruxelles4, Beth Israel Deaconess Medical Center5, National Taiwan University6, University of Turin7, University of Copenhagen8, St George’s University Hospitals NHS Foundation Trust9, Hannover Medical School10, University of Padua11, Catholic University of Korea12, Tokyo Medical and Dental University13, University of Bordeaux14, Sunnybrook Health Sciences Centre15, Cardiovascular Institute of the South16, Xiamen University17, Paris Diderot University18, University of Girona19, Kansai Medical University20, Lankenau Medical Center21, University of Ulsan22
TL;DR: The risk of fever-related AE in BrS markedly varies according to age group, sex, and ethnicity, and taking these factors into account could help the clinical management of patients with BrS with fever.
69 citations
TL;DR: Ranolazine blocks INaL in experimental models of LQT3 harboring the SCN5A-D1790G mutation and shortened the QT interval of L QT3 patients.
Abstract: 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 ( I Na and I NaL), but ranolazine preferentially reduces I NaL. 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. We then performed a long-term clinical evaluation of ranolazine in LQT3 patients carrying the D1790G mutation. In the experimental study, I NaL was significantly higher in D1790G than in wild-type channels expressed in the TSA201 cells. Ranolazine exerted a concentration-dependent block of I NaL of the SCN5A-D1790G channel without reducing peak I Na significantly. In the clinical study, among 8 patients with LQT3 and confirmed D1790G mutation, ranolazine had no effects on the sinus rate or QRS width but shortened the QTc from 509±41 to 451±26 ms, a mean decrease of 56±52 ms (10.6%; P =0.012). The QT-shortening effect of ranolazine remained effective throughout the entire study period of 22.8±12.8 months. Ranolazine reduced the QTc at all heart rates but less so during extreme nocturnal bradycardia. A type I Brugada ECG was never noticed.
Conclusions— Ranolazine blocks I NaL in experimental models of LQT3 harboring the SCN5A-D1790G mutation and shortened the QT interval of LQT3 patients.
Clinical Trial Registration— URL: ; Unique identifier: [NCT01728025][1].
[1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01728025&atom=%2Fcircae%2F9%2F10%2Fe004370.atom
55 citations
Tel Aviv University1, University of Amsterdam2, University of Bordeaux3, Catholic University of Korea4, National Taiwan University5, Tokyo Medical and Dental University6, Hospital Sant Joan de Déu Barcelona7, Beth Israel Deaconess Medical Center8, Sunnybrook Health Sciences Centre9, Cardiovascular Institute of the South10, Xiamen University11, Paris Diderot University12, University of Turin13, St George’s University Hospitals NHS Foundation Trust14, Université libre de Bruxelles15, Copenhagen University Hospital16, Osaka City University17, Hannover Medical School18, University of Padua19, Lankenau Medical Center20, University of Ulsan21
TL;DR: In this article, the authors compared clinical, electrocardiographic, electrophysiologic, and genetic profiles of patients with Brugada syndrome presenting their first arrhythmic event after prophylactic implantation of an implantable cardioverter-defibrillator (ICD) is limited.
54 citations
Tel Aviv University1, University of Amsterdam2, University of Bordeaux3, University of Turin4, University of Barcelona5, Catholic University of Korea6, National Taiwan University7, Tokyo Medical and Dental University8, Beth Israel Deaconess Medical Center9, Sunnybrook Health Sciences Centre10, Cardiovascular Institute of the South11, Xiamen University12, Paris Diderot University13, St George’s University Hospitals NHS Foundation Trust14, University of Girona15, Université libre de Bruxelles16, University of Copenhagen17, Kansai Medical University18, Hannover Medical School19, University of Padua20, Lankenau Medical Center21, University of Ulsan22
TL;DR: It is confirmed that female patients with BrS are much rarer, display less type 1 Brugada ECG, and exhibit lower inducibility rates than do males, as well as the relationship between gender vs age at the onset of AEs and ethnicity.
53 citations
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652 citations