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      Programmed Ventricular Stimulation for Risk Stratification in the Brugada Syndrome: A Pooled Analysis

      research-article
      , MD, PhD 1 , , MD, PhD 2 , , MD 3 , 4 , , MD 5 , , MD 6 , , MD 7 , , MD 8 , , MD 9 , , MD 10 , , PhD 11 , , MD, PhD 3 , 4 , , MD 12 , 13 , , MD 14 , 15 , , MD, PhD 16 , , MD, PhD 17 , 18 , , MD, PhD 12 , 13 , 19 , , MD 10 , , MD 9 , , MD, PhD 20 , , MD 7 , , PhD 21 , , MD 20 , , MD, PhD 3 , 4 , , MD, MPH 12 , 13 , 19
      Circulation
      Sudden cardiac death, electrophysiology

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          Abstract

          Background

          The role of programmed ventricular stimulation (PVS) in identifying Brugada syndrome patients at highest risk for sudden death is uncertain.

          Methods and Results

          We performed a systematic review and pooled analysis of prospective observational studies of Brugada syndrome patients without a history of sudden cardiac arrest who underwent PVS. We estimated incidence rates and relative hazards of cardiac arrest or ICD shock. We analyzed individual-level data from 8 studies, comprising 1312 patients who experienced 65 cardiac events (median follow-up of 38.3 months). A total of 527 patients were induced into arrhythmias with up to triple extrastimuli. Induction was associated with cardiac events during follow-up (HR 2.66, 95%CI 1.44–4.92, P<0.001), with the greatest risk observed among those induced with single or double extrastimuli. Annual event rates varied substantially by syncope history, presence of spontaneous type 1 ECG pattern, and arrhythmia induction. The lowest risk occurred in individuals without syncope and with drug-induced type 1 patterns (0.23%, 95%CI 0.05–0.68 [no induced arrhythmia with up to double extrastimuli]; 0.45%, 95%CI 0.01–2.49 [induced arrhythmia]) and the highest risk occurred in individuals with syncope and spontaneous type 1 patterns (2.55%, 95%CI 1.58–3.89 [no induced arrhythmia]; 5.60%, 95%CI 2.98–9.58 [induced arrhythmia]).

          Conclusions

          In Brugada syndrome patients, arrhythmias induced with PVS are associated with future ventricular arrhythmia risk. Induction with fewer extrastimuli is associated with higher risk. However, clinical risk factors are important determinants of arrhythmia risk, and lack of induction does not necessarily portend low ventricular arrhythmia risk particularly in patients with high-risk clinical features.

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          Author and article information

          Journal
          0147763
          2979
          Circulation
          Circulation
          Circulation
          0009-7322
          1524-4539
          31 December 2015
          21 January 2016
          16 February 2016
          16 February 2017
          : 133
          : 7
          : 622-630
          Affiliations
          [1 ]Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, MA
          [2 ]Service de cardiologue du CHU de Nantes, CHU de Nantes, Hôpital Nord, Nantes Cefex, France
          [3 ]Molecular Cardiology, IRCCS Fondazione Salvatore Maugeri, Pavia, Italy
          [4 ]Dipartimento di Medicina, Molecolare Università di Pavia, Pavia, Italy
          [5 ]Division of Cardiology, Casa di Cura Pederzoli, Peschiera del Garda (Verona), Italy
          [6 ]Arrhythmia Unit, Cardiovascular Surgery and Cardiology Institute, Havana, Cuba
          [7 ]Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan
          [8 ]Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padova, Italy
          [9 ]Institut Universitaire de Cardiologie et Pneumologie de Québec, Quebec City, Canada
          [10 ]Department of Electrophysiology and Pacing, Onassis Cardiac Surgery Center, Athens, Greece
          [11 ]Boston University and National Heart, Lung and Blood Institute’s Framingham Heart Study, Framingham, MA
          [12 ]Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA
          [13 ]Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, MA
          [14 ]Heart centre AMC, Department of Clinical and Experimental Cardiology, Academic Medical Center, University of Amsterdam, the Netherlands
          [15 ]Princess Al-Jawhara Al-Brahim Centre of Excellence in Research of Hereditary Disorders, Jeddah, Kingdom of Saudi Arabia
          [16 ]Bordeaux University Hospital, LIRYC Institute/INSERM 1045, Bordeaux, France
          [17 ]1st Department of Medicine-Cardiology, University Medical Centre Mannheim, Mannheim, Germany
          [18 ]DZHK (German Centre for Cardiovascular Research), partner site Heidelberg/Mannheim, Mannheim, Germany
          [19 ]Program in Medical and Population Genetics, The Broad Insitute of Harvard and MIT, Cambridge, MA
          [20 ]Department of Cardiology, General Hospital of Conegliano, Conegliano, Treviso, Italy
          [21 ]SUNY Upstate Medical University, Syracuse, NY
          Author notes
          Correspondence: Steven A. Lubitz, MD, MPH, Cardiac Arrhythmia Service and Cardiovascular Research Center, Massachusetts General Hospital, 55 Fruit Street, GRB 109, Boston, MA 02114, Phone: 617-643-7339, Fax: 617-726-3852, slubitz@ 123456mgh.harvard.edu
          Article
          PMC4758872 PMC4758872 4758872 nihpa748173
          10.1161/CIRCULATIONAHA.115.017885
          4758872
          26797467
          fca2ad05-57ed-4ee2-935d-685cd0e54851
          History
          Categories
          Article

          electrophysiology,Sudden cardiac death
          electrophysiology, Sudden cardiac death

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