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Twelve-lead ambulatory electrocardiographic monitoring in Brugada syndrome: Potential diagnostic and prognostic implications

  • Belinda Gray
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia

    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Camperdown, New South Wales, Australia
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  • Adrienne Kirby
    Affiliations
    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    NHMRC Clinical Trials Centre, Camperdown, New South Wales, Australia
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  • Peter Kabunga
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
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  • Saul B. Freedman
    Affiliations
    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    Department of Cardiology, Concord Repatriation General Hospital, Concord, New South Wales, Australia

    Heart Research Institute, Charles Perkins Centre, University of Sydney, Camperdown, New South Wales, Australia
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  • Laura Yeates
    Affiliations
    Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Camperdown, New South Wales, Australia
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  • Ajita Kanthan
    Affiliations
    Department of Cardiology, Blacktown Hospital, Blacktown, New South Wales, Australia
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  • Caroline Medi
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia

    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Camperdown, New South Wales, Australia
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  • Anthony Keech
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia

    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    NHMRC Clinical Trials Centre, Camperdown, New South Wales, Australia
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  • Christopher Semsarian
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia

    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    Agnes Ginges Centre for Molecular Cardiology, Centenary Institute, Camperdown, New South Wales, Australia
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  • Raymond W. Sy
    Correspondence
    Address reprint requests and correspondence: Dr Raymond W. Sy, Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, NSW 2042, Australia.
    Affiliations
    Department of Cardiology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia

    Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia

    Department of Cardiology, Concord Repatriation General Hospital, Concord, New South Wales, Australia
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      Background

      Patients with Brugada syndrome (BrS) are diagnosed and risk stratified on the basis of a spontaneous or drug-induced type 1 electrocardiographic (ECG) pattern, often at single time points not accounting for variation throughout the day.

      Objectives

      The purpose of this study was to prospectively assess the overall burden of type 1 Brugada ECG changes using 12-lead 24-hour Holter monitoring and evaluate association with cardiac events.

      Methods

      From July 1, 2013 to December 31, 2015, patients with BrS were recruited from 3 Australian centers and the Australian Genetic Heart Disease Registry. All patients underwent clinical review, baseline ECG, and 12-lead 24-hour Holter assessment with precordial leads placed in the left and right second, third, and fourth intercostal spaces. The frequency, temporal, and spatial burden of type 1 BrS ECG pattern were analyzed and assessed for association with cardiac events.

      Results

      A total of 54 patients with BrS were recruited (n=44, 81% men; mean age 44 ± 13 years); the mean follow-up was 2.3 ± 2.5 years. Eleven of 32 patients (34%) initially classified as “drug-induced BrS” demonstrated a spontaneous type 1 pattern at least once over 24 hours. Patients with cardiac events had a significantly higher temporal burden of type 1 ST-segment elevation in the 24-hour monitoring period (total area under the curve 21% vs 15%; P = .008), being most pronounced between the hours of 1600 and 2400 (P = .027).

      Conclusion

      Patients with BrS traditionally classified as drug-induced can exhibit spontaneous ECG changes with longer-term monitoring, particularly in the evening. Temporal burden on 12-lead Holter monitor was associated with cardiac events. Ambulatory 12-lead ECG monitoring may have potential utility in the diagnosis and risk stratification of patients with BrS.

      Keywords

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