Christopher C Cheung1, Greg Mellor2, Marc W Deyell1, Bode Ensam2, Velislav Batchvarov2, Michael Papadakis2, Jason D Roberts3, Richard Leather4, Shubhayan Sanatani5, Jeffrey S Healey6, Vijay S Chauhan7, David H Birnie8, Jean Champagne9, Paul Angaran10, George J Klein3, Raymond Yee3, Christopher S Simpson11, Mario Talajic12, Martin Gardner13, John A Yeung-Lai-Wah1, Santabhanu Chakrabarti1, Zachary W Laksman1, Sanjay Sharma2, Elijah R Behr2, Andrew D Krahn14. 1. Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada. 2. Cardiology Clinical Academic Group, St. George's University Hospitals NHS Foundation Trust, London, United Kingdom; Institute of Molecular and Clinical Sciences, St. George's University of London, London, United Kingdom. 3. Section of Cardiac Electrophysiology, Division of Cardiology, Western University, London, Ontario, Canada. 4. Division of Cardiology, Royal Jubilee Hospital, Victoria, British Columbia, Canada. 5. Children's Heart Centre, Department of Pediatrics, University of British Columbia, Vancouver, British Columbia, Canada. 6. Division of Cardiology, McMaster University, Hamilton, Ontario, Canada. 7. Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada. 8. University of Ottawa Heart Institute, University of Ottawa, Ottawa, Ontario, Canada. 9. Institut Universitaire de Cardiologie et Pneumologie de Québec, Université Laval, Québec City, Québec, Canada. 10. Division of Cardiology, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. 11. Division of Cardiology, Queen's University, Kingston, Ontario, Canada. 12. Institut de Cardiologie de Montréal, Département of Médecine, Université de Montréal, Montréal, Québec, Canada. 13. Division of Cardiology, Dalhousie University, Halifax, Nova Scotia, Canada. 14. Division of Cardiology, University of British Columbia, Vancouver, British Columbia, Canada. Electronic address: akrahn@mail.ubc.ca.
Abstract
OBJECTIVES: The authors studied the response rates and relative sensitivity of the most common agents used in the sodium-channel blocker (SCB) challenge. BACKGROUND: A type 1 Brugada electrocardiographic pattern precipitated by an SCB challenge confers a diagnosis of Brugada syndrome. METHODS: Patients undergoing an SCB challenge were prospectively enrolled across Canada and the United Kingdom. Patients with no prior cardiac arrest and family histories of sudden cardiac death or Brugada syndrome were included. RESULTS: Four hundred twenty-five subjects underwent SCB challenge (ajmaline, n = 331 [78%]; procainamide, n = 94 [22%]), with a mean age of 39 ± 15 years (54% men). Baseline non-type 1 Brugada ST-segment elevation was present in 10%. A total of 154 patients (36%) underwent signal-averaged electrocardiography, with 41% having late potentials. Positive results were seen more often with ajmaline than procainamide infusion (26% vs. 4%, p < 0.001). On multivariate analysis, baseline non-type 1 Brugada ST-segment elevation (odds ratio [OR]: 6.92; 95% confidence interval [CI]: 3.15 to 15.2; p < 0.001) and ajmaline use (OR: 8.76; 95% CI: 2.62 to 29.2; p < 0.001) were independent predictors of positive results to SCB challenge. In the subgroup undergoing signal-averaged electrocardiography, non-type 1 Brugada ST-segment elevation (OR: 9.28; 95% CI: 2.22 to 38.8; p = 0.002), late potentials on signal-averaged electrocardiography (OR: 4.32; 95% CI: 1.50 to 12.5; p = 0.007), and ajmaline use (OR: 12.0; 95% CI: 2.45 to 59.1; p = 0.002) were strong predictors of SCB outcome. CONCLUSIONS: The outcome of SCB challenge was significantly affected by the drug used, with ajmaline more likely to provoke a type 1 Brugada electrocardiographic pattern compared with procainamide. Patients undergoing SCB challenge may have contrasting results depending on the drug used, with potential clinical, psychosocial, and socioeconomic implications.
OBJECTIVES: The authors studied the response rates and relative sensitivity of the most common agents used in the sodium-channel blocker (SCB) challenge. BACKGROUND: A type 1 Brugada electrocardiographic pattern precipitated by an SCB challenge confers a diagnosis of Brugada syndrome. METHODS:Patients undergoing an SCB challenge were prospectively enrolled across Canada and the United Kingdom. Patients with no prior cardiac arrest and family histories of sudden cardiac death or Brugada syndrome were included. RESULTS: Four hundred twenty-five subjects underwent SCB challenge (ajmaline, n = 331 [78%]; procainamide, n = 94 [22%]), with a mean age of 39 ± 15 years (54% men). Baseline non-type 1 Brugada ST-segment elevation was present in 10%. A total of 154 patients (36%) underwent signal-averaged electrocardiography, with 41% having late potentials. Positive results were seen more often with ajmaline than procainamide infusion (26% vs. 4%, p < 0.001). On multivariate analysis, baseline non-type 1 Brugada ST-segment elevation (odds ratio [OR]: 6.92; 95% confidence interval [CI]: 3.15 to 15.2; p < 0.001) and ajmaline use (OR: 8.76; 95% CI: 2.62 to 29.2; p < 0.001) were independent predictors of positive results to SCB challenge. In the subgroup undergoing signal-averaged electrocardiography, non-type 1 Brugada ST-segment elevation (OR: 9.28; 95% CI: 2.22 to 38.8; p = 0.002), late potentials on signal-averaged electrocardiography (OR: 4.32; 95% CI: 1.50 to 12.5; p = 0.007), and ajmaline use (OR: 12.0; 95% CI: 2.45 to 59.1; p = 0.002) were strong predictors of SCB outcome. CONCLUSIONS: The outcome of SCB challenge was significantly affected by the drug used, with ajmaline more likely to provoke a type 1 Brugada electrocardiographic pattern compared with procainamide. Patients undergoing SCB challenge may have contrasting results depending on the drug used, with potential clinical, psychosocial, and socioeconomic implications.
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