TY - JOUR
T1 - Prognostic significance of fever-induced Brugada syndrome
AU - Mizusawa, Yuka
AU - Morita, Hiroshi
AU - Adler, Arnon
AU - Havakuk, Ofer
AU - Thollet, Aurélie
AU - Maury, Philippe
AU - Wang, Dao W.
AU - Hong, Kui
AU - Gandjbakhch, Estelle
AU - Sacher, Frédéric
AU - Hu, Dan
AU - Amin, Ahmad S.
AU - Lahrouchi, Najim
AU - Tan, Hanno L.
AU - Antzelevitch, Charles
AU - Probst, Vincent
AU - Viskin, Sami
AU - Wilde, Arthur A.M.
N1 - Funding Information:
Dr Mizusawa, Dr Tan, and Dr Wilde were supported by the Netherlands CardioVascular Research Initiative: the Dutch Heart Foundation, the Dutch Federation of University Medical Centres, the Netherlands Organization for Health Research and Development, and the Royal Netherlands Academy of Sciences. Dr Morita is affiliated with the endowed department sponsored by Japan Medtronic Inc. and was supported by Japan Society for the Promotion of Science KAKENHI (grant nos. 24591051 and 15K09082) and the Ministry of Health, Labor and Welfare of Japan for Clinical Research on Intractable Diseases (grant nos. H24-033 and H26-040). Dr Wang was supported by the National Natural Science Foundation of China (project no. 81170159) and by the National Key Basic Research Program of China (973 Program) (program no. 2013CB531105). Dr Antzelevitch was supported by the National Heart, Lung, and Blood Institute (grant no. HL47678).
Publisher Copyright:
© 2016 Heart Rhythm Society.
PY - 2016/7/1
Y1 - 2016/7/1
N2 - Background In Brugada syndrome (BrS), spontaneous type 1 electrocardiogram (ECG) is an established risk marker for fatal arrhythmias whereas drug-induced type 1 ECG shows a relatively benign prognosis. No study has analyzed the prognosis of fever-induced type 1 ECG (F-type1) in a large BrS cohort. Objectives The objectives of this study were to assess the prognosis of F-type1 in asymptomatic BrS and to compare the effects of fever and drugs on ECG parameters. Methods One hundred twelve patients with BrS who developed F-type1 were retrospectively enrolled. Prognosis was evaluated in 88 asymptomatic patients. In a subgroup (n = 52), ECG parameters of multiple ECGs (at baseline, during fever, and after drug challenge) were analyzed. Results Eighty-eight asymptomatic patients had a mean age of 45.8 ± 18.7 years, and 71.6% (67 of 88) were men. Twenty-one percent (18 of 88) had a family history of sudden cardiac death, and 26.4% (14 of 53) carried a pathogenic SCN5A mutation. Drug challenge was positive in 29 of 36 patients tested (80.6%). The risk of ventricular fibrillation in asymptomatic patients was 0.9%/y (3 of 88; 43.6 ± 37.4 months). ST-segment elevation in lead V2 during fever and after drug challenge was not significantly different (0.41 ± 0.21 ms during fever and 0.40 ± 0.30 ms after drug challenge; P >.05). Fever shortened the PR interval compared to baseline, whereas drug challenge resulted in prolonged PR interval and QRS duration (PR interval: 169 ± 29 ms at baseline, 148 ± 45 ms during fever, and 202 ± 35 ms after drug challenge; QRS duration: 97 ± 18 ms at baseline, 92 ± 28 ms during fever, and 117 ± 21 ms after drug challenge). Conclusion Patients with BrS who develop F-type1 are at risk of arrhythmic events. F-type1 appears to develop through a more complex mechanism as compared with drug-induced type 1 ECG.
AB - Background In Brugada syndrome (BrS), spontaneous type 1 electrocardiogram (ECG) is an established risk marker for fatal arrhythmias whereas drug-induced type 1 ECG shows a relatively benign prognosis. No study has analyzed the prognosis of fever-induced type 1 ECG (F-type1) in a large BrS cohort. Objectives The objectives of this study were to assess the prognosis of F-type1 in asymptomatic BrS and to compare the effects of fever and drugs on ECG parameters. Methods One hundred twelve patients with BrS who developed F-type1 were retrospectively enrolled. Prognosis was evaluated in 88 asymptomatic patients. In a subgroup (n = 52), ECG parameters of multiple ECGs (at baseline, during fever, and after drug challenge) were analyzed. Results Eighty-eight asymptomatic patients had a mean age of 45.8 ± 18.7 years, and 71.6% (67 of 88) were men. Twenty-one percent (18 of 88) had a family history of sudden cardiac death, and 26.4% (14 of 53) carried a pathogenic SCN5A mutation. Drug challenge was positive in 29 of 36 patients tested (80.6%). The risk of ventricular fibrillation in asymptomatic patients was 0.9%/y (3 of 88; 43.6 ± 37.4 months). ST-segment elevation in lead V2 during fever and after drug challenge was not significantly different (0.41 ± 0.21 ms during fever and 0.40 ± 0.30 ms after drug challenge; P >.05). Fever shortened the PR interval compared to baseline, whereas drug challenge resulted in prolonged PR interval and QRS duration (PR interval: 169 ± 29 ms at baseline, 148 ± 45 ms during fever, and 202 ± 35 ms after drug challenge; QRS duration: 97 ± 18 ms at baseline, 92 ± 28 ms during fever, and 117 ± 21 ms after drug challenge). Conclusion Patients with BrS who develop F-type1 are at risk of arrhythmic events. F-type1 appears to develop through a more complex mechanism as compared with drug-induced type 1 ECG.
KW - Brugada syndrome
KW - Drug-induced type 1 ECG
KW - Fever-induced type 1 ECG
KW - Prognosis
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U2 - 10.1016/j.hrthm.2016.03.044
DO - 10.1016/j.hrthm.2016.03.044
M3 - Article
C2 - 27033637
AN - SCOPUS:84965041821
SN - 1547-5271
VL - 13
SP - 1515
EP - 1520
JO - Heart Rhythm
JF - Heart Rhythm
IS - 7
ER -