Key result
Symptomatic patients with Brugada syndrome showed greater daytime fluctuations in sinus node response compared to asymptomatic patients (SDNN variation 39.0 vs 34.1 ms; P<0.05).
Why the study?
Do autonomic characteristics and ST-segment elevation differ between symptomatic and asymptomatic patients with Brugada syndrome?
Observational (n=118)
Do autonomic characteristics and ST-segment elevation differ between symptomatic and asymptomatic patients with Brugada syndrome?
Absolute Event Rate: 39% vs 34.1%
p-value: p=< 0.05
Analysis of autonomic nervous system parameters and type 1 Brugada burden did not identify sensitive predictors of arrhythmic events in Brugada syndrome, though symptomatic patients showed greater fluctuations in sinus node response.
Symptomatic and asymptomatic Brugada patients show similar autonomic profiles and STE; leaves open need for better risk stratification tools.
AIM: Modulation of ST-segment elevation (STE) and tachyarrhythmic events by the autonomic nervous system (ANS) has been reported in patients with Brugada syndrome (BS). This study examined and compared the autonomic characteristics and STE in symptomatic vs. asymptomatic patients with BS. METHODS AND RESULT: We studied 40 symptomatic and 78 asymptomatic patients (mean age = 46.1 ± 13.7 years; 88 men) who underwent 24 h, 12-lead electrocardiograms, and exercise and a head-up tilt tests. Heart rate variability was examined and STE was measured at 5 points between 100 and 140 ms after the onset of 1 min averaged QRS complexes, and the type 1 Brugada pattern was automatically identified. 'Type 1 Brugada burden' was the percentage of averaged type 1 complexes. All measurements were made over 24 h, and during day and night times. During daytime, the variation coefficients of standard deviation of normal-to-normal intervals were 39.0 ± 12.3 vs. 34.1 ± 14.5 ms (P< 0.05) and high frequency normalized units were 39.9 ± 16.9 vs. 33.9 ± 16.2% (P< 0.05) in symptomatic vs. asymptomatic patients, respectively. ST-segment elevation was similar in symptomatic and asymptomatic patients at all time points. The type 1 Brugada burden in V2 was 38.7 ± 33.6% in the symptomatic vs. 24.3 ± 35.2% in the asymptomatic sample, a statistically non-significant difference. CONCLUSION: This analysis of ANS did not identify sensitive predictors of arrhythmic events in patients with BS. We observed, however, greater fluctuations in sinus node response to ANS in symptomatic patients. The type 1 Brugada electrocardiographic pattern was not as reliable a predictor of arrhythmic risk as previously reported.
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Béhar et al. (2016) conducted an observational in Brugada syndrome (n=118). Symptomatic status vs. Asymptomatic status was evaluated on Variation coefficients of standard deviation of normal-to-normal intervals during daytime (p=< 0.05). Symptomatic patients with Brugada syndrome showed greater daytime fluctuations in sinus node response compared to asymptomatic patients (SDNN variation 39.0 vs 34.1 ms; P<0.05).
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