Key result
Baseline ST elevation in Brugada syndrome strongly correlates with V1 response during Class I antiarrhythmic challenge.
Why the study?
The effect of class I antiarrhythmic challenge in Brugada syndrome is difficult to anticipate and potentially associated with complications, prompting an assessment of response to the challenge.
Does baseline ECG predict the response to class I antiarrhythmic challenge in patients with drug-induced Brugada syndrome?
Observational (n=157)
Yes
Does baseline ECG predict the response to class I antiarrhythmic challenge in patients with drug-induced Brugada syndrome?
In patients with drug-induced Brugada syndrome, the amplitude of sodium blockade effect on ST elevation correlates with baseline ST amplitude, but drug effect on QRS duration correlates poorly with baseline QRS duration.
Baseline ST elevation may predict class I challenge response in Brugada syndrome; hypothesis-generating and should not yet change testing protocols.
Drug challenge is useful to identify patients with Brugada syndrome (BS) without spontaneous ECG type 1 pattern. Effect of class I antiarrhythmic challenge is difficult to anticipate and potentially associated with complications. Assess the response to class I antiarrhythmic challenge. We included patients from the French multicenter MUTAVIT registry with a drug induced BS. Using digitized ECG, we automatically quantified 12‑lead ECG parameters on lead V1-V3. Among 157 patients (72 % males, mean age 43 ± 13 years), baseline ECG did not show a type 2 or 3 BS pattern in 58 %. Drug infusion induced a QRS prolongation from 96 ± 20 to 117 ± 25 ms and an increase of ST amplitude from 107 ± 82 to 345 ± 231 μV (lead V2). Amplitude of drug-challenge effect was associated with homogeneous response across groups (with and without baseline BS pattern). Baseline ST elevation correlated with a pronounced response to the induction test (on V1: r = 0.697 (0.568; 0.792), p < 0.001, R 2 = 0.486). Conversely, on-drug QRS duration was poorly correlated with baseline QRS duration (on V2: r = 0.215 (0.0527; 0.366), p < 0.05, R 2 = 0.046). SCN5A variant carriers had longer QRS duration at baseline but not during drug challenge. Male patients had prolonged baseline QRS and baseline and post-induction ST amplitude. Amplitude of sodium blockade effect on ST elevation was correlated with baseline ST amplitude but dugs effect on QRS duration was only slightly correlated with baseline QRS duration. Presence of (likely) pathogenic SCN5A variant was associated with different baseline ECG characteristics and response to sodium channel blockade. • Amplitude of sodium blockade effect on ST elevation was correlated with baseline ST amplitude. • Drugs effect on QRS duration was only slightly correlated with baseline QRS duration. • Amplitude of the drug challenge effect showed a consistent response across groups regardless of baseline patterns. • Presence of a pathogenic SCN5A P/LP variant was linked to distinct baseline ECG characteristics and different response to sodium channel blockade.
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Laporte et al. (2025) conducted an observational in Brugada syndrome (n=157). Class I antiarrhythmic challenge was evaluated on Correlation of baseline ST elevation with response to the induction test on V1 (r = 0.697, 95% CI 0.568-0.792, p=<0.001). Class I antiarrhythmic challenge in Brugada syndrome patients showed baseline ST elevation strongly correlated with response to the induction test on V1 (r=0.697; 95% CI 0.568-0.792; p<0.001).
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