Journal of electrocardiology · 2025
Baseline quantitative ECG parameters do not fully predict class 1 antiarrhythmic effect in Brugada patient: Drug-induced ECG changes in Brugada patients.
СтатьяМногоцентровое исследованиеНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Laporte Pierre-Léo, Vaglio Martino, Denjoy Isabelle, Maison-Blanche Pierre, Maury Philippe, Hermida Alexis, Klug Didier, Maltret Alice, Badilini Fabio, Leenhardt Antoine, Extramiana Fabrice
Аннотация
BACKGROUND: 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.
OBJECTIVE: Assess the response to class I antiarrhythmic challenge.
METHODS: 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.
RESULTS: 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, R2 = 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, R2 = 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.
CONCLUSION: 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.
OBJECTIVE: Assess the response to class I antiarrhythmic challenge.
METHODS: 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.
RESULTS: 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, R2 = 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, R2 = 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.
CONCLUSION: 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.