The presence of an S-wave duration ≥40 ms in lead I was a powerful independent predictor of ventricular fibrillation or sudden cardiac death in patients with Brugada syndrome (HR 39.1).
Cohort (n=347)
Does the presence of a significant S-wave in lead I predict ventricular fibrillation or sudden cardiac death in patients with Brugada syndrome without prior cardiac arrest?
A wide or large S-wave in lead I is a strong independent predictor of ventricular fibrillation and sudden cardiac death in Brugada syndrome patients without prior cardiac arrest.
Effect estimate: HR 39.1
BACKGROUND: Risk stratification in asymptomatic patients remains by far the most important yet unresolved clinical problem in the Brugada syndrome (BrS). OBJECTIVES: This study sought to analyze the usefulness of electrocardiographic parameters as markers of sudden cardiac death (SCD) in BrS. METHODS: This study analyzed data from 347 consecutive patients (78.4% male; mean age 45 ± 13.1 years) with spontaneous type 1 BrS by ECG parameters but with no history of cardiac arrest (including 91.1% asymptomatic at presentation, 5.2% with a history of atrial fibrillation AF, and 4% with a history of arrhythmic syncope). Electrocardiographic characteristics at the first clinic visit were analyzed to predict ventricular fibrillation (VF)/SCD during follow-up. RESULTS: During the follow-up (48 ± 38 months), 276 (79.5%) patients remained asymptomatic, 39 (11.2%) developed syncope, and 32 (9.2%) developed VF/SCD. Patients who developed VF/SCD had a lower prevalence of SCN5A gene mutations (p = 0.009) and a higher prevalence of positive electrophysiological study results (p < 0.0001), a family history of SCD (p = 0.03), and AF (p < 0.0001). The most powerful marker for VF/SCD was a significant S-wave (≥0.1 mV and/or ≥40 ms) in lead I. In the multivariate analysis, the duration of S-wave in lead I ≥40 ms (hazard ratio: 39.1) and AF (hazard ratio: 3.7) were independent predictors of VF/SCD during follow-up. Electroanatomic mapping in 12 patients showed an endocardial activation time significantly longer in patients with an S-wave in lead I, mostly because of a significant delay in the anterolateral right ventricular outflow tract. CONCLUSIONS: The presence of a wide and/or large S-wave in lead I was a powerful predictor of life-threatening ventricular arrhythmias in patients with BrS and no history of cardiac arrest at presentation. However, the prognostic value of a significant S-wave in lead I should be confirmed by larger studies and by an independent confirmation cohort of healthy subjects.
Calò et al. (Tue,) conducted a cohort in Brugada syndrome (n=347). Significant S-wave in lead I (≥0.1 mV and/or ≥40 ms) vs. Absence of significant S-wave in lead I was evaluated on Ventricular fibrillation (VF) or sudden cardiac death (SCD) (HR 39.1). The presence of an S-wave duration ≥40 ms in lead I was a powerful independent predictor of ventricular fibrillation or sudden cardiac death in patients with Brugada syndrome (HR 39.1).