Ventricular conduction delay as marker of risk in Brugada Syndrome. Results from the analysis of clinical and electrocardiographic features of a large cohort of patients.

BACKGROUND: Brugada Syndrome is a genetic arrhythmogenic disease with a variable clinical spectrum. The role of clinical and ECG parameters in the risk stratification is still uncertain. AIMS: In a large cohort of Brugada patients we analysed clinical and ECG features to determine the variables with prognostic value for the occurrence of a first documented arrhythmic event and for recurrences. METHODS: We enrolled 614 patients, subdivided into 3 groups according to their clinical presentation: 531 (88%) asymptomatic, 69 (10%) with previous unexplained syncope and 14 (2%) with aborted sudden death. We also compared the ECG characteristics of patients with a single documented arrhythmic event (either at presentation or at follow-up, 17 patients), with those of patients with arrhythmic recurrences (13 patients). RESULTS: The event rate was 1.3% in the asymptomatic patients and 15% among patients with unexplained syncope (median follow-up 6 years), p < 0.0001. In both groups a QRS duration ≥110 ms in lead II and/or V6 and/or S wave duration ≥40 ms in lead I and/or II were significant risk factors for the occurrence and timing of events at follow-up. The same ECG risk factors were also significantly associated with arrhythmic recurrences. CONCLUSIONS: The arrhythmic risk of Brugada patients is related not only to the symptoms at presentation, but also to the presence of a ventricular conduction delay (QRS duration ≥ 110 ms and/or S wave duration ≥ 40 ms). The ECG conduction parameters also affect the timing of events and recurrences.

Long-term events following atrial fibrillation rate control or transcatheter ablation: a multicenter observational study.

BACKGROUND: Atrial fibrillation increases thromboembolic risk. Oral anticoagulation with antivitamin K (AVK) reduces thromboembolic event rate, but increases hemorrhagic risk. OBJECTIVE: The aim of the present study was to describe long-term cerebral thromboembolic/hemorrhagic event rates in atrial fibrillation patients managed by rhythm control, pursued by atrial fibrillation transcatheter ablation (AFTCA), and rate control strategy. METHODS AND RESULTS: One thousand and five hundred consecutive patients referring to three medical care centers for atrial fibrillation were retrospectively divided into three groups: AFTCA maintaining AVK (group A); AFTCA discontinuing AVK (group B); and rate control strategy and AVK (group C). Thromboembolic and hemorrhagic events were recorded in 60 ±â€Š28 months of follow-up. Thromboembolic events did not differ between the groups (5/500, 1% group A; 7/500, 1.4% group B; 11/500, 2.2% group C; P = 0.45), and hemorrhagic events were greater in group A (9/500, 1.8%) and C (12/500, 2.4%) than in group B (no events; P = 0.003). Among patients with CHA2DS2 VASc score 2 or less, thromboembolic events did not differ in the group discontinuing AVK (group B, 4/388, 1%) or not (group A, 1/319, 0.3%; P = 0.38), whereas hemorrhagic events were more common in patients on AVK (5/319, 1.5% group A and 3/175, 1.7% group C; P = 0.02) compared with those discontinuing AVK (0/388, group B). Following AFTCA (groups A and B), 299/1000 experienced atrial fibrillation relapses; all thromboembolic events (12/299, 4%) occurred within these patients (P < 0.001). CONCLUSION: Considering this multicenter design study, AVK continuation following AFTCA, especially within patients with low-to-intermediate thromboembolic risk, confers a hemorrhagic risk greater to the thromboembolic protective effect. All thromboembolic events following AFTCA occur within patients experiencing atrial fibrillation relapses; therefore, in patients with high thromboembolic risk routine rhythm monitoring is essential after AVK discontinuation.