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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.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.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).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.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.

Atrial fibrillation increases thromboembolic risk. Oral anticoagulation with antivitamin K (AVK) reduces thromboembolic event rate, but increases hemorrhagic risk.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.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 ± 28 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).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.