Background The role of programmed ventricular stimulation (PVS) in identifying Brugada syndrome patients at highest risk for sudden death is uncertain. Methods and Results We performed a systematic review and pooled analysis of prospective observational studies of Brugada syndrome patients without a history of sudden cardiac arrest who underwent PVS. We estimated incidence rates and relative hazards of cardiac arrest or ICD shock. We analyzed individual-level data from 8 studies, comprising 1312 patients who experienced 65 cardiac events (median follow-up of 38.3 months). A total of 527 patients were induced into arrhythmias with up to triple extrastimuli. Induction was associated with cardiac events during follow-up (HR 2.66, 95%CI 1.44–4.92, P<0.001), with the greatest risk observed among those induced with single or double extrastimuli. Annual event rates varied substantially by syncope history, presence of spontaneous type 1 ECG pattern, and arrhythmia induction. The lowest risk occurred in individuals without syncope and with drug-induced type 1 patterns (0.23%, 95%CI 0.05–0.68 [no induced arrhythmia with up to double extrastimuli]; 0.45%, 95%CI 0.01–2.49 [induced arrhythmia]) and the highest risk occurred in individuals with syncope and spontaneous type 1 patterns (2.55%, 95%CI 1.58–3.89 [no induced arrhythmia]; 5.60%, 95%CI 2.98–9.58 [induced arrhythmia]). Conclusions In Brugada syndrome patients, arrhythmias induced with PVS are associated with future ventricular arrhythmia risk. Induction with fewer extrastimuli is associated with higher risk. However, clinical risk factors are important determinants of arrhythmia risk, and lack of induction does not necessarily portend low ventricular arrhythmia risk particularly in patients with high-risk clinical features.

Background: The early diagnosis and treatment of heart failure in β-thalassaemic patients is related to survival. Iron alone or in combination with other factors causes diastolic dysfunction, which usually precedes systolic dysfunction. NT-proBNP is a sensitive biomarker of ventricular dysfunction. Aim: To evaluate NT-proBNP in non heart failure β-thalassaemic patients. Methods: Fifty-two β-thalassaemia major patients (mean age: 27.2 ± 12.5 years) with normal LV systolic function, underwent NT-proBNP measurement and a thorough Doppler-echocardiographic and pulsed tissue-Doppler study, 4 days following blood transfusion. Fifty-two age matched healthy controls were also studied. Results: NT-proBNP and E/E′ ratio were increased in thalassaemic patients compared with controls [(469 ± 171 vs 262 ± 51 pmol/l, p < 0.001) and (10.8 ± 4.0 vs 6.6 ± 1.1, p < 0.001)] and were well correlated (r: 0.54, p < 0.01). Although NT-proBNP levels were increased in patients with higher E/E′ ratios (E/E′ < 8: 354 ± 119, 8-15: 516 ± 177, > 15: 565 ± 114 pmol/l, ANOVA p: 0.002) this increase only became statistically significant in the 3rd decade of life, while E/E′ ratio increased in the 4th decade. Conclusion: NT-proBNP increases in β-thalassaemia major patients and is related to age and LV diastolic dysfunction. NT-proBNP appears to be an early biomarker of LV diastolic dysfunction, compared with the conventional Echo-Doppler indexes.