An increasing body of evidence has demonstrated the essential role of inflammation in the genesis and maintenance of atrial fibrillation (AF). The aim of the present study was to investigate whether success or failure of electrical pulmonary vein isolation (PVI) in patients with AF is related with the presence of a pre-ablative inflammatory state as determined by known clinical parameters and conventional markers of inflammation including high-sensitivity C-reactive protein, white blood cell (WBC) count, and fibrinogen. Seventy-two patients with paroxysmal (64%) or persistent AF (36%) underwent successful electrical PVI. The mean duration of arrhythmia was 5.5 ± 2.9 years. After a mean follow-up period of 12.5 ± 5.7 months, 44 patients (61%) were in sinus rhythm. In univariate Cox proportional hazard regression analysis, hypertension, body mass index (BMI), left ventricular ejection fraction, left ventricular end-diastolic diameter, left atrial diameter (LAD), WBC count, and high-sensitivity C-reactive protein were significantly associated with AF recurrence ( P < 0.05). In multivariate Cox proportional hazard regression analysis, hypertension [hazard ratio (HR) 3.127; 95% confidence interval (CI) 1.269–7.706, P = 0.013], LAD (HR 1.077; 95% CI 1.014–1.144, P = 0.015), and WBC count (HR 1.423; 95% CI 1.067–1.897, P = 0.016) were independent pre-ablative predictors of AF recurrence following PVI. Conventional markers of the inflammatory cascade such as WBC count and high-sensitivity C-reactive protein as well as elements of the metabolic syndrome such as hypertension and increased BMI were significantly associated with AF recurrence. The impact of a pre-ablative inflammatory state in the overall success rate of PVI needs further elucidation.
The present study investigated whether several ECG markers of ventricular repolarization are associated with ventricular tachycardia/fibrillation (VT/VF) inducibility in subjects with type 1 ECG pattern of Brugada syndrome (BS). The clinical data of 23 individuals (19 males, age 42.69 ± 14.63) with spontaneous ( n = 10) or drug-induced ( n = 13) type 1 ECG pattern of BS who underwent programmed ventricular stimulation were analysed. Sustained VT/VF was induced in 17 subjects (74%) and was significantly associated with the presence of spontaneous type 1 ECG of BS ( P = 0.012). Among the studied ECG repolarization markers, subjects with inducible VT/VF displayed an increased Tpeak – Tend interval in leads V 2 (88.82 ± 15.70 vs. 78.33 ± 4.08 ms, P = 0.02) and V 6 (76.33 ± 10.08 vs. 66.66 ± 5.16 ms, P = 0.04) and a greater Tpeak – Tend /QT ratio in lead V 6 (0.214 ± 0.028 vs. 0.180 ± 0.014, P = 0.009) compared with those without arrhythmias. Ventricular tachycardia/fibrillation inducibility was not associated with arrhythmic events during a mean follow-up period of 4.61 ± 2.14 years ( P = 0.739). The Tpeak – Tend interval and Tpeak – Tend /QT ratio were associated with VT/VF inducibility in BS. The utility of Tpeak – Tend /QT ratio as a new marker of arrhythmogenesis in BS requires further studies, including a large number of patients.