AimsRisk stratification in individuals with type 1 Brugada electrocardiogram (ECG) pattern (type 1 ECG) for primary prevention of sudden death (SD).Methods and resultsThree hundred and twenty patients (258 males, median age 43 years) with type 1 ECG were enrolled. No patient had previous cardiac arrest. Fifty-four per cent of patients had a spontaneous and 46% a drug-induced type 1 ECG. One-third had syncope, two-thirds were asymptomatic. Two hundred and forty-five patients underwent electrophysiologic study (EPS) and 110 patients received an implantable cardiac defibrillator (ICD). During follow-up [median length 40 months (IQ20-67)], 17 patients had major arrhythmic events (MAE) (14 resuscitated ventricular fibrillation (VF) and three SD). Both a spontaneous type 1 ECG and syncope significantly increased the risk (2.6 and 3.0% event rate per year vs. 0.4 and 0.8%). Major arrhythmic events occurred in 14% of subjects with positive EPS, in no subjects with negative EPS and in 5.3% of subjects without EPS. All MAE occurred in subjects who had at least two potential risk factors (syncope, family history of SD, and positive EPS). Among these patients, those with spontaneous type 1 ECG had a 30% event rate.Conclusion(1) In subjects with the Brugada type 1 ECG, no single clinical risk factor, nor EPS alone, is able to identify subjects at highest risk; (2) a multiparametric approach (including syncope, family history of SD, and positive EPS) helps to identify populations at highest risk; (3) subjects at highest risk are those with a spontaneous type 1 ECG and at least two risk factors; (4) the remainder are at low risk.

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.

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Background— Catheter ablation of ganglionated plexi (GP) in the left atrium has been proposed in different subgroup of patients with atrial fibrillation (AF). Anatomic studies found a high prevalence of GP in the posterior surface of the right atrium (RA). Experimental data suggested the potential role of right atrial GP in the AF initiation and maintenance. The aim of our study was to assess the efficacy of GP ablation in RA in patients with vagal AF. Methods and Results— Thirty-four patients without structural heart diseases were randomly assigned for a selective ablation procedure targeted on the elimination of vagal reflex evoked by high frequency stimulation or an extensive approach at anatomic sites of GP. All patients underwent Holter ECG and heart rate variability evaluation at baseline and at 3, 6, 12, and 18 months of follow-up. At a mean follow-up of 19.7±5.2 months, AF recurred in 5 of 17 patients with anatomic ablation and in 13 of 17 patients with a selective approach ( P =0.01). No patient had major complications. After ablation, heart rate variability parameters showed a significant parasympathetic (and sympathetic) denervation in the first 6 months, which was more prominent in patients with anatomic GP ablation and in those without AF recurrence. Conclusions— This study demonstrates that in a selected population of vagal paroxysmal AF, the anatomic ablation of GPs in the RA is effective in about 70% of patients. These results confirm that atrial vagal denervation can abolish AF, as suggested by experimental and clinical data.

EAM using a specific parameter setting proved highly effective at identifying the MDAI in MAT, even in patients with previous surgery and multiple re-entrant loops. Ablation of the MDAI yielded acute arrhythmia suppression with low rate of recurrence during follow-up.

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The prognosis of dilated cardiomyopathy is generally poor. The cause of ventricular dysfunction often cannot be identified. In most cases, the clinical history of cardiomyopathy is irreversible but, in some cases, potentially curable causes may be identified. The development of cardiomyopathy may be correlated to atrial or to ventricular arrhythmias. In this scenario, atrial fibrillation is the most frequent cause of ventricular dysfunction, even if it may also be secondary to heart failure. The diagnosis of tachycardia-induced cardiomyopathy can be made only after the improvement of the left ventricular function once the cardiac frequency has slowed down.

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