Among our study patients without supraventricular tachyarrhy

Among our study patients without supraventricular tachyarrhythmia, the prevalence of a spontaneous type 1 Brugada ECG and symptoms were higher and QRS duration was longer than in those with supraventricular tachyarrhythmia. Previous studies have revealed a spontaneous type 1 Brugada ECG and prolonged QRS duration in symptomatic Brugada syndrome patients [24,25]. In addition, the PR and AH intervals were longer in our study patients without supraventricular tachyarrhythmia than in those with supraventricular tachyarrhythmia; however, the differences did not reach statistical significance. Another group of investigators also reported more prevalent PR prolongation (≥0.22s) among symptomatic than among asymptomatic patients, but the difference was not statistically significant [26]. The higher prevalence of a spontaneous type 1 ECG and longer PR and AH intervals among patients without supraventricular tachyarrhythmia might be related to the higher prevalence of symptoms related to ventricular tachyarrhythmia. The mechanism underlying syncope or resuscitated cardiac arrest in patients with supraventricular tachyarrhythmia is often unknown. Resuscitation occurs mainly in cases of Wolff-Parkinson-White syndrome with a short refractory enos inhibitor of the accessory pathway [27,28]. In young patients with a history of palpitations, syncope may be a benign symptom. An abnormal vasomotor response to the hemodynamic stress of tachycardia has been suggested as one mechanism responsible for syncope [29]. Activation of cardiac mechanoreceptors during tachycardia may lead to the withdrawal of sympathetic tone, enhanced vagal tone, and hypotension [30]. The presence of concealed or intermittent forms of Brugada syndrome makes diagnosis of the disease even more difficult in these cases [30]. Thus, if syncope or cardiac arrest cannot be explained by the supraventricular tachyarrhythmia or the conduction properties of an accessory pathway, Brugada syndrome should be considered an additional disorder. If there is any doubt that the supraventricular tachyarrhythmia is responsible for the clinical event, patients should be given an antiarrhythmic drug such as pilsicainide or flecainide, which may provoke typical ECG signs of Brugada syndrome [1]. Supraventricular tachyarrhythmia is an important cause of inappropriate ICD shocks in patients with Brugada syndrome [10,13,31]. Bordachar et al. [10] reported that the number of inappropriate ICD interventions (occurring in 14% of patients) exceeded the number of appropriate ICD interventions (occurring in 10% of patients). Kharazi et al. [32] reported a similar finding, i.e., 41% of patients had inappropriate shocks, whereas 17% had appropriate shocks, and Sacher et al. [14] found inappropriate shocks to be 2.5 times more common than appropriate shocks in a large population of Brugada syndrome patients treated with ICD. Dual-chamber ICDs are useful in preventing such inappropriate shocks in patients with paroxysmal AF; however, the benefit must be weighed against the increased complication rate associated with the atrial lead placement. A less invasive and sometimes simpler option is the use of rate-lowering drugs. Careful programming of single-chamber ICDs is also recommended to avoid inappropriate shocks in those without documented AF. Class I antiarrhythmic drugs are often used for the treatment of paroxysmal AF. Matsumoto et al. [33] described a patient with intermittent or concealed Brugada syndrome who developed VF after the administration of pilsicainide for the treatment of AF. Therefore, Brugada syndrome should be considered before the administration of class Ic antiarrhythmic drugs in patients with AF.
Conclusion
Conflict of interest
Introduction Post-ablation atrial tachycardia (AT) is observed in 2.9%–31% of patients undergoing catheter ablation for atrial fibrillation (AF) [1,2]. The most common macroreentrant tachycardia circulates around the mitral annulus, which is observed in 10%–61% cases of ATs in the left atrium (LA) following ablation for AF [1–4]. This type of AT can be treated by catheter ablation therapy through which a bidirectional conduction block is established through the mitral isthmus (MI) between the left inferior pulmonary vein (PV) and the mitral annulus.