Ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) in the absence of overt structural heart disease is a common entity. Exclusion of occult structural disease such as arrhythmogenic right ventricular cardiomyopathy is critical as this diagnosis impacts both ablation outcomes and long-term prognosis. VT is most commonly due to triggered activity. Induction of the target arrhythmia in the laboratory is often problematic, and is frequently facilitated by catecholamine infusion. Recent data indicate that high-density three-dimensional activation mapping facilitates identification of target sites for ablation, and that the spatial resolution of pacemapping may be more limited than previously recognized. A standard 12-lead electrocardiogram is useful in providing an initial approximation of the site of origin within the outflow tract, and may contain subtle clues to potentially confounding foci on the left ventricular endocardial or epicardial surface. When sufficient arrhythmia is present to permit mapping, successful ablation can be expected in 90-95% of patients, with a recurrence risk of approximately 5%. In experienced centers, major complications are

Early AF recurrence peaks within the first few weeks after PVI, but continues at a lower level until the completion of monitoring. A blanking period of 3 months is justified to identify patients with AF recurrences that do not portend procedure failure. Freedom from AF in the first 2 weeks following ablation significantly predicts long-term AF freedom.

Ventricular arrhythmia (VA) in structurally normal hearts can be broadly considered under non-life-threatening monomorphic and life-threatening polymorphic rhythms. Monomorphic VA is classified on the basis of site of origin in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The morphology of the QRS complexes on electrocardiogram is an excellent tool to identify the site of origin of the rhythm. Although these arrhythmias are common and generally carry an excellent prognosis, rare sudden death events have been reported. Very frequent ventricular ectopy may also result in a cardiomyopathy in a minority of patients. Suppression of VA may be achieved using calcium-channel blockers, beta-adrenergic blockers, and class I or III antiarrhythmic drugs. Radiofrequency ablation has emerged as an excellent option to eliminate these arrhythmias, although certain foci including aortic cusps and epicardium may be technically challenging. Polymorphic ventricular tachycardia (VT) is rare and generally occurs in patients with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and short QT syndrome. Unlike monomorphic VT, these arrhythmic syndromes are associated with sudden death. While the cardiac gross morphology is normal, suggesting a structurally normal heart, abnormalities exist at the molecular level and predispose them to arrhythmias. Another fascinating area, idiopathic ventricular fibrillation and early repolarization syndrome, are undergoing research for a genetic basis.

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