Sustained and non-sustained ventricular tachycardia and no associated heart disease (idiopathic ventricular tachycardia)

Patients with ventricular arrhythmias (VAs) and without underlying structural heart disease or baseline electrical disorders (‘idiopathic’ VAs) usually have a benign clinical course. Only rarely do these benign arrhythmias trigger polymorphic ventricular tachycardia and idiopathic ventricular fibrillation. Due to their focal origin and to the absence of underlying myocardial scar, the 12-lead electrocardiogram (ECG) very precisely establishes the right or left ventricular site of origin of the arrhythmia and can help regionalize the origin of ventricular tachycardia for ablation. A 12-lead ECG obtained during the baseline rhythm and 24 h ECG Holter monitoring are indicated in order to identify structural or electrical disorders leading to polymorphic ventricular tachycardia/ventricular fibrillation and to determine the VA burden. The most frequent origin of idiopathic VAs is the right ventricular outflow tract. Other origins include the left ventricular outflow tract, the left ventricular fascicles (fascicular ventricular tachycardias), the left and right ventricular papillary muscles, the crux cordis, the mitral and tricuspid annuli, and the right ventricular moderator band. Recognizing the typical anatomic sites of origin combined with a 12-lead ECG assessment facilitates localization. Antiarrhythmic drug therapy (including use of beta blockers) or catheter ablation may be indicated to suppress or eliminate idiopathic VAs, particularly if there are severe arrhythmia-related symptoms or if the arrhythmia burden is high and ‘tachycardia’-induced cardiomyopathy is suspected. Catheter ablation is frequently preferred to prevent lifelong drug therapy in young patients.