Ventricular arrhythmias, especially those of non‐ischemic heart diseases, arise mostly from the outflows. Differences in embryonic origin and phenotype may account for arrhythmogenic propensity of right ventricular outflow tract (RVOT). The anatomy of the ventricles may be divided

into inflow, apex, and outflow. As far as RVOT (pulmonary infundibulum) is concerned, it goes from the moderation band to the semilunar pulmonary valves. Since some myocardium extends distally from the “nadir” of the valve ring, arrhythmias may originate from the “pulmonary artery.” This is true also on the aortic side, where the myocardium located within the coronary Valsalva sinuses may be the source of “aortic” arrhythmias. Arrhythmias with substrate from the RVOT may be genetically determined (arrhythmogenic cardiomyopathy), immune mediated (sarcoidosis) or infective (viral myocarditis), or form without substrate (idiopathic RVOT tachycardia). It is still controversial whether Brugada syndrome occurs in normal hearts or presents a substrate at the infundibular level.

Electroanatomical mapping plays a crucial role in establishing the existence of lacking electrical activity (“electric scars”), but it is unable to establish the precise nature of the underlying disease. Endomyocardial biopsy in this setting is the gold standard for diagnosis.