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Brugada syndrome (BrS) is a controversial disease whose pathophysiology is still far from being fully understood. Unlike other cardiological disorders, a definite etiology has not yet been established so that it could be summarized under two main chapters: "functional" or "organic", "repolarization" or "depolarization" disorder. Despite initial descriptions leaned towards the organic substrate and delayed depolarization features, functional and repolarization theories have attracted most of the Cardiological attention for many years. Data from electrocardiography, endocavitary tracings, electroanatomic mapping and histopathology, however, demonstrated that BrS is mainly characterized by structural myocardial changes mostly at the right ventricular outflow tract (RVOT), but also at the right ventricle (RV) and by delayed conduction at the same sites. Conduction disorders at different levels may also be present and identify patients at high risk for major arrhythmic events. The aim of the present review is to provide the current state of art of the pathophysiology of BrS, focusing on electro‐vectorcardiography and electrophysiological features, histopathology, echocardiography, and cardiac magnetic resonance imaging (CMRI). [ABSTRACT FROM AUTHOR]

A 43-year-old woman presented to the emergency room with a sustained ventricular tachycardia (VT). ECG showed a QRS in left bundle branch block morphology with inferior axis. Echocardiography, ventricular angiography, and cardiac magnetic resonance imaging (CMRI) revealed a normal right ventricle and a left ventricular diverticulum. Electrophysiology studies with epicardial voltage mapping identified a large fibrotic area in the inferolateral layer of the right ventricular wall and a small area of fibrotic tissue at the anterior right ventricular outflow tract. VT ablation was successfully performed with combined epicardial and endocardial approaches. [ABSTRACT FROM AUTHOR]