Even a Pooled Analysis Does Not Resolve the Debate of Electrophysiology Testing in Brugada Syndrome.

619 Since the first description, investigative work into the pathophysiology and clinical management of Brugada syndrome (BrS) has been active. Like other channelopathies, BrS is a cause of sudden cardiac arrest (SCA) in young, otherwise healthy, individuals. Initially attributed to the loss of sodium channel function, BrS has also been attributed to the loss of calcium channel function. Thus, the disease is not solely a sodium channelopathy, but rather related to an imbalance between inward and outward currents during phase 1 of the action potential. The hallmark ECG feature is a type 1 pattern of a coved ST-segment elevation of ≥2 mm followed by a negative T wave, present in >1 right precordial lead (V 1 through V 3 ), occurring either spontaneously or provoked with a sodium channel antagonist. However, the ECG in BrS can demonstrate type 1, 2, or 3 patterns, or be normal; and these changes can occur either spontaneously or be related to autonomic tone, physiological parameters (eg, fever), and ECG lead position. BrS, therefore, is a dynamic disease, influenced by ethnicity, sex, genotype, autonomic tone, regionally abnormal myocardium, and varied physiological and pharmacological stimuli. With this interplay of pathophysiology, risk stratification of patients with BrS ECG pattern is challenging. Programmed electric stimulation (PES) has been reported to be a useful tool for risk stratification; however, this recommendation is controversial.