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

Since the first description(1), 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 loss of sodium channel function, BrS has also been attributed to 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 electrocardiogram (ECG) feature is a type-1 pattern of a coved ST-segment elevation ≥2 mm followed by a negative T-wave, present in greater than 1 right precordial lead (V1-V3), 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 related to autonomic tone, physiologic parameters (e.g., fever) and ECG lead position. Brugada syndrome, therefore, is a dynamic disease, influenced by ethnicity, gender, genotype, autonomic tone, regionally abnormal myocardium(2), and varied physiologic and pharmacologic stimuli. With this interplay of pathophysiology, risk stratification of patients with Br ECG pattern is challenging. Programmed electrical stimulation (PES) has been reported to be a useful tool for risk stratification; however, this recommendation is controversial(3-11).