Our understanding of Brugada syndrome (BrS) has evolved since the syndrome was 
first described in 1992. BrS is considered to be a primary inherited 
channelopathy often involving the inward sodium current and the diagnosis has 
traditionally required the exclusion of overt structural heart disease. In view 
of recently published observations about BrS, we propose that the term BrS may 
actually encompass a heterogeneous group of disorders with a variety of genetic 
and clinical phenotypes. This disease has classically been described as a 
primary electrical disorder involving the sodium channel leading to the 
characteristic electrocardiogram (ECG) changes of BrS. We challenge the current 
understanding and propose that patients with structurally normal hearts, family 
history of sudden cardiac death, with associated genetic abnormalities only 
account for a subset of patients with the "Brugada pattern" ECG. There may also 
be some patients with a diagnosis of BrS who may also have features which 
overlap with arrhythmogenic right ventricular cardiomyopathy. In these patients 
there may be an underlying structural abnormality. In this context, it is 
possible that catheter ablation may abolish the "Brugada pattern" ECG changes as 
well as abolishing the risk of life threatening arrhythmias in these patients. 
Given the recent developments in the field, we propose a novel comprehensive 
multimodality model for risk stratification and assessment of patients with BrS. 
Identification of variations of diseases may facilitate more specific risk 
stratification models and management paradigms in patients with Brugada ECG 
pattern.