Key result
Review details Brugada syndrome pathophysiology, presentation, and management, noting a ~0.4% worldwide prevalence.
Why the study?
To review current hypotheses regarding pathophysiology, clinical presentations, sudden cardiac death prevention strategies, and treatment of recurrent arrhythmias in Brugada syndrome.
This review provides a clinical update on the pathophysiology, presentation, and management of Brugada syndrome.
Offers clinicians an updated Brugada syndrome synthesis; leaves open need for prospective trials on risk stratification.
Brugada syndrome (BrS) was initially described in southeast Asians with a structurally normal heart presenting with polymorphic ventricular tachycardia and fibrillation. This condition is marked by J-point elevation ≥ 2 mm with coved-type ST segment elevation followed by negative T wave inversions in at least one precordial lead (V1 or V2) when other etiologies have been excluded. These changes on electrocardiogram (EKG) can either be spontaneous or manifest after sodium channel blockade. The worldwide prevalence of BrS is about 0.4%; however, it is higher in the Asian population at 0.9%. This article will review the current hypotheses regarding the pathophysiology, spectrum of clinical presentation, strategies for prevention of sudden cardiac death and the treatment for recurrent arrhythmias in BrS.
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Rojas et al. (2021) conducted a review in Brugada syndrome. Brugada syndrome, characterized by specific EKG changes and a worldwide prevalence of 0.4% (0.9% in Asian populations), is reviewed regarding its pathophysiology, presentation, and management.
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