The diagnostic challenge of type 3 Brugada pattern: clinical implications and provocative testing strategies

Pedro Luis Matus Rojo; Donaldo Emiliano Silva Lopez; Héctor Daniel Zamora Andrade; Pedro Emmanuel Escárzaga López; Celina Guadalupe Camacho  Mascareño; Erick Adolfo Meza Soto

doi:10.18203/2320-6012.ijrms20251674

Authors

Pedro Luis Matus Rojo Autonomous University of Sinaloa, Los Mochis General Hospital, Los Mochis, Sinaloa, Mexico
Donaldo Emiliano Silva Lopez Monterrey Institute of Technology, Monterrey Campus, Nuevo León, Mexico
Héctor Daniel Zamora Andrade Autonomous University of Sinaloa, Los Mochis General Hospital, Los Mochis, Sinaloa, Mexico
Pedro Emmanuel Escárzaga López Autonomous University of Sinaloa, Los Mochis General Hospital, Los Mochis, Sinaloa, Mexico
Celina Guadalupe Camacho Mascareño Autonomous University of Sinaloa, Los Mochis General Hospital, Los Mochis, Sinaloa, Mexico
Erick Adolfo Meza Soto Autonomous University of Sinaloa, Los Mochis General Hospital, Los Mochis, Sinaloa, Mexico

DOI:

https://doi.org/10.18203/2320-6012.ijrms20251674

Keywords:

Brugada syndrome, Type 3 Brugada pattern, Provocative testing, Sodium channel blockers

Abstract

The Brugada syndrome (BrS) is a channelopathy associated with an increased risk of sudden cardiac death (SCD), characterized by distinctive electrocardiographic (ECG) patterns. While type 1 Brugada pattern is diagnostic, type 2 and 3 patterns are non-diagnostic and require further evaluation. The type 3 Brugada pattern, characterized by a <2 mm saddleback ST-segment elevation followed by a positive T-wave, poses significant diagnostic uncertainty due to its dynamic nature and overlap with benign ECG variants. Provocative testing with sodium channel blockers (e.g., ajmaline, flecainide, or procainamide) is often necessary to unmask a diagnostic type 1 pattern. However, the indications, timing, and safety of pharmacological challenge remain debated, particularly in asymptomatic individuals or those with low pretest probability. This review explores the diagnostic dilemmas of type 3 Brugada pattern, analyzes risk stratification criteria, and provides evidence-based recommendations on when to perform provocative testing. Key considerations include clinical history, family history of SCD, syncope of unknown origin, and the presence of arrhythmic symptoms. A structured diagnostic approach is essential to avoid both underdiagnosis and overmedicalization in this clinically ambiguous population.

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