Right ventricular outflow tract electroanatomical abnormalities in asymptomatic and high‐risk symptomatic patients with Brugada syndrome: Evidence for a new risk stratification tool?

Abstract

Introduction: Microstructural abnormalities at the epicardium of the right ventricular outflow tract (RVOT) may provide the arrhythmia substrate in Brugada syndrome (BrS). Endocardial unipolar electroanatomical mapping allows the identification of epicardial abnormalities. We evaluated the clinical implications of an abnormal endocardial substrate as perceived by high-density electroanatomical mapping (HDEAM) in patients with BrS. Methods: Fourteen high-risk BrS patients with aborted sudden cardiac death (SCD) (12 males, mean age: 41.9 ± 11.8 years) underwent combined endocardial-epicardial HDEAM of the right ventricle/RVOT, while 40 asymptomatic patients (33 males, mean age: 42 ± 10.7 years) underwent endocardial HDEAM. Based on combined endocardial-epicardial procedures, endocardial HDEAM was considered abnormal in the presence of low voltage areas (LVAs) more than 1 cm 2 with bipolar signals less than 1 mV and unipolar signals less than 5.3 mV. Programmed ventricular stimulation (PVS) was performed in all patients.Results: The endocardial unipolar LVAs were colocalized with epicardial bipolar LVAs (p = .0027). Patients with aborted SCD exhibited significantly wider endocardial unipolar (p < .01) and bipolar LVAs (p < .01) compared with asymptomatic individuals. A substrate size of unipolar LVAs more than 14.5 cm 2 (area under the curve [AUC]: 0.92, p < .001] and bipolar LVAs more than 3.68 cm 2 (AUC: 0.82,

Heterogeneities in Ventricular Conduction Following Treatment with Heptanol: A Multi-Electrode Array Study in Langendorff-Perfused Mouse Hearts

“…Conduction velocity (CV) is an important variable for the propagation of cardiac action potentials (APs) [ 1 , 2 ]. Defects in conduction are found with aging [ 3 ], and in many pathological states, such as heart failure [ 4 ], diabetic cardiomyopathy [ 5 ], long QT syndrome [ 6 ], and Brugada syndrome [ 7 , 8 ]. Therefore, the elucidation of the relative contributions of abnormal conduction to the arrhythmic substrate can provide opportunities for the development of novel pharmacotherapy that can potentially restore conduction.…”

Case report: Lamin A/C gene mutation in patient with drug-induced type 1 Brugada syndrome at high arrhythmic risk

“…it may be considered a good tool to identify those at low arrhythmic risk, showing a high negative predictive value (95% in asymptomatic; 100% in symptomatic). Recently, the electroanatomical mapping has been considered an additional tool for SCD risk stratification among BrS patients ( 9 ); in particular an extensive RVOT electroanatomical abnormalities identify asymptomatic BrS patients at high risk ( 10 ). In order to better characterize the BrS electrophysiological substrate, we usually propose the ventricular endocardial electroanatomical mapping for all BrS patients followed at our center.…”

Pathogenesis and Management of Brugada Syndrome: Recent Advances and Protocol for Umbrella Reviews of Meta-Analyses in Major Arrhythmic Events Risk Stratification

“…However, some investigators suggest that this may lead to overdiagnosis, and specific symptoms or clinical data are required to confirm diagnosis [ 29 , 30 ]. Clinical, ECG, and laboratory markers have been found to be useful in diagnostics and risk stratification in diverse groups of patients [ 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 ]. Despite progress in SCD prevention, the optimal diagnostics and risk stratification in BrS are a major clinical challenge [ 42 , 43 , 44 ].…”

“…In BrS individuals, the presence of structural anomalies in the epicardium of the RVOT may contribute to arrhythmias [ 38 ]. Endocardial unipolar electroanatomical mapping technology may identify RVOT electrical abnormalities with VF inducibility during PVS and assist in BrS risk stratification [ 38 , 58 ]. Endocardial high-density electroanatomical mapping may permit BrS risk stratification in asymptomatic patients (referred for PVS) [ 38 ].…”