Table 2.

Concealed substrates in Brugada syndrome.

Structural Findings for Underlying Anatomical Arrhythmogenic Substrates in BrS.	Studies
Echocardiogram - Decreased biventricular function at TEI index through sodium channel blocking test. - Reduction in the RV longitudinal strain. - Morphologic and wall-motion abnormalities of the RV.	[51] [52] [53]
Cardiac magnetic resonance - Lower right ventricular ejection fraction. - LV/RV dilation, with a wider involvement of the RV than LV. - Enlarged RVOT area, larger RV end-systolic volumes, lower LV and RV ejection fraction. - Fibrosis and abnormal late fractionated potentials, indicative of slowed conduction in the RVOT region.	[49] [54] [55] [9]
Endomyocardial biopsy - Lymphocytic myocarditis with inflammatory infiltrates and focal necrosis, with or without microaneurysms. - Parvovirus B19 with VF. - RV hypertrophy and fibrosis, mainly at RVOT level, with epicardial fatty infiltration. - Epicardial interstitial fibrosis, along with increased collagen throughout the heart and a reduction of the expression of gap junctions in the RVOT.	[56] [57] [58] [59] [60] [9] [61]
EAM - Electroanatomical substrate on the epicardial rather than endocardial surface of the RVOT.	[62] [63] [64]

Subtle substrate abnormalities with a potential arrhythmogenic role in BrS are shown, as documented by the multimodal diagnostic workup. BrS = Brugada syndrome; EAM = electroanatomical map; RV = right ventricular; RVOT = right ventricular outflow tract.