Recent body surface potential mapping studies suggest that the induction rate of VT in Brugada syndrome (BrS) correlates with the area of ST elevation and the presence of late potentials, but also that ST elevation might be primarily caused by abnormality in depolarization rather than in repolarization, especially in the right ventricle outflow tract (RVOT). A preliminary study with magnetocardiographic (MCG) mapping at rest has shown an abnormal current distribution located in the RVOT. In this study we describe MCG patterns at rest, during physical effort and during flecainide test in an asymptomatic patient with BrS, restudied three times during three years follow-up. Method: An asymptomatic 28 years old man, with a type 2 BrS ECG at rest, but normal physical examination, echocardiogram and MRI, was studied with 12-lead ECG and multichannel MCG mapping, recorded with a 36-channel DC-SQUID system (CMI-2436), (sensitivity 20 fT/Hz½), at rest, during effort and flecainide tests. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) gradient orientation (a angle) was computed at the integral of the second quarter of the ST interval and at the T-wave apex. Current density imaging (CDI) and the strength (in mAm) of the equivalent current dipole (ECD) were calculated during all the first and second quarter of the J-T interval, to estimate potentially arrhythmogenic current flowing. Results: Molecular screening of the SCNC 5A open reading frame revealed a de novo missense mutation in the DII-DIII linker, thus confirming the diagnosis of BrS. Flecainide induced typical type-1 ST elevation in V1-V3 leads, but no changes of MF a angles, which were normal at rest and under effort. After flecainide, CDI evidenced a shift of the current density at the J-point, from right to left epicardial surface, without a significant increase of the J-T ECD strength. Conclusions: In this asymptomatic BrS patient, in spite of positive flecainide at the ECG, MCG mapping didn’t show abnormalities of VR parameters. In three years of follow-up no arrhythmia occurred. Further work is necessary to establish the predictive value of MCG mapping as an additional method for non-invasive risk-stratification in asymptomatic BrS patients with abnormal flecainide-test.

Brisinda, D., Fenici, R., Bottelli, G., Napolitano, C., P. R. I. O. R. I., .. S. G., Meloni, A. M., Magnetocardiographic Mapping in an Asymptomatic Brugada Patient, with a de novo SCN5A Mutation-Effects of Flecainide and of Exercise Tests, Poster, in Proceedings of 15th International Conference on Biomagnetism. BIOMAG 2006, (Vancouver, 20-26 August 2006), N/A, Vancouver 2006: 221-221 [http://hdl.handle.net/10807/17220]

Magnetocardiographic Mapping in an Asymptomatic Brugada Patient, with a de novo SCN5A Mutation-Effects of Flecainide and of Exercise Tests

Brisinda, Donatella;Fenici, Riccardo;
2006

Abstract

Recent body surface potential mapping studies suggest that the induction rate of VT in Brugada syndrome (BrS) correlates with the area of ST elevation and the presence of late potentials, but also that ST elevation might be primarily caused by abnormality in depolarization rather than in repolarization, especially in the right ventricle outflow tract (RVOT). A preliminary study with magnetocardiographic (MCG) mapping at rest has shown an abnormal current distribution located in the RVOT. In this study we describe MCG patterns at rest, during physical effort and during flecainide test in an asymptomatic patient with BrS, restudied three times during three years follow-up. Method: An asymptomatic 28 years old man, with a type 2 BrS ECG at rest, but normal physical examination, echocardiogram and MRI, was studied with 12-lead ECG and multichannel MCG mapping, recorded with a 36-channel DC-SQUID system (CMI-2436), (sensitivity 20 fT/Hz½), at rest, during effort and flecainide tests. For MCG assessment of ventricular repolarization (VR), magnetic field (MF) gradient orientation (a angle) was computed at the integral of the second quarter of the ST interval and at the T-wave apex. Current density imaging (CDI) and the strength (in mAm) of the equivalent current dipole (ECD) were calculated during all the first and second quarter of the J-T interval, to estimate potentially arrhythmogenic current flowing. Results: Molecular screening of the SCNC 5A open reading frame revealed a de novo missense mutation in the DII-DIII linker, thus confirming the diagnosis of BrS. Flecainide induced typical type-1 ST elevation in V1-V3 leads, but no changes of MF a angles, which were normal at rest and under effort. After flecainide, CDI evidenced a shift of the current density at the J-point, from right to left epicardial surface, without a significant increase of the J-T ECD strength. Conclusions: In this asymptomatic BrS patient, in spite of positive flecainide at the ECG, MCG mapping didn’t show abnormalities of VR parameters. In three years of follow-up no arrhythmia occurred. Further work is necessary to establish the predictive value of MCG mapping as an additional method for non-invasive risk-stratification in asymptomatic BrS patients with abnormal flecainide-test.
2006
Inglese
Proceedings of 15th International Conference on Biomagnetism. BIOMAG 2006
15th International Conference on Biomagnetism
Vancouver
Poster
20-ago-2006
26-ago-2006
Brisinda, D., Fenici, R., Bottelli, G., Napolitano, C., P. R. I. O. R. I., .. S. G., Meloni, A. M., Magnetocardiographic Mapping in an Asymptomatic Brugada Patient, with a de novo SCN5A Mutation-Effects of Flecainide and of Exercise Tests, Poster, in Proceedings of 15th International Conference on Biomagnetism. BIOMAG 2006, (Vancouver, 20-26 August 2006), N/A, Vancouver 2006: 221-221 [http://hdl.handle.net/10807/17220]
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