Multichannel Magnetocardiographic Mapping at Rest, after Effort and during Flecainide test, in a Patient with Idiopathic Brugada ECG Pattern

Donatella Brisinda, Riccardo Fenici, Anna Maria Meloni, Peter Fenici

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The Brugada syndrome (BS) [1] is an autosomal dominant familial disease, predominant in males. Mutations affecting the gene SCN5A that encodes for the cardiac sodium channel have been described. It is characterized by an ECG pattern with ST segment elevation in the precordial leads V1 to V3, and right bundle branch block morphology of the QRS complex. Syncope and/or sudden death may be caused by fast polymorphic ventricular tachycardia or ventricular fibrillation. An idiopathic Brugada ECG pattern (IBEP) may be present in 0.5 to 1 per 1000 asymptomatic individuals, but limited follow-up time doesn¿t allow conclusions on the prognostic value of IBEP alone. Method: We have studied an asymptomatic 28 years old man, with a type 2 IBEP at rest and normal physical examination and echocardiogram. Both rest ECG and flecainide-test were highly consistent with the diagnosis of BS, although the latter was less abnormal at two follow-up examinations. Flecainide-test was carried during simultaneous 12-lead ECG and multichannel magnetocardiographic mapping (MCG). MCG was recorded with a 36-channel DC-SQUID system (sensitivity: 20 fT/Hz, at 1 Hz) from a 36-point grid (20 x 20 cm) [2]. Magnetic ventricular repolarization (VR), was analyzed measuring the following parameters: 1) the orientation of the magnetic field (MF) distribution, at the integral of the second quarter from the J-point to the T-wave apex (ST α) and at the apex of the T-wave (T α) [3]. 2) The dynamics of MF distribution in the time interval between S100 (ST point at 100 ms from the end of S-wave) and T wave apex (Tmax) [2], measured as: a) changes in direction of the current vector, in time windows of 30 ms; b) changes of MF pole distance, in time windows of 30 ms, and c) changes in ratio between MF poles strength, in time windows of 30 ms. 3) The stability of VR, quantified as the time point of the ST interval (measured as the interval from the onset of the QRS) when the magnetic field orientation was stably within 50 degrees of the orientation at the peak of the T-wave. 4) The equivalent current dipole (ECD) strength of the ST integral, as an index of current flowing during the ST, potentially responsible for phase-2 reentry. Results: In spite of a typical type 2 ST elevation in the V1-V3 ECG leads, which changed to type 1 during flecainide-test, all MCG VR parameters were within normal limits, and unchanged after flecainide and effort. The strength of the ST-ECD increased from 9.1±0.5 Am to 10.8±0.9 Am during flecainide. However this increase in current strength, was not significantly different from that observed after effort in a normal subject. Both parents and one brother had normal ECG and MCG. Conclusions: This is the first MCG study of a patient with IBEP. The patient was aymptomatic and without arrhythmias, but with a ST-segment elevation 2 mm, in V2-V3, and positive flecainide test, therefore with a theoretical risk of serious arrhythmias [1]. MCG didn¿t show VR abnormalities after flecainide, in spite of positive ECG response. We are waiting for the results of genetic analysis to confirm a true BS. However our data suggests that MCG could be an independent method for more precise risk-stratification in asymptomatic patients with IBEP and abnormal flecainide-test.
Lingua originaleEnglish
pagine (da-a)125-127
Numero di pagine3
RivistaBiomedizinische Technik
Stato di pubblicazionePubblicato - 2004


  • Brugada ECG Pattern
  • Magnetocardiographic Mapping


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