Myocardial Iodine-123-Metaiodobenzylguanidine (I-MIBG) Imaging in Brugada Syndrome

(I-MIBG) Imaging in Brugada Syndrome To the Editor: We read with interest a recent article in Circulation by Wichter et al1 on cardiac autonomic dysfunction in Brugada syndrome. The authors demonstrated that regionally reduced iodine-123-metaiodobenzylguanidine (I-MIBG) uptake in the inferior and septal left ventricular wall was present in 8 (47%) of 17 patients with Brugada syndrome but in none of 10 age-matched control subjects. The study may provide new insight into the pathogenesis and arrhythmogenesis of Brugada syndrome. However, we have some questions concerning other indices of I-MIBG imaging, clinical characteristics of the study patients, and timing of I-MIBG imaging. In normal subjects, regional MIBG uptake may be nonhomogeneous and apparently lower in the inferior and septal wall than in the anterior wall2: 80 11% versus 95 5% (mean SD).3 Additionally, a heterogeneous I-MIBG distribution in the left ventricle may be a physiological phenomenon mediated by the parasympathetic nerve fibers predominantly located in the inferior wall. Therefore, it is possible that segmental (inferior and septal) reduction of I-MIBG uptake in patients with Brugada syndrome is a normal variant. Cardiac I-MIBG markers that have been used include not only regional uptake heterogeneity but also global myocardial uptake (heart-to-mediastinum ratio) and washout kinetics. Our recent study showed that the heart-to-mediastinum ratio has independent and incremental prognostic value.4 It seems essential to investigate other indices such as the heart-tomediastinum ratio and washout kinetics in patients with Brugada syndrome. We also think that subjects with right bundle branch block but no ST-segment elevation, or asymptomatic subjects with Brugada-type ST shift but no ST-segment augmentation by a sodium channel blocker loading test, should be enrolled as control subjects. We previously found an asymptomatic Brugada-type ST shift in 12 (0.14%) of 8612 general Japanese subjects.5 We performed I-MIBG imaging in 11 of these 12 subjects. Segmental reduction of I-MIBG uptake in the inferior wall was found in 5 (45%) of those 11 subjects (unpublished data, 1999). None were patients with proven Brugada syndrome because sodium channel blocker loading tests failed to enhance ST-segment elevation. Reduced IMIBG uptake in the inferior left ventricular wall does not necessarily explain the pathogenesis and arrhythmogenesis of Brugada syndrome. Finally, the timing of I-MIBG imaging was not defined in the article. We speculate that I-MIBG uptake would be persistently impaired by rescue DC shock or after ventricular arrhythmia. We would like to know about the difference between acute and chronic phases, the time course, and the pharmacological change in I-MIBG uptake.