INTRODUCTION: Cardiac magnetic resonance imaging (CMR) is a powerful diagnostic tool for evaluating cardiac structure and function. Recently, right ventricular wall-motion abnormalities were described using electron beam tomography in patients with Brugada syndrome. In the present study, we prospectively evaluated CMR findings in patients with Brugada syndrome compared to matched controls. METHODS AND RESULTS: CMR was performed on 20 consecutive patients with proven Brugada syndrome. The imaging protocol included breath-hold dark blood prepared T1-weighted multislice turbo spin-echo and gradient-echo images. Ventricular volumes and dimensions were compared to age- and sex-matched normal volunteers. The right ventricular outflow tract area was significantly enlarged in patients with Brugada syndrome compared to controls (11 vs 9 cm2, P = 0.018). There was a trend to larger right ventricular end-diastolic and end-systolic volumes and lower right ventricular ejection fraction in patients with Brugada syndrome compared to controls. However, none of the differences reached significance (P = 0.3, P = 0.08, and P = 0.06, respectively). There was no statistically significant difference in the left ventricular parameters between patients and controls. High intramyocardial T1 signal similar to fat signal was observed in 4 (20%) of the 20 patients compared to none of the controls. CONCLUSION: The findings support the view that subtle structural changes, such as right ventricular outflow tract dilation may point to a localized arrhythmogenic substrate in patients with Brugada syndrome.
INTRODUCTION: Cardiac magnetic resonance imaging (CMR) is a powerful diagnostic tool for evaluating cardiac structure and function. Recently, right ventricular wall-motion abnormalities were described using electron beam tomography in patients with Brugada syndrome. In the present study, we prospectively evaluated CMR findings in patients with Brugada syndrome compared to matched controls. METHODS AND RESULTS: CMR was performed on 20 consecutive patients with proven Brugada syndrome. The imaging protocol included breath-hold dark blood prepared T1-weighted multislice turbo spin-echo and gradient-echo images. Ventricular volumes and dimensions were compared to age- and sex-matched normal volunteers. The right ventricular outflow tract area was significantly enlarged in patients with Brugada syndrome compared to controls (11 vs 9 cm2, P = 0.018). There was a trend to larger right ventricular end-diastolic and end-systolic volumes and lower right ventricular ejection fraction in patients with Brugada syndrome compared to controls. However, none of the differences reached significance (P = 0.3, P = 0.08, and P = 0.06, respectively). There was no statistically significant difference in the left ventricular parameters between patients and controls. High intramyocardial T1 signal similar to fat signal was observed in 4 (20%) of the 20 patients compared to none of the controls. CONCLUSION: The findings support the view that subtle structural changes, such as right ventricular outflow tract dilation may point to a localized arrhythmogenic substrate in patients with Brugada syndrome.
Authors: Charles Antzelevitch; Gan-Xin Yan; Michael J Ackerman; Martin Borggrefe; Domenico Corrado; Jihong Guo; Ihor Gussak; Can Hasdemir; Minoru Horie; Heikki Huikuri; Changsheng Ma; Hiroshi Morita; Gi-Byoung Nam; Frederic Sacher; Wataru Shimizu; Sami Viskin; Arthur A M Wilde Journal: Europace Date: 2017-04-01 Impact factor: 5.214