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Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
114 consecutive patients matched in age underwent prospectively cardiac catheterization and quantitative biventricular contrast angiography to rule out a structural heart disease. Studied population included: 51 patients with a BrS-ECG (BrS group, 7F, 44M, 43 ± 11 y) who had a spontaneous or ajmaline-induced BrS coved type ECG, 49 patients with localized ARVD/C but without ST segment elevation in the right precordial leads (14F, 35M, 39±13y), and 14 control patients (7 F, 7 M, 38 ± 16 y). Among BrS group, the authors identified three main angiographic phenotypes: BrS group I = patients with normal RV (n = 15, 29%); BrS group II = patients with segmental RV wall motion abnormalities but no structural arguments for ARVD/C (n = 26, 51%); BrS group III = patients with localized abnormalities suggestive of focal ARVD/C (n = 10, 20%).Seventy-one percent of patients with BrS-ECG had abnormal RV wall motion. In BrS group III, 8/10 patients (16% of BrS patients) finally fulfilled international ESC/WHF 2000 ARVD/C criteria and 5/10 (10% of BrS patients) fulfilled BrS diagnostic criteria. An overlap was observed in 4 patients (8% of BrS patients) who fulfilled both ARVD/C and BrS criteria. Among the 45 genotyped patients, only one presented a SCN5A mutation, whereas a TRPM4 mutation was found in another patient. Both belonged to BrS group II. MOG1 gene analysis was negative for all patients, as were PKP2, DSP, DSG2, and DSC2 analyzes performed in BrS group III.
This is the first study to show prospectively an overlap between BrS and ARVD/C.The main finding of the study is that 71% of patients with a BrS-ECG had abnormal RV wall motion and 16% had structural alterations corresponding to localized (anteroapical and/or diaphragmatic) ARVD/C. Moreover, 8% of BrS-ECG patients fulfilled both BrS and ARVD/C criteria.These findings support the hypothesis of an overlap between BrS and localized or concealed forms of ARVD/C, but also that Brugada ECG pattern is not specific of a pathophysiological entity, i.e., BrS, but can be due to other conditions such as myocarditis or localized RV cardiomyopathy. BrS ECG pattern may be an indicator of ARVC, particularly in its clinically concealed phase, thus requiring morphological RV evaluation, such as MRI, contrast echocardiography and/or contrast angiography.As pointed out by the authors this overlap between BrS and ARVD/C does not mean that these two diseases are the same one, but that a substantial proportion of patients with a Brugada ECG pattern present RV structural alterations.In this study genetic screening was poorly contributive for both diseases. One of the explanations of the low prevalence of SCN5A mutations in thus series may lie in the high proportion of structural abnormalities and of localized ARVD/C.
1: Rouzet F, Algalarrondo V, Burg S, et al. Contraction delay of the RV outflow tract in patients with Brugada syndrome is dependent on the spontaneous ST-segment elevation pattern. Heart Rhythm. 2011 Dec;8(12):1905-12.
2: Yodogawa K, Morita N, Kobayashi Y, et al. A new approach for the comparison of conduction abnormality between arrhythmogenic right ventricular cardiomyopathy/dysplasia and Brugada syndrome. Ann Noninvasive Electrocardiol. 2011 Jul;16(3):263-9.
3: Duthoit G, Fressart V, Hidden-Lucet F, et al. Brugada ECG pattern: a physiopathological prospective study based on clinical, electrophysiological, angiographic, and genetic findings. Front Physiol.2012;3:474.
4: Iacoviello M, Forleo C, Puzzovivo A, et al. Altered two-dimensional strain measures of the right ventricle in patients with Brugada syndrome and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Eur J Echocardiogr. 2011 Oct;12(10):773-81.
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