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Background: Brugada syndrome (BrS) is characterized by a high risk of sudden cardiac death. The clinical value of deformation imaging in patients with BrS is unknown. We aimed to assess whether echocardiographic speckle tracking parameters differ between: 1) BrS patients and healthy controls, 2) BrS patients with and without life-threatening ventricular arrhythmias., Methods: Left ventricle (LV) and right ventricle (RV) longitudinal strain and mechanical dispersion (MD) were derived from echocardiography at inclusion. Clinical and ECG data were retrospectively assessed. A life-threatening ventricular arrhythmia was defined as an aborted cardiac arrest or sustained ventricular tachyarrhythmia., Results: We included 175 BrS patients and 82 controls. LV and RV longitudinal strain were lower (-18.1 ± 2.6% vs. -18.8 ± 2.0%, p = 0.01 and - 24.4 ± 5.4% vs. 25.6 ± 3.7%, p = 0.04), while MD was higher [38 ± 11 ms vs. 33 ± 8 ms, p = 0.001 and 15 (8-25) ms vs. 11 (6-19) ms, p = 0.03] in BrS patients compared to controls. BrS patients who experienced a life-threatening ventricular arrhythmia (n = 19) had higher LV MD compared to those without events (43 ± 11 ms vs. 37 ± 11 ms, p = 0.02). An LV MD ≥40 ms was optimally associated with life-threatening ventricular arrhythmias [odds ratio 4.62 (95%CI 1.58-13.50), p = 0.005]., Conclusions: BrS patients had lower longitudinal strain and more heterogeneous contractions than healthy controls. Furthermore, BrS patients with a history of life-threatening ventricular arrhythmia had more heterogeneous LV contractions than those without. Therefore, LV MD may be a risk marker in BrS and its evaluation in prospective studies is needed., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background and objectives Right ventricular (RV) conduction delay has been suggested as an underlying pathophysiological mechanism in Brugada syndrome (BS). In this cross-sectional study we non-invasively assessed the value of echocardiographic markers reflecting ventricular ejection delay to further assess electromechanical abnormalities in BS and to identify patients at risk for life-threatening arrhythmic events. Furthermore, we sought to assess differences in ejection delays between genders because male BS patients demonstrate a more malignant clinical phenotype. Methods 124 BS patients (57.3% males) and 62 controls (CTR) (48.4% males) were included. Using Tissue Velocity Imaging, the ejection delay, determined as the time from QRS onset to the onset of the sustained systolic contraction, was measured for both RV free wall (RVED) and lateral LV wall (LVED). From these parameters, the interventricular ejection delay between both walls (IVED) was calculated. Results BS patients had longer RVEDs and IVEDs compared to the CTR. BS patients with a previous history of syncope or spontaneous ventricular arrhythmia showed the longest RVEDs and IVEDs. Male BS patients demonstrated longer RVEDs and IVEDs than females. Male BS patients with malignant events had the longest delays. No significant differences regarding LVED were observed between BS patients and CTR. Conclusions We demonstrated that a previous history of malignant events was associated with longer RVEDs. Our findings supported the RV conduction delay mechanism behind BS and demonstrated for the first time that the predominant malignant male Brugada phenotype might also be the result of a more delayed RV conduction in males. [ABSTRACT FROM AUTHOR]