Esther Scheirlynck1, Sophie Van Malderen2, Andreea Motoc3, Øyvind H Lie4, Carlo de Asmundis5, Juan Sieira6, Gian-Battista Chierchia7, Pedro Brugada8, Bernard Cosyns9, Steven Droogmans10. 1. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium; Life sciences and Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Electronic address: esther.scheirlynck@vub.be. 2. Life sciences and Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Electronic address: svmalder@msn.com. 3. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium; Life sciences and Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Electronic address: andreeaiulia.motoc@uzbrussel.be. 4. Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute for Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address: Oyvind.Haugen.Lie@rr-research.no. 5. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium. Electronic address: carlo.deasmundis@uzbussel.be. 6. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium. Electronic address: juan.sieira@uzbrussel.be. 7. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium. Electronic address: jeanbaptiste.chierchia@uzbrussel.be. 8. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium. Electronic address: pedro.brugadaiterradellas@uzbrussel.be. 9. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium; Life sciences and Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Electronic address: bernard.cosyns@uzbrussel.be. 10. Department of Cardiology, Universitair Ziekenhuis Brussel, Centrum voor Hart- en Vaatziekten, Brussels, Belgium; Life sciences and Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Electronic address: steven.droogmans@uzbrussel.be.
Abstract
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.
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.
Authors: Tom Kai Ming Wang; Richard A Grimm; L Leonardo Rodriguez; Patrick Collier; Brian P Griffin; Zoran B Popović Journal: PLoS One Date: 2021-08-20 Impact factor: 3.240
Authors: Marta Fonseca; Leonor Parreira; José Maria Farinha; Rita Marinheiro; Ana Esteves; Sara Gonçalves; Rui Caria Journal: Indian Pacing Electrophysiol J Date: 2021-02-16