Sophie C H Van Malderen1, Dirk Kerkhove2, Dominic A M J Theuns3, Caroline Weytjens2, Steven Droogmans2, Kaoru Tanaka4, Dorien Daneels5, Sonia Van Dooren5, Marije Meuwissen5, Maryse Bonduelle5, Pedro Brugada6, Guy Van Camp2. 1. Department of Electrophysiology (Heart Rhythm Management Centre), Vrije Universiteit Brussel (VUB), UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium; Department of Electrophysiology, Thoraxcenter, Erasmus MC, 's Gravendijkwal 230, 3015 CE Rotterdam, The Netherlands.. Electronic address: s.vanmalderen@erasmusmc.nl. 2. Department of Non-invasive Cardiology, Vrije Universiteit Brussel (VUB), UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. 3. Department of Electrophysiology, Thoraxcenter, Erasmus MC, 's Gravendijkwal 230, 3015 CE Rotterdam, The Netherlands. 4. Department of Cardiac Radiology, Vrije Universiteit Brussel (VUB), UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. 5. Centre for Medical Genetics, Reproduction and Genetics, Reproduction Genetics and Regenerative Medicine, Vrije Universiteit Brussel (VUB), UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. 6. Department of Electrophysiology (Heart Rhythm Management Centre), Vrije Universiteit Brussel (VUB), UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium.
Abstract
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.
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 BSpatients demonstrate a more malignant clinical phenotype. METHODS: 124 BSpatients (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:BSpatients had longer RVEDs and IVEDs compared to the CTR. BSpatients with a previous history of syncope or spontaneous ventricular arrhythmia showed the longest RVEDs and IVEDs. Male BSpatients demonstrated longer RVEDs and IVEDs than females. Male BSpatients with malignant events had the longest delays. No significant differences regarding LVED were observed between BSpatients 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.
Authors: Estefanía Martínez-Barrios; Elena Arbelo; Sergi Cesar; José Cruzalegui; Victoria Fiol; Nuria Díez-Escuté; Clara Hernández; Ramon Brugada; Josep Brugada; Oscar Campuzano; Georgia Sarquella-Brugada Journal: Front Cardiovasc Med Date: 2022-04-11