Speckle tracking echocardiography data in Brugada syndrome patients

Brugada syndrome is characterized by typical electrocardiogram changes and a high risk for sudden cardiac death (Priori et al., 2013). In addition to the well known electrical substrate, morphological and functional alterations appeared to be present in a subset of the Brugada syndrome patients (Catalano et al., 2009). Echocardiographic speckle tracking enables us to detect subtle contraction alterations (Smiseth et al.,2016). We performed transthoracic echocardiography with speckle tracking analysis in 82 healthy controls and 175 Brugada syndrome patients. Main findings are presented and discussed in the article “Contraction alterations in Brugada syndrome; association with life-threatening ventricular arrhythmias” (Scheirlynck et al., 2019). This related Data article contains segmental longitudinal strain values for RV and LV, and the comparison of echocardiographic parameters between Brugada syndrome patients with spontaneous and drug-induced type 1 pattern and between patients with and without ventricular arrhythmia inducibility during electrophysiological study.


Data
Brugada syndrome is a heritable channelopathy characterized by typical electrocardiogram changes and a high risk for sudden cardiac death [1,2]. Initially considered as a purely electrical disease, the use of cardiac imaging in Brugada syndrome only gained interest recently. Mild morphological and functional abnormalities affecting the right ventricular outflow tract [3e8] -and to a lesser extent the right ventricle (RV) and the left ventricle (LV) [9À11] e were observed. Echocardiographic speckle tracking can reveal subtle alterations in myocardial contraction patterns [12]. We acquired transthoracic echocardiography in 82 healthy controls and 175 Brugada syndrome patients [13]. Speckle tracking analysis was performed for the left (16 segments) and right ventricle (3 segments) (Fig. 1). Segmental longitudinal strain values of healthy individuals and Brugada syndrome patients are reported and Specifications Table   Subject Medicine Specific subject area Echocardiography in Brugada syndrome patients Type of data Mechanical dispersion, which is defined as the standard deviation of the time-interval from onset of the QRS-complex until the peak myocardial shortening in the 16 left ventricle, 3 right ventricle free   wall and 6 right ventricle segments, was calculated in all patients, as a measure of contraction heterogeneity (Fig. 2). Echocardiographic data were reported for specific subgroups of Brugada syndrome patients. First, we compared patients who presented a spontaneous type 1 electrocardiogram pattern with patients who were diagnosed based on a drug-induced type 1 pattern (Table 2).
Secondly, we compared patients in whom a sustained ventricular arrhythmia could be induced during electrophysiological study compared to patients in whom no ventricular arrhythmia could be induced (Table 3). A total of 168 patients (96%) underwent electrophysiological testing.

Study population
Brugada syndrome patients were recruited from the database of the University Hospital of Brussels. All had been diagnosed with Brugada syndrome based either on a spontaneous or drug induced ST segment elevation with a type 1 morphology of !2 mm in 1 or more leads among the right precordial leads (V 1 eV 2 ) positioned in the second, third, or fourth intercostal space [1,2]. Included patients were at least 18 years old. We excluded patients with a history of ischemic or structural heart disease. We also excluded patients with atrial fibrillation or pacing during transthoracic echocardiography (TTE) or with insufficient image quality for speckle tracking analysis of both left and right ventricle, defined as inappropriate tracking of 2 or more segments on a single view.
Healthy controls with similar age and sex distribution were recruited among hospital employees and their family members.
Written informed consent was obtained from all subjects. This study was performed in accordance with the Declaration of Helsinki and was approved by the Ethics Committee of UZ Brussel.

Echocardiography
TTE was performed using a commercial cardiac ultrasound system (Vivid 9; GE Vingmed Ultrasound, Horten, Norway), equipped with a 2D broad-band M3S transducer (2.5 MHz). In each patient standard parasternal long-and short-axis images, apical 4-, 2-and 3-chamber views and a RV focused 4-chamber view were acquired [14]. Lead II was used for ECG recordings. Loops of 3 consecutive heart beats at >50 frames per second were digitally stored for offline analysis (EchoPac, version 201, GE Vingmed Ultrasound, Horten, Norway).
The LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) were measured and the ejection fraction (EF) was calculated by modified Simpson's biplane method. Tricuspid annular plane systolic excursion (TAPSE) was obtained by M-mode through the tricuspid annulus on the 4-chamber view. RV outflow tract (RVOT) proximal and distal diameters were measured from the parasternal short-axis view. End-diastolic and end-systolic RV area (RVA) were obtained from the RV focused 4chamber view and fractional area change (FAC) was calculated [15]. Speckle tracking analysis was performed on the 3 apical views for the LV and on the RV focused 4chamber view for the RV [14,16]. When necessary, the automated region of interest was adjusted to optimise tracking. GLS was defined as the mean of the peak systolic strain in the 16 LV segments and RV longitudinal strain (RVLS) from the 3 RV free wall segments (Fig. 1). The time to peak myocardial longitudinal strain in each segment was measured as the time from onset of the QRS complex on the ECG to maximum myocardial shortening. MD was defined as the standard deviation of the time to peak in respectively the 16 LV segments, the 6 RV segments and the 3 RV free wall segments (Fig. 2) [17,18].

Drug-challenge
Ajmaline (1 mg/kg) was administered intravenously over a 5-min period to unmask the diagnostic type 1 electrocardiogram pattern in case of non-diagnostic baseline electrocardiogram. The test was considered positive if type 1 ECG appeared in !1 right precordial leads. The drug infusion was discontinued if QRS prolongation exceeded 30%, frequent premature ventricular beats or type 1 Brugada ECG occurred or development of high-degree atrio-ventricular block.

Electrophysiological study
Electrophysiological study protocol consisted of a single site of stimulation at the right ventricular apex, three basic pacing cycles (600, 500, and 430 ms), and introduction of up to 3 ventricular premature beats down to a minimum of 200 ms. A patient was considered inducible if a sustained (!30 seconds) ventricular fibrillation or ventricular tachycardia was induced.

Statistics
Continuous data was presented as mean ± standard deviation or median with interquartile range (IQR). Categorical data was presented as number (%). Comparisons were performed using T-test, Mann-Whitney U test, c2 or Fischer's exact test as appropriate.