ABSTRACT
Introduction: Paediatric Inflammatory Multisystem Syndrome Temporarily associated with SARS-CoV-2 (PIMS-TS) is commonly associated with cardiovascular compromise. We have previously described the time course and magnitude of left ventricular (LV) systolic dysfunction in children and young adults with PIMSTS. However, it remains unknown if this inflammatory process can cause LV dyssynchrony. We aim to establish whether paediatric patients with PIMS TS develop LV dyssynchrony as assessed by echocardiography. Methods: Comprehensive transthoracic echocardiography in 10 PIMS-TS patients was performed during the acute stage of the initial illness when LV systolic function (3D Ejection Fraction (EF)) was worst and then again at six months post PIMS-TS. At both time points, we compared: 3D EF, LV fractional shortening (FS) and global longitudinal strain (GLS). Intraventricular LV dyssynchrony was assessed byMmode, PW tissue Doppler Velocities (TDI), 2-D speckle tracking and 3D echocardiography, while the interventricular dyssynchrony was also assessed by TDI at both time points. Results: Any improvement in 3D-LV EF at six months post illness (57.8±5.5 %) vs acute phase (51.8± 9.9%) was not statistically significant (p=0.166), whereas the LV FS (29.9± 9.5% vs 36.5± 12.5%, p=0.043) and GLS (-13.8±1.9% vs -18.6±3.1%, p=0.005) were significantly lower during the acute phase of the illness compared to six months later. Regarding dyssynchrony, none of the measures differed at follow up compared with acute phase;the septal to posterior wall motion delay assessed by Mmode (46.1±2.7msec vs 38.6±2.1msec, p=0.417), the basal septal to basal lateral peak velocity delay assessed by TDI (23.2±1.9.msec vs 24±1.9msec, p=0.930), the 2D speckle tracking-derived strain delay index was 1.1±1.2% at the time of the worst LV systolic performance and 0.62±0.26% at 6 months in the recovery period (p=0.219). The 3D echocardiography demonstrated that the 3D systolic dyssynchrony index (SDI) remained similar throughout the follow up period (3.04±1.23% at baseline vs 3.22±1.25% at 6 months, p=0.466). Conclusions: Despite the fact that in patients with PIMS TS cardiac involvement show a decline on LV systolic performance, this does not appear to be associated with LV dyssynchrony as assessed by echocardiography. We recommend larger patient cohort studies to investigate this further.
ABSTRACT
Introduction: Patients with PIMS-TS present with features of vasculitis (bright coronary arteries and diffuse coronary ectasia on transthoracic echocardiography) and prothrombotic features (e.g. elevated D Dimers) indicating involvement of the endothelial layer in the inflammatory process. Impairment in endothelial function may contribute to the acute but also to possible long-term consequences in patients with PIMSTS. The aim of this pilot study is to assess non-invasively the endothelial (dys)function using reactive hyperemic peripheral arterial tonometry (RH-PAT) 6 months after the acute inflammatory phase. Methods: Ten patients with previous diagnosis of PIMS-TS were compared to age-matched controls. The endothelial function was assessed using the EndoPAT device which provides the reactive hyperemic index (RHI) of endothelial function in a 15-min test. Cardiac function indices by means of LV fractional shortening (FS) was also assessed. Results: There were no significant differences regarding age (11.2 ± 3.0 vs 13.6 ± 2.4, p = 0.063), height, weight and body surface area, (BSA: 1.49 ± 0.36 vs 1.52 ± 0.25, p = 0.856) in patients with previous diagnosis of PIMS-TS and controls respectively. The two groups also had similar LV systolic function assessed by FS (36.3 ± 9.1% vs 36.7 ± 7.1%, p = 0.922). The RHI in the PIMS TS group was similar to the control group (1.65 ± 0.43 vs 1.81 ± 0.60, p = 0.533 respectively). Conclusions. Patients with PIMS-TS who may present with features of vasculitis during the acute phase, do not show evidence of endothelial dysfunction during the long term follow-up, suggesting resolution. Further studies are required to accurately determine the endothelial (dys)function during the acute phase of the inflammatory syndrome and course.