Aims The prevalence of obesity is increasing among children in the developed world. The association of obesity and abnormal cardiac function is still debated. The reported changes may reflect the role of comorbidities that contribute to ventricular dysfunction. Obese children, without arterial hypertension, may be a unique clinical opportunity to evaluate the effect of obesity, per se, on myocardial function, excluding the influence of possible comorbidities. We sought to define the preclinical effects of obesity on the cardiovascular system, of healthy children with excess weight who have no other clinically appreciable cause of heart disease, using the more sensitive ultrasonic-derived strain and strain rate (SR) imaging.

Previous reports have demonstrated that myocardial velocities are not sufficiently sensitive in foetal heart studies. Strain (S) imaging is a new non-invasive ultrasonic technique able to quantify regional myocardial deformation properties. Strain imaging has a superior sensitivity than myocardial velocity for non-invasive assessment of ventricular function. However, Doppler-derived strain imaging has been used to quantify myocardial deformation properties in the foetal heart with rather limited results, because of angle dependency, sensitivity to extracardial movement, the need for good-quality images, long and time-consuming post-processing and the low reproducibility of Doppler-derived strain. Recently, a novel method for motion estimation based on two-dimensional (2D) tissue tracking strain (2D-S) echocardiography using time-domain processing has been developed, providing rapid assessment of regional myocardial strain that is independent of both cardiac translation and angle dependency, with a very good reproducibility. However, no information on 2D-S in human foetuses has so far been provided. We studied 100 consecutive normal foetuses (gestation range: 20–32 weeks; no evidence of structural cardiovascular disease by 2D echo and Doppler study) using 2D-S imaging. Left ventricle (LV) and right ventricle (RV) peak myocardial negative strain values were obtained. Strain data were obtained from all the studied subjects, the duration of post processing was 3 ± 2 min for each patient dataset. Peak longitudinal deformation parameters were homogeneous in all the three studied walls (strain: septum = −25 ± 5%; lateral wall = −25 ± 4%; RV free wall = −24 ± 4%; P = NS). There were significant correlations between gestational age and peak longitudinal strain ( P < 0.001; R : −0.73). Inter and intra-observer variability for strain was good, <3 and <6%, respectively. This study demonstrated that 2D-S is a feasible and reproducible approach to assess regional ventricular function in the foetal heart, ready for the clinical application.

Multisystem Inflammatory Syndrome in Children (MIS-C) is a known severe condition affecting children previously exposed to SARS-CoV-2. The aim of our study was to describe the early cardiac abnormalities in patients with MIS-C, evaluated by speckle tracking echocardiography (STE) and cardiac MRI (CMR). Clinical, laboratory and microbiological data were measured for all patients. All children underwent standard transthoracic echocardiography, STE with analysis of left ventricle global longitudinal strain (GLS). Seventeen (75%) of the children were evaluated with CMR. Twenty-three patients (13M, 10F) were recruited, mean age was 8.1 ± 4 years. Cardiovascular symptoms were present in 10 (43.5%). Nine children (39.1%) shared Kawasaki Disease-like symptoms. Four patients (17.4%) needed ICU admission. In-hospital survival was 100%. TnI was elevated in 15 (65.2%) and BNP in 20 (86.9%) patients. The median time to STE evaluation was 8 days and to CMR was 18 days after fever onset. Mean LVEF was 59 ± 10%. Coronary dilation was observed in six (26.1%) patients. STE showed a reduced mean LVGLS (−17 ± 4.3%). LGE with a non-ischemic pattern was evident in six out of seventeen patients (35.2%). The elevation of myocardial necrosis markers, the reduction of LVGLS and the presence of LGE on CMR in about a quarter of MIS-C patients supports the hypothesis of a post-viral immune-mediated myocarditis-like pathogenesis.