Multisystem inflammatory syndrome in children is an inflammatory syndrome related to severe acute respiratory syndrome coronavirus 2 with a high risk of cardiovascular complications (vasoplegia, cardiac shock). We investigated the cardiac outcomes in multisystem inflammatory syndrome in children, focusing on the identification of predictors for late cardiac function impairment.

Clinical characteristics, conventional echocardiography (left ventricle ejection fraction, fractional shortening), 4-chamber left ventricular global longitudinal strain, and cardiac MRI of multisystem inflammatory syndrome in children patients (n = 48) were collected during admission, 6 weeks, 6 months, >12–≤18 months, and >18–≤24 months post-onset. Paired over-time patterns were assessed and multivariable regression analyses were performed to identify predictors for late global longitudinal strain impairment.

In total, 81.3% of patients had acute cardiac dysfunction (left ventricle ejection fraction <50% and/or fractional shortening <28%). The left ventricle ejection fraction and fractional shortening reached a plateau level ≤6 weeks, while the global longitudinal strain continued to decrease in the first 6 months post-onset (median –17.3%, P < 0.001 [versus acute]). At 6 months, 35.7% of the patients still had an abnormal global longitudinal strain, which persisted in 5/9 patients that underwent echocardiography >12–≤18 months post-onset and in 3/3 patients >18–≤24 months post-onset. In a multivariable analysis, soluble troponin T (>62.0 ng/L [median]) was associated with reduced global longitudinal strain at 6 months. Our cardiac MRI findings indicated acute myocardial involvement (increased T1/T2 value) in 77.8% (7/9), which recovered quickly without signs of fibrosis on convalescent cardiac MRIs.

Late global longitudinal strain impairment is seen in some multisystem inflammatory syndrome in children patients up to one-year post-onset. Careful cardiac follow-up in patients with elevated troponin in the acute phase and patients with persistent abnormal global longitudinal strain is warranted until resolution of the global longitudinal strain since the long-term implications of such abnormalities are still unclear.

There is a paucity of functional data on mid-to-late preterm infants between 30+0 and 34+6 weeks gestation. We aimed to characterise transitional cardiopulmonary and haemodynamic changes during the first 48 hours in asymptomatic mid-to-late preterm infants.

Forty-five healthy preterm newborns (mean ± standard deviation) gestation of 32.7 ± 1.2 weeks) underwent echocardiography on Days 1 and 2. Ventricular mechanics were assessed by speckle tracking-derived deformation, rotational mechanics, tissue Doppler imaging, and right ventricle-focused measures (tricuspid annular plane systolic excursion, fractional area change). Continuous haemodynamics were assessed using the NICOM™ system to obtain left ventricular output, stroke volume, heart rate, and total peripheral resistance by non-invasive cardiac output monitoring.

Right ventricular function increased (all measures p < 0.005) with mostly stable left ventricular performance between Day 1 and Day 2. NICOM-derived left ventricular output [mean 34%, 95% confidence interval 21–47%] and stroke volume [29%, 16–42%] increased with no change in heart rate [5%, −2 to 12%]. There was a rise in mean blood pressure [11%, 1–21%], but a decline in total peripheral resistance [−14%, −25 to −3%].

Left ventricular mechanics remained persevered in mid-to-late premature infants, but right ventricular function increased. Non-invasive cardiac output monitoring is feasible in preterm infants with an increase in left ventricular output driven by an improvement in stroke volume during the transitional period.

Recent studies have revealed that atherosclerosis progresses faster than expected in young adults with a history of Kawasaki disease. However, it is unclear as to when these arterial changes become measurable. In this study, we evaluated subclinical arterial stiffness in young children with a history of Kawasaki disease using two-dimensional ultrasound speckle tracking.

A total of 75 children with a history of Kawasaki disease (mean age, 8.2 ± 2.8 years) and 50 healthy controls (mean age 8.3 ± 3.5 years) were included. The two regions of interest for speckle tracking were manually positioned at the anterior and posterior carotid arterial wall using a Philips iE33 (Philips Medical Systems, Bothell, WA, USA). The peak systolic strain, time to peak systolic strain, early systolic strain rate, and late systolic strain rate were continuously monitored between the two regions of interest. Furthermore, the intimal-medial thickness, stiffness β, and pressure-elastic modulus, as conventional measures of arterial stiffness, were concurrently obtained.

The peak systolic strain and late systolic strain rate differed significantly between the patients with Kawasaki disease and controls (6.69% versus 8.60%, p < 0.01, and −0.28/second versus −0.51/second, p < 0.0001, respectively). There was no difference in the time to peak systolic strain, early systolic strain rate, and conventional measures.

The arteries of patients with Kawasaki disease appear to develop mild sclerotic changes shortly after the onset of the disease.