Although COVID-19 is known to have cardiac effects in children, seen primarily in severe disease, more information is needed about the cardiac effects following COVID-19 in non-hospitalised children and adolescents during recovery. This study aims to compare echocardiographic markers of cardiac size and function of children following acute COVID-19 with those of healthy controls.

This single-centre retrospective case–control study compared 71 cases seen in cardiology clinic following acute COVID-19 with 33 healthy controls. Apical left ventricle, apical right ventricle, and parasternal short axis at the level of the papillary muscles were analysed to measure ventricular size and systolic function. Strain was analysed on vendor-independent software. Statistical analysis was performed using t-test, chi-square, Wilcoxon rank sum, and regression modelling as appropriate (p < 0.05 significant).

Compared to controls, COVID-19 cases had slightly higher left ventricular volumes and lower left ventricular ejection fraction and right ventricular fractional area change that remained within normal range. There were no differences in right or left ventricular longitudinal strain between the two groups. Neither initial severity nor persistence of symptoms after diagnosis predicted these differences.

Echocardiographic findings in children and adolescents 6 weeks to 3 months following acute COVID-19 not requiring hospitalisation were overall reassuring. Compared to healthy controls, the COVID-19 group demonstrated mildly larger left ventricular size and lower conventional measures of biventricular systolic function that remained within the normal range, with no differences in biventricular longitudinal strain. Future studies focusing on longitudinal echocardiographic assessment of patients following acute COVID-19 are needed to better understand these subtle differences in ventricular size and function.

Although maternal stressor exposure has been associated with shorter telomere length (TL) in offspring, this literature is based largely on White samples. Furthermore, timing of maternal stressors has rarely been examined. Here, we examined how maternal stressors occurring during adolescence, pregnancy, and across the lifespan related to child TL in Black and White mothers.

Mothers (112 Black; 110 White; Mage = 39) and their youngest offspring (n = 222; Mage = 8) were part of a larger prospective cohort study, wherein mothers reported their stressors during adolescence (assessed twice during adolescence for the past year), pregnancy (assessed in midlife for most recent pregnancy), and across their lifespan (assessed in midlife). Mother and child provided saliva for TL measurement. Multiple linear regression models examined the interaction of maternal stressor exposure and race in relation to child TL, controlling for maternal TL and child gender and age. Race-stratified analyses were also conducted.

Neither maternal adolescence nor lifespan stressors interacted with race in relation to child TL. In contrast, greater maternal pregnancy stressors were associated with shorter child TL, but this effect was present for children of White but not Black mothers. Moreover, this effect was significant for financial but not social pregnancy stressors. Race-stratified models revealed that greater financial pregnancy stressors predicted shorter telomeres in offspring of White, but not Black mothers.

Race and maternal stressors interact and are related to biological aging across generations, but these effects are specific to certain races, stressors, and exposure time periods.

In this study, we assessed the acute changes in biventricular longitudinal strain after atrial septal defect transcatheter closure and its relation to the device size.

Hundred atrial septal defect patients and 40 age-matched controls were included. Echocardiography and strain study were performed at baseline and 24 hours and 1 month after the intervention. The study group was divided into two subgroups; group 1: smaller devices were used (mean device size = 1.61 ± 0.05 cm, n = 74) and group 2: larger devices were used (mean device size = 2.95 ± 0.07 cm, n = 26).

At baseline, there was a significant difference between the study group and controls as regards right ventricular global longitudinal strain with significant hyperkinetic apex (p = 0.033, p = 0.020, respectively). There was a significant immediate reduction in right ventricular global longitudinal strain (from −24.43 ± 0.49% to −21.62 ± 0.47%, p < 0.001), which showed insignificant improvement after 1-month follow-up. While only left ventricular global longitudinal strain increased after 1 month. Within 24 hours of device closure, all the basal- and mid-lateral segments strains and apical right ventricular strains showed a significant reduction. There was a significant negative correlation between the indexed large device size and an immediate change in the right ventricular global longitudinal strain (r = −0.425, p = 0.034).

Significant right ventricular global longitudinal strain reduction starts as early as 24 hours after transcatheter closure, irrespective of the device size used. The rapid impact of closure was mainly on the biventricular basal and lateral segments and right ventricular apical ones, especially with the large sized atrial septal defect.

Anthracycline-associated cardiotoxicity in childhood cancer survivors may relate to global or segmental left ventricular abnormalities from associated thromboembolic events and myocardial microinfarcts. We characterized left ventricular segmental changes by two-dimensional speckle-tracking echocardiography in anthracycline-treated asymptomatic childhood cancer survivors.

Childhood cancer survivors’ echocardiograms with normal left ventricular fractional shortening >1 year after anthracycline chemotherapy were studied. Cancer-free control children had normal echocardiograms. Apical two-, three-, and four-chamber peak systolic left ventricular longitudinal and global longitudinal strain, and peak systolic left ventricular radial and circumferential strain at papillary muscle levels were analyzed. The mean (standard deviation) age was 12.7 (3.8) years in 41 childhood cancer survivors. The median (interquartile range) follow-up after anthracycline chemotherapy was 4.73 (2.15–8) years. The median (range) cumulative anthracycline dose was 160.2 (60–396.9) mg/m2. In childhood cancer survivors, the mean (standard deviation) left ventricular longitudinal strain was lower in two- (−18.6 [3.2] versus −21.3 [2.5], p < 0.001), three- (−16.3 [6.0] versus −21.7 [3.0], p < 0.001), and four- (−17.6 [2.7] versus −20.8 [2.0], p < 0.001) chamber views compared to controls. The left ventricular global longitudinal strain (−17.6 [2.7] versus −21.3 [2.0]) and circumferential strain (−20.8 [4.3] versus −23.5 [2.6], p < 0.001) were lower in childhood cancer survivors. Among childhood cancer survivors, 12 out of 16 left ventricular segments had significantly lower longitudinal strain than controls.

Asymptomatic anthracycline-treated childhood cancer survivors with normal left ventricular fractional shortening had lower global longitudinal and circumferential strain. The left ventricular longitudinal strain was lower in majority of the segments, suggesting that anthracycline cardiotoxicity is more global than regional.

Anthracycline chemotherapeutic agents carry the well-recognised risk of cardiac toxicity. The aim of this study was to determine the long-term effect of anthracycline chemotherapy on the biventricular function in childhood cancer survivors using tissue Doppler imaging and two-dimensional speckle tracking echocardiography.

The study included 45 survivors of childhood cancers and 50 healthy age-matched control patients. Cardiac function was prospectively studied with conventional echocardiography, tissue Doppler imaging, and speckle tracking echocardiography after completion of treatment. The same analysis was performed on matched controls.

There was no difference in age, gender, height, and weight between the study and control groups. The mean anthracycline dose was 240 ± 106 mg/m2 and the mean remission duration was 8.2 ± 5 years (1–20 years) in the study group. Conventional echocardiography showed similar ejection fraction, shortening fraction, and left ventricle end-diastolic diameter in both groups. Mitral lateral and septal tissue Doppler imaging showed normal but according to control group relatively sub-normal systolic and diastolic function in patient group. The global longitudinal and circumferential strain and strain rates were significantly lower in the patient group compared to control group. Correlation analysis revealed a negative and significant correlation between total anthracycline dose and global longitudinal and circumferential strain and strain rates.

Sub-clinical systolic and diastolic dysfunction may not be detected by conventional echocardiographic methods which are frequently used in daily practice. Sub-clinical systolic and diastolic dysfunction may be detected more sensitively by echocardiographic method such as speckle tracking echocardiography in childhood cancer survivors.

Myocardial strain measurements are increasingly used to detect complications following heart transplantation. However, the temporal association of these changes with allograft rejection is not well defined. The aim of this study was to describe the evolution of strain measurements prior to the diagnosis of rejection in paediatric heart transplant recipients.

All paediatric heart transplant recipients (2004–2015) with at least one episode of acute rejection were identified. Longitudinal and circumferential strain measurements were assessed at the time of rejection and retrospectively on all echocardiograms until the most recent negative biopsy. Smoothing technique (LOESS) was used to visualise the changes of each variable over time and estimate the time preceding rejection at which alterations are first detectable.

A total of 58 rejection episodes were included from 37 unique patients. In the presence of rejection, there were decrements from baseline in global longitudinal strain (−18.2 versus −14.1), global circumferential strain (−24.1 versus −19.6), longitudinal strain rate (−1 versus −0.8), circumferential strain rate (−1.3 versus −1.1), peak longitudinal early diastolic strain rate (1.3 versus 1), and peak circumferential early diastolic strain rate (1.5 versus 1.3) (p<0.01 for all). The earliest detectable changes occurred 45 days prior to rejection with simultaneous alterations in myocardial strain and ejection fraction.

Changes in graft function can be detected non-invasively prior to the diagnosis of rejection. However, changes in strain occur concurrently with a decline in ejection fraction. Strain measurements aid in the non-invasive detection of rejection, but may not facilitate earlier diagnosis compared to more traditional measures of ventricular function.