The Effect of Maternal Race, Ethnicity, and Nativity on Macrosomia Among Infants Born in the United States.

OBJECTIVES:  This study aims to elucidate the influence of race, ethnicity, and nativity on macrosomia rates, hypothesizing that higher rates are observed among White non-Latina mothers and United States (US)-born mothers. STUDY DESIGN:  We analyzed data from 1,791,718 US births sourced from the National Center for Health Statistics of the Centers for Disease Control and Prevention. Logistic regression analyses were conducted to examine the associations between macrosomia rates and maternal race, ethnicity, and nativity. RESULTS:  After excluding non-singleton, preterm, post-term births, and those with missing data, six maternal cohorts were identified: White non-Latina US-born (1,147,096) and foreign-born (75,542), Black non-Latina US-born (174,540) and foreign-born (32,200), and Latina US-born (223,968) and foreign-born (137,515). White non-Latina US-born mothers had the highest rates of excessive gestational weight gain (58.9%). Black non-Latina US-born mothers exhibited the highest rates of pre-pregnancy diabetes (0.7%) and obesity (29.5%). Macrosomia rates were highest among White non-Latina US-born mothers (10.7%) compared to other cohorts. After adjusting for socioeconomic and health-related factors, this group maintained the highest odds of macrosomia (OR: 1.876; 95%CI 1.832-1.922, P<0.001). CONCLUSION: Our findings reveal that White non-Latina US-born mothers experience the highest macrosomia rates, which persist after adjusting for known confounders. These results have significant implications for the development of gestational surveillance tools and targeted public health interventions aimed at improving pregnancy outcomes among high-risk cohorts.

Clinical spectrum of COVID-19 complications in young adults: combined analysis of the American Heart Association COVID-19 Cardiovascular Disease Registry and the Outcomes Registry for Cardiac Conditions in Athletes.

BACKGROUND: While young adults 18-24 years old bear a significant proportion of COVID-19 diagnoses, the risk factors for hospitalisation and severe COVID-19 complications in this population are poorly understood. OBJECTIVE: The objective of this study was to identify risk factors for hospitalisation and other COVID-19 complications across the health spectrum of young adults diagnosed with COVID-19 infection. STUDY DESIGN: Retrospective cohort study. PARTICIPANTS: Young adults (aged 18-24) with confirmed COVID-19 infection from the American Heart Association (AHA) COVID-19 Cardiovascular Disease Registry of hospitalised patients and the Outcomes Registry for Cardiac Conditions in Athletes (ORCCA) study of collegiate athletes. The AHA registry included 636 young adults from 152 hospitals. The ORCCA registry consisted of 3653 competitive college athletes from 42 colleges and universities. INTERVENTION: None (exposure to COVID-19). PRIMARY AND SECONDARY OUTCOME MEASURES: Main outcomes included hospitalisation, death, major adverse cardiovascular events (MACE) and other severe clinical events. RESULTS: In comparison to the ORCCA registry, patients in the AHA registry were more likely to be female (59% vs 33%); had higher average body mass index (BMI) (32.4 vs 25.6); and had increased prevalence of diabetes (10% vs 0.4%), hypertension (7% vs 0.6%), chronic kidney disease (2% vs 0%) and asthma (14% vs 8%), all with p<0.01. There were eight (2%) deaths in the AHA hospitalised registry compared with zero in the ORCCA cohort. BMI was a statistically significant predictor of death in the hospitalised cohort (OR 1.05, 95% CI 1.00, 1.10). No significant predictors of MACE or other severe clinical events were identified. CONCLUSIONS: The risk of cardiac events in young adults aged 18-24 diagnosed with COVID-19 infection is low. Patients who were hospitalised (AHA registry) were more likely to have pre-existing medical comorbidities and higher BMI than healthy collegiate athletes (ORCCA registry). Once hospitalised, elevated BMI is associated with increased mortality although other drivers of MACE and other severe clinical events remain unclear.

Cardiac Troponin Testing as a Component of Return to Play Cardiac Screening in Young Competitive Athletes Following SARS-CoV-2 Infection.

Background Initial protocols for return to play cardiac testing in young competitive athletes following SARS-CoV-2 infection recommended cardiac troponin (cTn) to screen for cardiac involvement. This study aimed to define the diagnostic yield of cTn in athletes undergoing cardiovascular testing following SARS-CoV-2 infection. Methods and Results This prospective, observational cohort study from ORCCA (Outcomes Registry for Cardiac Conditions in Athletes) included collegiate athletes who underwent cTn testing as a component of return to play protocols following SARS-CoV-2 infection. The cTn values were stratified as undetectable, detectable but within normal limits, and abnormal (>99% percentile). The presence of probable or definite SARS-CoV-2 myocardial involvement was compared between those with normal versus abnormal cTn levels. A total of 3184/3685 (86%) athletes in the ORCCA database met the inclusion criteria for this study (age 20±1 years, 32% female athletes, 28% Black race). The median time from SARS-CoV-2 diagnosis to cTn testing was 13 days (interquartile range, 11, 18 days). The cTn levels were undetectable in 2942 athletes (92%), detectable but within normal limits in 210 athletes (7%), and abnormal in 32 athletes (1%). Of the 32 athletes with abnormal cTn testing, 19/32 (59%) underwent cardiac magnetic resonance imaging, 30/32 (94%) underwent transthoracic echocardiography, and 1/32 (3%) did not have cardiac imaging. One athlete with abnormal troponin met the criteria for definite or probable SARS-CoV-2 myocardial involvement. In the total cohort, 21/3184 (0.7%) had SARS-CoV-2 myocardial involvement, among whom 20/21 (95%) had normal troponin testing. Conclusions Abnormal cTn during routine return to play cardiac screening among competitive athletes following SARS-CoV-2 infection appears to have limited diagnostic utility.

Transplanted allogeneic cardiac progenitor cells secrete GDF-15 and stimulate an active immune remodeling process in the ischemic myocardium.

BACKGROUND: Despite promising results in clinical studies, the mechanism for the beneficial effects of allogenic cell-based therapies remains unclear. Macrophages are not only critical mediators of inflammation but also critical players in cardiac remodeling. We hypothesized that transplanted allogenic rat cardiac progenitor cells (rCPCs) augment T-regulatory cells which ultimately promote proliferation of M2 like macrophages by an as-yet undefined mechanism. METHODS AND RESULTS: To test this hypothesis, we used crossover rat strains for exploring the mechanism of myocardial repair by allogenic CPCs. Human CPCs (hCPCs) were isolated from adult patients undergoing coronary artery bypass grafting, and rat CPCs (rCPCs) were isolated from male Wistar-Kyoto (WKY) rat hearts. Allogenic rCPCs suppressed the proliferation of T-cells observed in mixed lymphocyte reactions in vitro. Transplanted syngeneic or allogeneic rCPCs significantly increased cardiac function in a rat myocardial infarct (MI) model, whereas xenogeneic CPCs did not. Allogeneic rCPCs stimulated immunomodulatory responses by specifically increasing T-regulatory cells and M2 polarization, while maintaining their cardiac recovery potential and safety profile. Mechanistically, we confirmed the inactivation of NF-kB in Treg cells and increased M2 macrophages in the myocardium after MI by transplanted CPCs derived GDF15 and it's uptake by CD48 receptor on immune cells. CONCLUSION: Collectively, these findings strongly support the active immunomodulatory properties and robust therapeutic potential of allogenic CPCs in post-MI cardiac dysfunction.