COVID‐19 Increases Markers of Endothelial Damage in Normotensive Pregnant Women

COVID‐19 (CV19) is a disease caused by SARS‐CoV‐2 and has caused a pandemic since discovered in 2019, resulting in over 5 million deaths worldwide. The impact of CV19 on pregnancy are still under investigation and are potentially long‐lasting. However studies have reported that pregnant women affected by CV19 have an increased risk of preterm delivery, pregnancy complications, organ failure, respiratory distress, increased inflammation, increased hospitalization and poor fetal outcomes compared to women who do not contract CV19 during pregnancy. Outside of the pregnant literature, data reports that comorbidities associated with CV19 are associated with inflammation and hypertension (i.e. endothelial damage, kidney damage). In the current study we investigated the relationship between endothelial damage and CV19, hypothesizing that women who contract CV19 during pregnancy will have an increase in endothelial damage and poor birth outcomes. Women were enrolled into an IRB approved study and whole blood was collected at the time of hospital admission for delivery. Pregnant women (n=7/group) were grouped into one of three categories: Normotensive with no history of CV19, early (eCV19) a positive CV19 test > 10 weeks prior to delivery or term (tCV19) a positive CV19 test < 10 weeks prior to delivery. After centrifugation, plasma and serum was frozen at ‐20ºC for future use. Endothelial cells (HUVECs) were exposed to 10% serum for 24 hours, followed by media collection after an additional 24hr serum‐free media exposure. Circulating ET‐1 was extracted from plasma samples and ET‐1, sVCAM and ICAM were assayed via ELISA from both circulating and media samples. Data are expressed as mean±SEM. Comparisons between groups were analyzed via ANOVA followed by post‐hoc analysis. P < 0.05 was considered statistically significant. Endothelin is increased plasma of eCV19 (7.08±0.31,p<0.0001) and tCV19 (6.82±0.25,p<0.0001) normotensive women when compared to normotensive women (0.94±0.22) without the CV19 virus. SVCAM is also increased in plasma of eCV19 (1338±69.37, p<0.0001) and tCV19 (1355±36.18, p<0.0001) when compared to normotensive women without CV19 (75.51±4.67). There is no significance across groups in ICAM measurement in plasma from these women p=0.9024. There is also an increase in endothelin 1 measured in HUVEC media in eCV19 normotensive women (10.10±4.04, p=0.0318) when compared to normotensive women without CV19 (2.05±0.64) and an increase in SVCAM in eCV19 (72.65±5.69, p=0.0008) and tCV19 (50.78±10.68, p=0.002) normotensive women when compared to non‐CV19 normotensive women (4.94±0.86). There was no significance in birth outcomes as Gestational Age at delivery (37.79‐38.92 weeks, p=0.72), baby weight (2880‐3534 grams, p=0.33), systolic blood pressure (118.7‐123.1 mmHg, p=0.43) across groups. Results above shows that despite all women being normotensive, CV19 causes an increase in endothelial dysfunction regardless of when a patient contracted the virus. These results suggests that CV19 causes vasculature damage as endothelial damage markers are increased in both normotensive women who contracted the virus early and late as opposed to normotensive women without the virus. Despite all women being normotensive; CV19 is shown to be causing a direct effect on vasculature causing increases in endothelial damage markers.