# Stress, inflammation and coronary endothelial injury in preeclampsia

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 2022 · $432,128

## Abstract

Hypertensive disorders of pregnancy, such as preeclampsia (PEC) cause significant maternal
morbidity and mortality, and have emerged as an important early life, and potentially modifiable, risk factor
of heart disease in younger women. PEC is diagnosed as new onset hypertension after 20 weeks gestation
with evidence of end organ damage, thought to occur because of placental ischemia and an imbalance of
angiogenesis. Importantly, PEC is associated with significantly increased CVD risk that persists into later
life, far beyond the pregnancy period. Understanding how PEC affects cardiovascular (CV) health both from
a biological and socio-behavioral perspective (ie. socially constructed gender roles and stress) is critical to
inform risk communication, stratification and to identify and target new treatments to reduce CV disease
(CVD), especially among young, high risk women.
 Although patients with PEC often have traditional pre-pregnancy CV risk factors such as type 2
diabetes and obesity, these risk factors do not fully explain the elevated CV risk conferred after a pregnancy
complicated by PEC. Two factors thought to contribute to the pathogenesis of PEC and injure endothelial
cells are an imbalance of angiogenesis and alterations in renin-angiotensin-system (RAS), driven by
placental ischemia and resulting in oxidative stress with systemic inflammation. From a socio-behavioral
perspective, there is evidence that social determinants of health and psychological stress influence PEC
severity and future CVD outcomes. Women’s lived experience, including how they experience socially
constructed gender roles, stress and neighborhood factors affect health outcomes significantly in PEC. We
recently developed noninvasive, reproducible MRI-based methods to measure coronary endothelial function
(CEF), offering a means to probe mechanisms contributing to coronary artery disease (CAD) pathophysiology
in postpartum women with recent PEC. Abnormal CEF plays a critical role in the development, progression
and clinical manifestations of CAD, independently predicts CV events, and is a target for medical
interventions. We propose in this application to determine in postpartum women with PEC: 1) whether CEF,
and markers of inflammation/imbalanced angiogenesis are inversely related and 2) whether measures of
stress (both psychosocial stress and physiologic measures) are associated with endothelial abnormalities
and postpartum hypertension. We will determine, in women with a history of PEC, whether reduced CEF can
be explained, at least in part, by increased inflammation/abnormal angiogenesis/stress. Together these
studies will offer new pathophysiologic insights into increased CVD risk in women with PEC, and which
factors contribute most to vascular dysfunction. This study, if funded, will address significant knowledge
gaps regarding sex and gender specific variables that affect postpartum vascular health in young
women and provide data to design future interventiona...

## Key facts

- **NIH application ID:** 10531778
- **Project number:** 1R01HL159715-01A1
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Allison G Hays
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $432,128
- **Award type:** 1
- **Project period:** 2022-09-02 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10531778

## Citation

> US National Institutes of Health, RePORTER application 10531778, Stress, inflammation and coronary endothelial injury in preeclampsia (1R01HL159715-01A1). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10531778. Licensed CC0.

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