Abstract Body (Do not enter title and authors here): Background: Hypertensive disorders of pregnancy (HDP) is a leading cause of pregnancy-related mortality in the United States and an important risk factor for postpartum cardiovascular disease (CVD). Previous animal data suggested that FSTL3 expression may be pathogenic in the development of cardiovascular dysfunction. The incidence of CVD during pregnancy has been increasing over time, which highlights the need to identify biomarkers that affect the development of the disease. We therefore hypothesized that peripartum FSTL3 levels would be associated with postpartum cardiovascular dysfunction and maternal morbidity.


Methods: Pregnant patients age ≥ 18 years and singleton < 41 weeks with preeclampsia or superimposed preeclampsia who delivered at the University of Chicago between May 2017 and November 2020 were included in this observational cohort study. The primary outcome was cardiovascular dysfunction defined as postpartum hypertension, cardiomyopathy (confirmed with echocardiography and cardiology consult), and pulmonary edema (confirmed with chest radiography). The secondary outcome was severe maternal morbidity. Categorical data were assessed with chi-square or Fisher’s Exact test. The association between FSTL3 levels and postpartum CV dysfunction was assessed using multivariable logistic regression.


Results: Our study included 408 patients, of which 212 were diagnosed with HDP. The median age was 28 years old (IQR 23, 33), the median BMI was 33.4 (IQR 28.6, 39.3), and the majority were African American (67.1%). Elevated FSTL3 levels were associated with postpartum CV dysfunction (OR 1.02 [95% CI: 1.01, 1.04]; p < 0.001). After multivariable adjustment for delivery gestational age, maternal age, BMI, nulliparous, HDP, smoking, and diabetes, the association between FSTL3 and CVD persisted (p = 0.02). Table 1 outlines the association between FSTL3 and maternal/neonatal outcomes.


Conclusion: This study demonstrates that the biomarker FSLT3 predicts postpartum cardiovascular dysfunction and is associated with maternal morbidity. Our findings suggest that FSLT3 may facilitate the development of CVD and that therapeutic strategies targeting FSLT3 may affect the course of postpartum cardiovascular dysfunction.