ArticleArteriosclerosis, thrombosis, and vascular biology2026
Endothelial Susceptibility-Related Genetic Variants and Hypertensive Disorders of Pregnancy-Brief Report.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe hypertensive disorders of pregnancy (HDPs), that is, preeclampsia and gestational hypertension, are characterized by endothelial dysfunction in pregnancy and are epidemiologically and genetically associated with risk for coronary artery disease (CAD). A recent study suggested that endothelial cell (EC)-acting CAD risk variants may identify individuals who benefit from more intensive lipid-lowering treatment. The present study evaluated whether the same EC CAD genetic risk score is also associated with HDPs using comprehensive statistical genetic approaches.
methodsWe examined 35 previously identified EC-acting and 205 non-EC-acting risk variants associated with CAD. First, using the nuMoM2b (Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be), a prospective, multicenter US pregnancy cohort, we calculated polygenic risk scores (PRS) comprised of either EC-acting or non-EC-acting CAD risk variants in genotyped, unrelated participants across multiple ancestry groups. Scores were adjusted for population genetic structure using 10 principal components, then tested for associations with HDPs using logistic regression models adjusted for age. Second, we tested the genetic association of EC-acting and non-EC-acting CAD variants with preeclampsia and gestational hypertension using 2-sample Mendelian randomization.
resultsAmong 6782 unrelated nuMoM2b participants (mean [SD] age, 27.0 [5.5] years, 1040 [15.3%] with HDPs in the index pregnancy), participants with higher EC-acting PRS had a higher incidence of HDPs. Each SD of higher EC-acting PRS was associated with 1.09-fold increased odds of HDP (95% CI, 1.02-1.17;
conclusionsPRS and 2-sample Mendelian randomization approaches suggest enrichment for EC-acting CAD genetic risk variants in women with HDPs. These findings support a shared genetic architecture between HDPs and CAD through endothelial dysfunction.
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