Evidence map›Paper›PMID 41920533›Full record

ArticleJAMA cardiology2026

Blood Pressure Genetic Risk and Incident Hypertension at 2 to 7 Years Post Partum.

Jan Hemeryck, Nore De Moor, Daniel Ezzat, Raiyan R Khan, Nathan Vandergrift, Lisa D Levine, Caroline Rouse, Lauren H Theilen, C Noel Bairey Merz, Lynn M Yee and 8 more

Abstract readMulticenter Study
In one paragraph

Article in JAMA cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Jan HemeryckCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.
Nore De MoorCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.
Daniel EzzatCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.
Raiyan R KhanDepartment of Computer Science, Columbia University, New York, New York.
Nathan VandergriftRTI International, Research Triangle Park, North Carolina.
Lisa D LevineDepartment of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.
Caroline RouseDepartment of Obstetrics and Gynecology, Indiana University, Indianapolis.
Lauren H TheilenDepartment of Obstetrics and Gynecology, University of Utah, Salt Lake City.
C Noel Bairey MerzBarbra Streisand Women's Heart Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Lynn M YeeDepartment of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Judith ChungDepartment of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of California, Irvine, Irvine, California.
Natalie A BelloDepartment of Cardiology, Cedars Sinai Medical Center, Smidt Heart Institute, Los Angeles, California.
George SaadeDepartment of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk.
Philip GreenlandDepartment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Janet M CatovDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania.
Sadiya S KhanDepartment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
William A GrobmanDepartment of Obstetrics and Gynecology, The Warren Alpert Medical School of Brown University, Providence, Rhode Island.
Michael C HonigbergCardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, Massachusetts.

Funding

Cardiac Effects of Mineralocorticoid Receptor Antagonism after Preeclampsia (CARDAMOM)R01HL181150 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Michael Honigberg · 2025 to 2026
$1.3M
American Heart Association-American Stroke Association 24RGRSG1275749American Heart Association-American Stroke Association 25SFRNCCKMS1443062American Heart Association-American Stroke Association 25SFRNPCKMS1463898NHLBI NIH HHS R01 HL181150
6 · The paper itself

Abstract

Importance: Hypertensive disorders of pregnancy (HDP; ie, preeclampsia/eclampsia and gestational hypertension) are associated with earlier development of chronic hypertension. Whether genetic risk for high systolic blood pressure (SBP) can stratify risk of new-onset hypertension after pregnancy is unclear. Objective: To test the association of genetic risk for high SBP with new-onset hypertension at 2 to 7 years after delivery, independent of clinical characteristics and HDP history. Design, Setting, and Participants: This was a cohort study of women enrolled during pregnancy between 2010 and 2013 and followed up at 2 to 7 years post partum. Included in the study were genotyped participants without pregestational chronic hypertension in the Nulliparous Pregnancy Outcomes Study: Monitoring Mothers-to-Be (nuMoM2b) Heart Health Study. The setting included 8 US clinical sites. Study data were analyzed from October 2024 to January 2026. Exposures: SBP genetic risk was calculated using a genome-wide SBP polygenic score and categorized as low (bottom quintile), intermediate (quintiles 2-4) or high (top quintile). Main Outcomes and Measures: The primary outcome was stage 1+ hypertension (≥130/80 mm Hg or use of antihypertensive medication) at 2 to 7 years post partum. Logistic regression tested the association of SBP genetic risk with development of hypertension, adjusted for sociodemographic factors, prepregnancy diabetes, first-trimester BP, HDP history, and postpartum body mass index (BMI). Key secondary analyses were stratified by HDP history and compared population attributable risk for high SBP genetic risk, HDP history, and postpartum BMI. Results: Among 2852 participants (mean [SD] age, 30.8 [5.5] years; 353 [12.4%] with prior HDP), 509 (17.8%) developed hypertension by 2 to 7 years (mean [SD], 3.2 [0.9] years) after delivery. SBP genetic risk was independently associated with incident hypertension (high vs low SBP genetic risk: adjusted odds ratio [aOR], 1.50; 95% CI, 1.09-2.07; P = .01). In stratified analyses, SBP genetic risk was associated with incident hypertension in those without prior HDP (aOR, 1.25; 95% CI, 1.12-1.40 per SD; P < .001) but not in those with prior HDP (aOR, 1.01; 95% CI, 0.79-1.28 per SD; P = .92; P for interaction = .10). High SBP genetic risk, HDP history, and BMI greater than or equal to 25 (calculated as weight in kilograms divided by height in meters squared) accounted for 4.7%, 10.8%, and 41.5%, respectively, of population attributable risk for hypertension. Conclusions and Relevance: Results of this cohort study reveal that higher SBP genetic risk was independently associated with higher risk of developing new-onset hypertension 2 to 7 years after delivery. However, HDP history and elevated BMI were more important contributors to hypertension risk.

Indexed as

Blood PressureHypertensionHypertension, Pregnancy-InducedAdultCohort StudiesFemaleFollow-Up StudiesGenetic Predisposition to DiseaseGenetic Risk ScoreHumansIncidencePostpartum PeriodPregnancyRisk FactorsUnited States

Identifiers

PMID41920533
PMCPMC13044786

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.