Article in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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.
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
14 authors.
So Mi Jemma ChoProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0003-2460-3335
Yunfeng RuanProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0002-3213-8309
Hyeok-Hee LeeRichard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Boston, MA (H.-H.L., E.A.S.).ORCID 0000-0002-2895-6835
Satoshi KoyamaProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0002-9286-0360
Stephen P JuraschekDepartment of Medicine, Harvard Medical School, Boston, MA (S.P.J., E.A.S., M.C.H., A.C.F., A.P.P., P.N.).ORCID 0000-0003-4168-2696
Norrina B AllenDepartment of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (N.B.A.).ORCID 0000-0002-6993-4384
Eugene YangDivision of Cardiology, University of Washington School of Medicine, Seattle (E.Y.).ORCID 0000-0003-3945-7529
John W McEvoyCardiology Department, Galway University Hospital and University of Galway School of Medicine, Ireland (J.W.M.E.).ORCID 0000-0001-6530-5479
Eric A SecemskyRichard A. and Susan F. Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Boston, MA (H.-H.L., E.A.S.).ORCID 0000-0003-3861-3163
Michael C HonigbergProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0001-8630-5021
Akl C FahedProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).
Aniruddh P PatelProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0001-7871-9638
Whitney E HornsbyProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0002-0672-0338
Pradeep NatarajanProgram in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of MIT and Harvard, Cambridge, MA (S.M.J.C., Y.R., S.K., M.C.H., A.C.F., A.P.P., W.E.H., P.N.).ORCID 0000-0001-8402-7435
Funding
Polygenic Risk Score Methods Development Consortium Coordinating CenterU01HG011697 · NHGRI · UNIVERSITY OF WASHINGTON · PI Kenneth M. Rice · 2021 to 2026
$8.8M
Enabling improved applicability and transferability of polygenic scores across populationsU01HG011719 · NHGRI · MASSACHUSETTS GENERAL HOSPITAL · PI Alicia Martin · 2021 to 2026
$5.5M
Effects of IL-1 beta inhibition on vascular inflammation in TET2 clonal hematopoiesisR01HL173028 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Michael Honigberg, Mabel Toribio · 2025 to 2026
$1.7M
Advancing the clinical actionability of polygenic scores for coronary artery diseaseK08HL168238 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI Aniruddh Patel · 2024 to 2026
$511k
Clonal hematopoiesis as a mediator of cardiovascular disease in women with premature menopauseK08HL166687 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI HONIGBERG, MICHAEL · 2023 to 2025
$507k
Integration of novel contextual and genomic blood pressure measures to enhance cardiovascular disease prediction and management in young adultsK99HL177340 · NHLBI · BROAD INSTITUTE, INC. · PI So Mi Cho · 2025 to 2026
$331k
Whole genome sequence interpretation for lipids to discover new genes and mechanisms for coronary artery diseaseK99HL169733 · NHLBI · BROAD INSTITUTE, INC. · PI KOYAMA, SATOSHI · 2023 to 2024
backgroundSuboptimal blood pressure (BP) control remains a major cardiovascular disease risk factor. Whether genetically predicted BP independently predicts long-term BP control is unknown. We examined the associations of BP polygenic scores (PGSs) with long-term BP control and treatment-resistant hypertension.
methodsWe identified 22 456 Mass General Brigham Biobank participants with hypertension. Longitudinal BP control was defined as the percentage of time above-target systolic BP (SBP) ≥130 mm Hg or diastolic BP (DBP) ≥80 mm Hg over 5 years. Using multivariable regression, we assessed the associations of BP PGS with duration above-target BP and lifetime treatment-resistant hypertension incidence. Incremental prognostic utility of BP PGSs was assessed based on the discrimination C-index, Brier score, and net reclassification index. Validation was performed in the population-based UK Biobank cohort using the SBP/DBP ≥140/90 mm Hg threshold.
resultsAmong 10 853 (48.3%) were female, the mean SBP/DBP (SD) at index date was 132 (18)/75 (11) mm Hg, and 4126 (18.4%) developed treatment-resistant hypertension over lifetime. In reference to the low (<20th percentile) PGS group, the high (≥80th percentile) BP PGS was associated with 8.01 (95% CI, 6.68%-9.34%) longer duration with above-target SBP and 6.19 (95% CI, 5.05%-7.33%) with high DBP. Each high SBP and DBP PGS conferred 2.36 (95% CI, 2.07-2.68) and 1.75 (95% CI, 1.55-1.99)-fold higher odds of treatment-resistant hypertension. Adding BP PGSs to traditional risk factors improved treatment-resistant hypertension prediction from C-index (95% CI), 0.74 (0.73-0.75) to 0.78 (0.77-0.79). BP PGSs consistently predicted longitudinal BP management to a comparable extent in the UK Biobank.
conclusionsHarnessing BP PGSs may inform anticipated trends in BP control to warrant vigilant monitoring and augment prioritization of intensive therapy.
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.
Blood Pressure Polygenic Score Predicts Long-Term Blood Pressure Control and Treatment-Resistant Hypertension. · full record | Socratic