Evidence map›Paper›PMID 39520444›Full record

ArticleJACC. Heart failure2025

Cardiovascular Risk Factors and Genetic Risk in Transthyretin V142I Carriers.

Naman S Shetty, Mokshad Gaonkar, Akhil Pampana, Nirav Patel, Alanna C Morrison, Alexander P Reiner, April P Carson, Bing Yu, Bruce M Psaty, Charles Kooperberg and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

27 authors.

Naman S ShettyDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA; Harvard Medical School, Boston, Massachusetts, USA.
Mokshad GaonkarDivision of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Akhil PampanaDivision of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Nirav PatelDivision of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Alanna C MorrisonHuman Genetics Center, University of Texas Health Science Center, Houston, Texas, USA.
Alexander P ReinerDepartment of Epidemiology, University of Washington, Seattle, Washington, USA; Division of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, Washington, USA.
April P CarsonDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Bing YuHuman Genetics Center, University of Texas Health Science Center, Houston, Texas, USA.
Bruce M PsatyDepartment of Epidemiology, University of Washington, Seattle, Washington, USA; Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, USA; Department of Health Systems and Population Health, University of Washington, Seattle, Washington, USA.
Charles KooperbergDivision of Public Health Sciences, Fred Hutchinson Cancer Center, Seattle, Washington, USA.
Diane FatkinCardiology Department, St. Vincent's Hospital, Sydney, New South Wales, Australia; Molecular Cardiology Division, Victor Chang Cardiac Research Institute, Sydney, New South Wales, Australia; St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia.
Eric BoerwinkleHuman Genetics Center, University of Texas Health Science Center, Houston, Texas, USA.
Jerome I RotterInstitute for Translational Genomics and Population Sciences, Department of Pediatrics, Lundquist Institute for Biomedical Innovation at the Harbor-UCLA Medical Center, Torrance, California, USA.
Kent D TaylorInstitute for Translational Genomics and Population Sciences, Department of Pediatrics, Lundquist Institute for Biomedical Innovation at the Harbor-UCLA Medical Center, Torrance, California, USA.
Lifang HouDepartment of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Marguerite R IrvinDepartment of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Michael E HallDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Mathew MaurerCardiac Amyloidosis Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, New York, USA.
Myriam FornageUniversity of Texas Health Science Center, Houston, Texas, USA.
Nicole D ArmstrongDepartment of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Nicole BartCardiology Department, St. Vincent's Hospital, Sydney, New South Wales, Australia; Molecular Cardiology Division, Victor Chang Cardiac Research Institute, Sydney, New South Wales, Australia; St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia.
Parag GoyalWeill Cornell Medicine Division of Cardiology, New York, New York, USA.
Stephen S RichCenter for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA.
Ramachandran S VasanUniversity of Texas School of Public Health San Antonio, San Antonio, Texas, USA.
Peng LiSchool of Nursing, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Garima AroraDivision of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Pankaj AroraDivision of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, USA; Section of Cardiology, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA. Electronic address: parora@uabmc.edu.

Funding

CHARGE Consortium: Omics Discovery for CVD and Aging PhenotypesR01HL105756 · NHLBI · UNIVERSITY OF WASHINGTON · PI Bruce M Psaty, NICHOLAS L SMITH · 2011 to 2026
$9.5M
MECHANISMS OF HYPERTENSION AND CARDIOVASCULAR DISEASEST32HL007457 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Martin E Young · 1985 to 2026
$8.6M
Natriuretic Peptide-Renin-Angiotensin-Aldosterone System Rhythm Axis and Nocturnal Blood PressureR01HL160982 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Pankaj Arora · 2022 to 2026
$3.7M
Atrial Natriuretic Peptide and Regulation of Cardiometabolic Health: A Genotype-Guided Human Physiological StudyR01HL163081 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Pankaj Arora · 2022 to 2026
$3.7M
The Effects of Neprilysin Inhibition on Cardiometabolic Health in Black IndividualsR01HL163852 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Pankaj Arora · 2022 to 2026
$3.6M
NHLBI NIH HHS R01 HL105756NHLBI NIH HHS R01 HL160982NHLBI NIH HHS R01 HL163081NHLBI NIH HHS R01 HL163852NHLBI NIH HHS T32 HL007457
6 · The paper itself

Abstract

backgroundNearly 3% to 4% of Black individuals in the United States carry the transthyretin V142I variant, which increases their risk of heart failure. However, the role of cardiovascular (CV) risk factors (RFs) in influencing the risk of clinical outcomes among V142I variant carriers is unknown.

objectivesThis study aimed to assess the impact of CV RFs on the risk of heart failure in V142I carriers.

methodsThis study included self-identified Black individuals without prevalent heart failure from 6 TOPMed (Trans-Omics for Precision Medicine) cohorts, the REGARDS (Reasons for Geographic And Racial Differences in Stroke) study, and the All of Us Research Program. The cohort was stratified based on the V142I genotype and the number of CV RFs (hypertension, diabetes, obesity, and hypercholesterolemia). Adjusted Cox models were used to assess the association of heart failure with the V142I genotype and CV RF profile, taking noncarriers with a favorable CV RF profile as reference.

resultsThe cross-sectional analysis, including 1,625 V142I carriers among 48,365 Black individuals, found that the prevalence of CV RFs did not vary by V142I carrier status. In the longitudinal analysis, there were 587 (3.2%) V142I carriers among 18,407 Black individuals (median age: 60 years [Q1-Q3: 52-68 years], 63.0% female). Among carriers, the heart failure risk was attenuated with a favorable (0 or 1 RF) CV RF profile (adjusted HR: 2.26; 95% CI: 1.58-3.23) compared with an unfavorable (3 or 4 RFs) CV RF profile (adjusted HR: 4.14; 95% CI: 2.79-6.14).

conclusionsA favorable CV RF profile lowers but does not abrogate V142I variant-associated heart failure risk. This study highlights the importance of having a favorable CV RF profile among V142I carriers for risk reduction of heart failure.

Indexed as

Heart Disease Risk FactorsHeart FailurePrealbuminAgedBlack or African AmericanCardiovascular DiseasesCross-Sectional StudiesDiabetes MellitusFemaleGenotypeHeterozygoteHumansHypercholesterolemiaHypertensionMaleMiddle AgedPrealbuminTTR protein, humanamyloidosisBlack individualscardiovascular risk factorsheart failuremortalityV142I

Identifiers

PMID39520444
PMCPMC13229499

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