Evidence map›Paper›PMID 34965472›Full record

ArticleJournal of cardiac failure2022

Apolipoprotein E Polymorphism, Cardiac Remodeling, and Heart Failure in the ARIC Study.

Senthil Selvaraj, Brian Claggett, Michelle C Johansen, Jonathan W Cunningham, Rebecca F Gottesman, Bing Yu, Eric Boerwinkle, Thomas H Mosley, Amil M Shah, Scott D Solomon

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiac failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 46% of its field
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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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

10 authors at 6 institutions in 1 country.

Senthil SelvarajDivision of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
Brian ClaggettDivision of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Michelle C JohansenDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jonathan W CunninghamDivision of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Rebecca F GottesmanDepartment of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland.
Bing YuHuman Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, The University of Texas Health Science Center at Houston, Houston, Texas.
Eric BoerwinkleHuman Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, The University of Texas Health Science Center at Houston, Houston, Texas; Baylor College of Medicine, Human Genome Sequencing Center, Houston, Texas.
Thomas H MosleyDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi.
Amil M ShahDivision of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Scott D SolomonDivision of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts. Electronic address: ssolomon@rics.bwh.harvard.edu.
Brigham and Women's Hospital · USJohns Hopkins University · USBaylor College of Medicine · USHospital of the University of Pennsylvania · USThe University of Texas Health Science Center at Houston · USUniversity of Mississippi Medical Center · US

Funding

Mapping the Progression to HFpEF in the Elderly through Longitudinal Changes in Cardiac FunctionR01HL135008 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI Amil M Shah · 2017 to 2026
$11.5M
The ARIC and Neurocognitive Longitudinal StudyR01HL070825 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI MOSLEY, THOMAS H · 2002 to 2004
$5.1M
Early Detection of Transthyretin Cardiac Amyloidosis: Defining a Novel Target for HFpEF Treatment and Prevention in Late LifeR01HL150342 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI DORBALA, SHARMILA, SHAH, AMIL M · 2020 to 2023
$4.1M
Quantifying cardiac structure and function to define the progression to hear failure in African AmericansR01HL143224 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAH, AMIL M · 2018 to 2021
$3.4M
Defining the role of Atrial Cardiopathy and Subclinical Cardiac Disease in Acute Ischemic Stroke: Critical Life Event SupplementK23NS112459 · NINDS · JOHNS HOPKINS UNIVERSITY · PI JOHANSEN, MICHELLE C. · 2020 to 2024
$1.0M
NHLBI NIH HHS HHSN268201700001CNHLBI NIH HHS HHSN268201700001INHLBI NIH HHS HHSN268201700002CNHLBI NIH HHS HHSN268201700002INHLBI NIH HHS HHSN268201700003CNHLBI NIH HHS HHSN268201700003INHLBI NIH HHS HHSN268201700004CNHLBI NIH HHS HHSN268201700004INHLBI NIH HHS HHSN268201700005CNHLBI NIH HHS HHSN268201700005INHLBI NIH HHS R01 HL070825NHLBI NIH HHS R01 HL135008NHLBI NIH HHS R01 HL143224NHLBI NIH HHS R01 HL150342
6 · The paper itself

Abstract

backgroundβ-Amyloid has recently been discovered in the myocardium of patients with Alzheimer's disease (AD). Whether genetic variation in apolipoprotein E (APOE) ɛ4, a common variant associated with Alzheimer's disease, is associated with incident heart failure (HF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and cardiac structure and function is unknown. METHODS AND

resultsWe studied 15,064 White and Black participants in the Atherosclerosis Risk in Communities, relating genotype status at visit 1 (1987-1989) to incident HF hospitalization using Cox regression. At visits 2, 4, and 5, we assessed NT-proBNP levels by genotype. At visits 3 and 5, we related Aβ peptides to incident HF. At visit 5 (2011-2013, n = 6251), we assessed the relationship of genotype with prevalent HF and echocardiographic parameters. The mean participant age was 54.7 ± 5.8 years, 45% were men, and 73% were White. At visit 5, there was no difference in prevalent HF by genotype. The APOE ε4 carriers did not have increased risk for HF hospitalization. The APOE ε4 genotype was not associated with cardiac structure and function or NT-proBNP levels. The Aβ peptides were not associated with incident HF after multivariable adjustment.

conclusionsA genetic predisposition to Alzheimer's disease through APOE ε4 is not associated with an increased prevalence of HF, HF hospitalization, myocardial remodeling, or biochemical evidence of HF.

Indexed as

Alzheimer DiseaseApolipoprotein E4Heart FailureApolipoproteins EBiomarkersFemaleHumansMaleMiddle AgedNatriuretic Peptide, BrainPeptide FragmentsVentricular RemodelingApoE protein, humanApolipoprotein E4Apolipoproteins EBiomarkersNatriuretic Peptide, BrainPeptide FragmentsAlzheimer's diseaseAPOE ɛ4cardiac remodelingheart failure

Identifiers

PMID34965472
PMCPMC11062481
OpenAlexW4200202592

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.