Evidence map›Paper›PMID 34521746›Full record

ArticleOpen heart2021

Using genetics to detangle the relationships between red cell distribution width and cardiovascular diseases: a unique role for body mass index.

Timothy E Thayer, Shi Huang, Eric Farber-Eger, Joshua A Beckman, Evan L Brittain, Jonathan D Mosley, Quinn S Wells

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Open heart, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 41% 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, 3 citations in OpenAlex.

  1. Article
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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

7 authors at 1 institution in 1 country.

Timothy E ThayerDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA timothy.thayer@vumc.org.ORCID 0000-0001-5317-6171
Shi HuangBiostatistics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Eric Farber-EgerVICTR, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID 0000-0003-0281-3796
Joshua A BeckmanDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Evan L BrittainDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Jonathan D MosleyDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Quinn S WellsDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

Genomic and Phenomic Architecture of Heart FailureR01HL140074 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WELLS, QUINN STANTON · 2018 to 2022
$2.0M
NHLBI NIH HHS R01 HL140074
6 · The paper itself

Abstract

objectiveRed cell distribution width (RDW) is an enigmatic biomarker associated with the presence and severity of multiple cardiovascular diseases (CVDs). It is unclear whether elevated RDW contributes to, results from, or is pleiotropically related to CVDs. We used contemporary genetic techniques to probe for evidence of aetiological associations between RDW, CVDs, and CVD risk factors.

methodsUsing an electronic health record (EHR)-based cohort, we built and deployed a genetic risk score (GRS) for RDW to test for shared genetic architecture between RDW and the cardiovascular phenome. We also created GRSs for common CVDs (coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, venous thromboembolism) and CVD risk factors (body mass index (BMI), low-density lipoprotein, high-density lipoprotein, systolic blood pressure, diastolic blood pressure, serum triglycerides, estimated glomerular filtration rate, diabetes mellitus) to test each for association with RDW. Significant GRS associations were further interrogated by two-sample Mendelian randomisation (MR). In a separate EHR-based cohort, RDW values from 1-year pre-gastric bypass surgery and 1-2 years post-gastric bypass surgery were compared.

resultsIn a cohort of 17 937 subjects, there were no significant associations between the RDW GRS and CVDs. Of the CVDs and CVD risk factors, only genetically predicted BMI was associated with RDW. In subsequent analyses, BMI was associated with RDW by multiple MR methods. In subjects undergoing bariatric surgery, RDW decreased postsurgery and followed a linear relationship with BMI change.

conclusionsRDW is unlikely to be aetiologically upstream or downstream of CVDs or CVD risk factors except for BMI. Genetic and clinical association analyses support an aetiological relationship between BMI and RDW.

Indexed as

Body Mass IndexEthnicityBiomarkersCardiovascular DiseasesErythrocyte IndicesFemaleGenetic MarkersHumansIncidenceMaleMendelian Randomization AnalysisMiddle AgedPhenomicsRisk AssessmentUnited StatesBiomarkersGenetic Markersbiomarkerscoronary artery diseaseepidemiologygenetic association studiesobesity

Identifiers

PMID34521746
PMCPMC8442102
OpenAlexW3199366604

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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 OpenQuestion graph.