Evidence map›Paper›PMID 37298077›Full record

ArticleInternational journal of molecular sciences2023

C-Reactive Protein Levels and Risk of Cardiovascular Diseases: A Two-Sample Bidirectional Mendelian Randomization Study.

Annapurna Kuppa, Himi Tripathi, Ahmed Al-Darraji, Wadea M Tarhuni, Ahmed Abdel-Latif

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 4 pooled it
31.0field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 4 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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23 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Annapurna KuppaDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Himi TripathiDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Ahmed Al-DarrajiDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Wadea M TarhuniCanadian Cardiac Research Center, Department of Internal Medicine, Division of Cardiology, University of Saskatchewan, Saskatoon, SK S7N 5A2, Canada.
Ahmed Abdel-LatifDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
University of Michigan–Ann Arbor · USUniversity of Saskatchewan · CA

Funding

Lysophosphatidic Acid Mediates Cardiac Inflammation After Acute InfarctionR01HL138488 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABDEL-LATIF, AHMED · 2017 to 2021
$1.9M
Role of Bioactive Lipids in Stem Cell Mobilization and Homing in Cardiac IschemiaR56HL124266 · NHLBI · UNIVERSITY OF KENTUCKY · PI ABDEL-LATIF, AHMED · 2014 to 2014
$375k
NHLBI NIH HHS R01 HL138488NHLBI NIH HHS R56 HL124266NIH HHS HL124266
6 · The paper itself

Abstract

Elevated C-reactive protein (CRP) levels are an indicator of inflammation, a major risk factor for cardiovascular disease (CVD). However, this potential association in observational studies remains inconclusive. We performed a two-sample bidirectional Mendelian randomization (MR) study using publicly available GWAS summary statistics to evaluate the relationship between CRP and CVD. Instrumental variables (IVs) were carefully selected, and multiple approaches were used to make robust conclusions. Horizontal pleiotropy and heterogeneity were evaluated using the MR-Egger intercept and Cochran's Q-test. The strength of the IVs was determined using F-statistics. The causal effect of CRP on the risk of hypertensive heart disease (HHD) was statistically significant, but we did not observe a significant causal relationship between CRP and the risk of myocardial infarction, coronary artery disease, heart failure, or atherosclerosis. Our primary analyses, after performing outlier correction using MR-PRESSO and the Multivariable MR method, revealed that IVs that increased CRP levels also increased the HHD risk. However, after excluding outlier IVs identified using PhenoScanner, the initial MR results were altered, but the sensitivity analyses remained congruent with the results from the primary analyses. We found no evidence of reverse causation between CVD and CRP. Our findings warrant updated MR studies to confirm the role of CRP as a clinical biomarker for HHD.

Indexed as

Cardiovascular DiseasesHeart DiseasesHypertensionC-Reactive ProteinGenome-Wide Association StudyHumansMendelian Randomization AnalysisC-Reactive Proteinbidirectional Mendelian randomization analysiscardiovascular diseasesC-reactive proteinhypertensive heart diseaseMendelian randomizationMR-PRESSOmultivariable MR analysisPhenoScannersensitivity analysistwo-sample Mendelian randomization

Identifiers

PMID37298077
PMCPMC10252732
OpenAlexW4378083418

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.