Evidence map›Paper›PMID 35600285›Full record

ArticleAmerican journal of cardiovascular disease2022

Plasma proteomic analysis of association between atrial fibrillation, coronary microvascular disease and heart failure.

Gunjan Dixit, John Blair, Cevher Ozcan

Open access · greenAbstract read
In one paragraph

Article in American journal of cardiovascular disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Serum amyloid A in HFpEF and cardiometabolic diseases.Basic research in cardiology · 2026
    Review
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  8. Article
  9. Coronary microvascular dysfunction, arrythmias, and sudden cardiac death: A literature review.American heart journal plus : cardiology research and practice · 2024
    Article
  10. Article
  11. 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

3 authors at 1 institution in 1 country.

Gunjan DixitDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago 5841 S. Maryland Avenue, MC 6080, Chicago 60637, IL, USA.
John BlairDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago 5841 S. Maryland Avenue, MC 6080, Chicago 60637, IL, USA.
Cevher OzcanDepartment of Medicine, Section of Cardiology, Heart and Vascular Center, University of Chicago 5841 S. Maryland Avenue, MC 6080, Chicago 60637, IL, USA.
University of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical association between atrial fibrillation (AF), coronary microvascular disease (CMD) and heart failure with preserved ejection fraction (HFpEF) is highly prevalent, however the mechanism behind this association is not known. We hypothesized that plasma proteomic analysis can identify novel biomarkers and the mechanistic pathways in concomitant AF, CMD and HFpEF. To discover circulating biomarkers for the association between AF, CMD and HFpEF, an unbiased label-free quantitative proteomics approach was used in plasma derived from patients who underwent coronary physiology studies (n=18). Circulating proteins were analyzed by liquid chromatography-mass spectrometry and screened to determine candidate biomarkers of the concomitant AF, CMD and HFpEF. We identified 130 dysregulated proteins across the groups with the independent patient replicates. Among those, 35 proteins were candidate biomarkers of the association between AF, CMD and HFpEF. We found significantly elevated SAA1, LRG1 and APOC3 proteins in the coexistence of AF, CMD and HFpEF, whereas LCP1, PON1 and C1S were markedly downregulated in their associations. AF was associated with reduced LCP1, KLKB1 and C4A in these patients. Combined downregulation of PON1 and C1S was a marker of concurrent HFpEF and CMD. PON1 was associated with HFpEF while C1S was a marker of CMD. These proteins are related to inflammation, extra cellular remodeling, oxidative stress, and coagulation. In conclusion, plasma proteomic profile provides biomarkers and mechanistic insight into the association of AF, CMD and HFpEF. SAA1, LRG1, APOC3, LCP1, PON1 and C1S are candidate markers for the risk stratification of their associations and potential underlying mechanistic pathways.

Indexed as

Atrial fibrillationbiomarkerscoronary microvascular dysfunctionheart failureproteomics

Identifiers

PMID35600285
PMCPMC9123414
OpenAlexW4285741417

What OpenQuestion holds

Textmetadata
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.