Evidence map›Paper›PMID 31822289›Full record

ArticleJournal of translational medicine2019

Fibrosis independent atrial fibrillation in older patients is driven by substrate leukocyte infiltration: diagnostic and prognostic implications to patients undergoing cardiac surgery.

Christie M Aguiar, Kareem Gawdat, Stephanie Legere, Jean Marshall, Ansar Hassan, Petra C Kienesberger, Thomas Pulinilkunnil, Mathieu Castonguay, Keith R Brunt, Jean-Francois Legare

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Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
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  11. Article
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  13. Review
  14. Immune remodeling and atrial fibrillation.Frontiers in physiology · 2022
    Review
  15. 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

10 authors.

Christie M AguiarIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada.ORCID 0000-0002-6968-1997
Kareem GawdatDepartment of Pathology, Dalhousie University, Halifax, NS, Canada.
Stephanie LegereDepartment of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.
Jean MarshallDepartment of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.
Ansar HassanIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada.
Petra C KienesbergerIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada.
Thomas PulinilkunnilIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada.
Mathieu CastonguayDepartment of Pathology, Dalhousie University, Halifax, NS, Canada.
Keith R BruntIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada.
Jean-Francois LegareIMPART Investigator Team Canada (https://impart.team/), Saint John, NB, Canada. legarej@me.com.

Funding

CIHR THC-135230
6 · The paper itself

Abstract

backgroundThe objectives of the study were to characterize and quantify cellular inflammation and structural remodeling of human atria and correlate findings with molecular markers of inflammation and patient surrogate outcome.

methodsVoluntary participants undergoing heart surgery were enrolled in the study and blood samples were collected prior to surgery, and right atrium samples were harvested intraoperatively. Blood samples were analyzed by flow cytometry and complete blood counts. Atrial samples were divided for fixed fibrosis analysis, homogenized for cytokine analysis and digested for single cell suspension flow cytometry.

resultsA total of 18 patients were enrolled and samples assessed. Isolated cells from the atria revealed a CD45+ population of ~ 20%, confirming a large number of leukocytes. Further characterization revealed this population as 57% lymphocytes and 26% monocyte/macrophages (MoΦ), with the majority of the latter cells being classical (CD14++/CD16-). Interstitial fibrosis was present in 87% of samples and correlated significantly with patient age. Older patients (> 65) had significantly more atrial fibrosis and cellular inflammation. AFib patients had no distinguishing feature of atrial fibrosis and had significantly greater CD45+ MoΦ, increased expression of MMP9 and presented with a significant correlation in length of stay to CCL-2/MCP-1 and NLR (neutrophil-to-lymphocyte ratio).

conclusionAtrial fibrosis is correlated with age and not determinate to AFib. However, severity of atrial leukocyte infiltration and markers of matrix degradation are determinant to AFib. This also correlated with CCL2 (or MCP-1) and NLR-indicative of marked inflammation. These data show the potential importance of diagnostic and prognostic assessments that could inform clinical decision making in regard to the intensity of AFib patient management.

Indexed as

Cardiac Surgical ProceduresAgedAged, 80 and overAge FactorsAtrial FibrillationBlood PlateletsCell CountCohort StudiesFemaleFibrosisHeart AtriaHumansLength of StayLeukocyte Common AntigensLeukocytesLymphocytesLeukocyte Common AntigensMatrix Metalloproteinase 9Atrial fibrillationCardiac fibrosisCardiac surgeryCytokinesHuman atriumInflammationLeucocyte infiltrationMacrophages (MoΦ)NLR

Identifiers

PMID31822289
PMCPMC6905054

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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.