Evidence map›Paper›PMID 34163372›Full record

ArticleFrontiers in physiology2021

Presence of Left Atrial Fibrosis May Contribute to Aberrant Hemodynamics and Increased Risk of Stroke in Atrial Fibrillation Patients.

Nikhil Paliwal, Rheeda L Ali, Matteo Salvador, Ryan O'Hara, Rebecca Yu, Usama A Daimee, Tauseef Akhtar, Pallavi Pandey, David D Spragg, Hugh Calkins and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Nikhil PaliwalAlliance for Cardiovascular Diagnostic and Treatment Innovation, Johns Hopkins University, Baltimore, MD, United States.
Rheeda L AliAlliance for Cardiovascular Diagnostic and Treatment Innovation, Johns Hopkins University, Baltimore, MD, United States.
Matteo SalvadorDepartment of Mathematics, Politecnico di Milano, Milan, Italy.
Ryan O'HaraDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, United States.
Rebecca YuDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, United States.
Usama A DaimeeDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Tauseef AkhtarDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Pallavi PandeyDepartment of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
David D SpraggDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Hugh CalkinsDivision of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Natalia A TrayanovaAlliance for Cardiovascular Diagnostic and Treatment Innovation, Johns Hopkins University, Baltimore, MD, United States.
Johns Hopkins University · USJohns Hopkins Medicine · USPolitecnico di Milano · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) patients are at high risk of stroke, with the left atrial appendage (LAA) found to be the most common site of clot formation. Presence of left atrial (LA) fibrosis has also been associated with higher stroke risk. However, the mechanisms for increased stroke risk in patients with atrial fibrotic remodeling are poorly understood. We sought to explore these mechanisms using fluid dynamic analysis and to test the hypothesis that the presence of LA fibrosis leads to aberrant hemodynamics in the LA, contributing to increased stroke risk in AF patients. We retrospectively collected late-gadolinium-enhanced MRI (LGE-MRI) images of eight AF patients (four persistent and four paroxysmal) and reconstructed their 3D LA surfaces. Personalized computational fluid dynamic simulations were performed, and hemodynamics at the LA wall were quantified by wall shear stress (WSS, friction of blood), oscillatory shear index (OSI, temporal directional change of WSS), endothelial cell activation potential (ECAP, ratio of OSI and WSS), and relative residence time (RRT, residence time of blood near the LA wall). For each case, these hemodynamic metrics were compared between fibrotic and non-fibrotic portions of the wall. Our results showed that WSS was lower, and OSI, ECAP, and RRT was higher in the fibrotic region as compared to the non-fibrotic region, with ECAP (

Indexed as

atrial fibrillationfibrosishemodynamicspersonalized simulationstroke

Identifiers

PMID34163372
PMCPMC8215291
OpenAlexW3166679106

What OpenQuestion holds

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LicenceCC BY
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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.