Evidence map›Paper›PMID 30977811›Full record

ArticleCardiovascular research2019

Arrhythmogenic propensity of the fibrotic substrate after atrial fibrillation ablation: a longitudinal study using magnetic resonance imaging-based atrial models.

Rheeda L Ali, Joe B Hakim, Patrick M Boyle, Sohail Zahid, Bhradeev Sivasambu, Joseph E Marine, Hugh Calkins, Natalia A Trayanova, David D Spragg

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.3field-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

42 citing papers in PubMed, 58 citations in OpenAlex.

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  13. Digital twins in medicine.Nature computational science · 2024
    Review
  14. Computational Modeling and Simulation of the Fibrotic Human Atria.Methods in molecular biology (Clifton, N.J.) · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Rheeda L AliInstitute for Computational Medicine, Johns Hopkins University, 3400 N Charles Street, 208 Hackerman, Baltimore, MD, USA.
Joe B HakimInstitute for Computational Medicine, Johns Hopkins University, 3400 N Charles Street, 208 Hackerman, Baltimore, MD, USA.
Patrick M BoyleInstitute for Computational Medicine, Johns Hopkins University, 3400 N Charles Street, 208 Hackerman, Baltimore, MD, USA.
Sohail ZahidDepartment of Biomedical Engineering, Johns Hopkins University, 3400 N Charles Street, 208 Hackerman, Baltimore, MD, USA.
Bhradeev SivasambuDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Joseph E MarineDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Hugh CalkinsDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Natalia A TrayanovaInstitute for Computational Medicine, Johns Hopkins University, 3400 N Charles Street, 208 Hackerman, Baltimore, MD, USA.
David D SpraggDivision of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USJohns Hopkins Medicine · USUniversity of Washington · US

Funding

Virtual Electrophysiology LaboratoryDP1HL123271 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2013 to 2017
$4.0M
Simulation Guidance of Ablation Therapy for Persistent Atrial FibrillationU01HL141074 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CALKINS, HUGH G, TRAYANOVA, NATALIA A. · 2018 to 2021
$3.1M
American Heart Association-American Stroke Association 16SDG30440006NHLBI NIH HHS DP1 HL123271NHLBI NIH HHS U01 HL141074
6 · The paper itself

Abstract

aimsInadequate modification of the atrial fibrotic substrate necessary to sustain re-entrant drivers (RDs) may explain atrial fibrillation (AF) recurrence following failed pulmonary vein isolation (PVI). Personalized computational models of the fibrotic atrial substrate derived from late gadolinium enhanced (LGE)-magnetic resonance imaging (MRI) can be used to non-invasively determine the presence of RDs. The objective of this study is to assess the changes of the arrhythmogenic propensity of the fibrotic substrate after PVI. METHODS AND

resultsPre- and post-ablation individualized left atrial models were constructed from 12 AF patients who underwent pre- and post-PVI LGE-MRI, in six of whom PVI failed. Pre-ablation AF sustained by RDs was induced in 10 models. RDs in the post-ablation models were classified as either preserved or emergent. Pre-ablation models derived from patients for whom the procedure failed exhibited a higher number of RDs and larger areas defined as promoting RD formation when compared with atrial models from patients who had successful ablation, 2.6 ± 0.9 vs. 1.8 ± 0.2 and 18.9 ± 1.6% vs. 13.8 ± 1.5%, respectively. In cases of successful ablation, PVI eliminated completely the RDs sustaining AF. Preserved RDs unaffected by ablation were documented only in post-ablation models of patients who experienced recurrent AF (2/5 models); all of these models had also one or more emergent RDs at locations distinct from those of pre-ablation RDs. Emergent RDs occurred in regions that had the same characteristics of the fibrosis spatial distribution (entropy and density) as regions that harboured RDs in pre-ablation models.

conclusionRecurrent AF after PVI in the fibrotic atria may be attributable to both preserved RDs that sustain AF pre- and post-ablation, and the emergence of new RDs following ablation. The same levels of fibrosis entropy and density underlie the pro-RD propensity in both pre- and post-ablation substrates.

Indexed as

Atrial Function, LeftAtrial RemodelingCatheter AblationCryosurgeryMagnetic Resonance ImagingAction PotentialsAtrial FibrillationComputer SimulationFibrosisHeart AtriaHeart RateHumansLongitudinal StudiesModels, CardiovascularPredictive Value of TestsPulmonary VeinsAtrial fibrillationCardiac MRIDriversFibrosisModelling

Identifiers

PMID30977811
PMCPMC6755354
OpenAlexW2935962098

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.