Evidence map›Paper›PMID 32242478›Full record

ReviewJournal of the American Heart Association2020

Characterization, Pathogenesis, and Clinical Implications of Inflammation-Related Atrial Myopathy as an Important Cause of Atrial Fibrillation.

Milton Packer

Open access · goldAbstract readReview
In one paragraph

Review in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  5. Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026
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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

1 author at 1 institution in 2 countries.

Milton PackerBaylor Heart and Vascular Institute Baylor University Medical Center Dallas TX.
Baylor University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Historically, atrial fibrillation has been observed in clinical settings of prolonged hemodynamic stress, eg, hypertension and valvular heart disease. However, recently, the most prominent precedents to atrial fibrillation are metabolic diseases that are associated with adipose tissue inflammation (ie, obesity and diabetes mellitus) and systemic inflammatory disorders (ie, rheumatoid arthritis and psoriasis). These patients typically have little evidence of left ventricular hypertrophy or dilatation; instead, imaging reveals abnormalities of the structure or function of the atria, particularly the left atrium, indicative of an atrial myopathy. The left atrium is enlarged, fibrotic and noncompliant, potentially because the predisposing disorder leads to an expansion of epicardial adipose tissue, which transmits proinflammatory mediators to the underlying left atrium. The development of an atrial myopathy not only leads to atrial fibrillation, but also contributes to pulmonary venous hypertension and systemic thromboembolism. These mechanisms explain why disorders of systemic or adipose tissue inflammation are accompanied an increased risk of atrial fibrillation, abnormalities of left atrium geometry and an enhanced risk of stroke. The risk of stroke exceeds that predicted by conventional cardiovascular risk factors or thromboembolism risk scores used to guide the use of anticoagulation, but it is strongly linked to clinical evidence and biomarkers of systemic inflammation.

Indexed as

Atrial Function, LeftAtrial RemodelingAdipose TissueAnimalsAtrial FibrillationFibrosisHeart AtriaHumansInflammationInflammation MediatorsPrognosisRisk AssessmentRisk FactorsInflammation Mediatorsatrial fibrillationatrial myopathystroke

Identifiers

PMID32242478
PMCPMC7428644
OpenAlexW3014209586

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.