Evidence map›Paper›PMID 31898271›Full record

ReviewJournal of thrombosis and thrombolysis2020

Tissue-level inflammation and ventricular remodeling in hypertrophic cardiomyopathy.

Richard C Becker, A Phillip Owens, Sakthivel Sadayappan

Open access · greenAbstract readReview
In one paragraph

Review in Journal of thrombosis and thrombolysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.9field-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

49 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  10. Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025
    Review
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  13. Interplay ofFrontiers in cardiovascular medicine · 2025
    Article
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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

3 authors at 1 institution in 1 country.

Richard C BeckerDivision of Cardiovascular Health and Disease, UC Heart, Lung and Vascular Institute, University of Cincinnati College of Medicine, UC Heart, University of Cincinnati Health System, CVC 4936, 231 Albert Sabin Way, Cincinnati, OH, 45267-0542, USA. richard.becker@uc.edu.ORCID http://orcid.org/0000-0002-9878-7707
A Phillip OwensDivision of Cardiovascular Health and Disease, UC Heart, Lung and Vascular Institute, University of Cincinnati College of Medicine, UC Heart, University of Cincinnati Health System, CVC 4936, 231 Albert Sabin Way, Cincinnati, OH, 45267-0542, USA.
Sakthivel SadayappanDivision of Cardiovascular Health and Disease, UC Heart, Lung and Vascular Institute, University of Cincinnati College of Medicine, UC Heart, University of Cincinnati Health System, CVC 4936, 231 Albert Sabin Way, Cincinnati, OH, 45267-0542, USA.
University of Cincinnati · US

Funding

Translational Research Skills Development Core (TRSDC): Training Future GeneratiU54HL112307 · NHLBI · DUKE UNIVERSITY · PI BECKER, RICHARD CLINTON · 2012 to 2016
$11.1M
Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
The role of protease-activated receptor 2 (PAR2) in the pathogenesis of Alzheimer’s Disease (AD)R01HL141404 · NHLBI · UNIVERSITY OF CINCINNATI · PI OWENS III, ALBERT PHILLIP · 2018 to 2022
$2.4M
Molecular mechanism of hypertrophic cardiomyopathy in populations of South Asian descendantsR01HL130356 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2016 to 2019
$1.6M
Tissue Factor & Clot Formation In Abdominal Aortic AneurysmR00HL116786 · NHLBI · UNIVERSITY OF CINCINNATI · PI OWENS III, ALBERT PHILLIP · 2015 to 2017
$736k
Tissue Factor & Clot Formation In Abdominal Aortic AneurysmK99HL116786 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI OWENS III, ALBERT PHILLIP · 2013 to 2014
$142k
NHLBI NIH HHS K99 HL116786NHLBI NIH HHS R00 HL116786NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01 HL130356NHLBI NIH HHS R01 HL141404NHLBI NIH HHS U54 HL112307
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is a common cardiac condition caused primarily by sarcomeric protein mutations with several distinct phenotypes, ranging from asymmetric septal hypertrophy, either with or without left ventricular outflow tract obstruction, to moderate left ventricular dilation with or without apical aneurysm formation and marked, end-stage dilation with refractory heart failure. Sudden cardiac death can occur at any stage. The phenotypic variability observed in HCM is the end-result of many factors, including pre-load, after-load, wall stress and myocardial ischemia stemming from microvascular dysfunction and thrombosis; however, tissue level inflammation to include leukocyte-derived extracellular traps consisting of chromatin and histones, apoptosis, proliferation of matrix proteins and impaired or dysfunctional regulatory pathways contribute as well. Our current understanding of the pathobiology, developmental stages, transition from hypertrophy to dilation and natural history of HCM with emphasis on the role of tissue-level inflammation in myocardial fibrosis and ventricular remodeling is summarized.

Indexed as

AnimalsCardiomyopathy, HypertrophicHumansInflammationMyocardiumNeutrophilsVentricular RemodelingExtracellular trapsHypertrophic cardiomyopathyInflammationThrombosis

Identifiers

PMID31898271
PMCPMC7001758
OpenAlexW2997464284

What OpenQuestion holds

Textmetadata
LicenceTDM
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.