Evidence map›Paper›PMID 30370501›Full record

ReviewPflugers Archiv : European journal of physiology2019

Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.

Richard J Marszalek, R John Solaro, Beata M Wolska

Open access · greenAbstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Mechanisms and prognostic impact of myocardial ischaemia in hypertrophic cardiomyopathy.The international journal of cardiovascular imaging · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
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 J MarszalekDepartment of Physiology and Biophysics and the Center for Cardiovascular Research, University of Illinois at Chicago, 835 S Wolcott Ave, Chicago, IL, 60612, USA.
R John SolaroDepartment of Physiology and Biophysics and the Center for Cardiovascular Research, University of Illinois at Chicago, 835 S Wolcott Ave, Chicago, IL, 60612, USA.
Beata M WolskaDepartment of Physiology and Biophysics and the Center for Cardiovascular Research, University of Illinois at Chicago, 835 S Wolcott Ave, Chicago, IL, 60612, USA.
University of Illinois Chicago · US

Funding

Sarcomeric Modifications and Progressive Cardiac MaladaptationP01HL062426 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DE TOMBE, PIETER P. · 2000 to 2020
$42.4M
Training Program in Personalized Cardiovascular Medicine (TPIPCVM)T32HL139439 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DARBAR, DAWOOD · 2018 to 2022
$2.1M
Myofilament signaling and cardiac disordersR01HL128468 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN, WOLSKA, BEATA M. · 2016 to 2019
$1.6M
NHLBI NIH HHS P01 HL062426NHLBI NIH HHS PO1 HL 62426NHLBI NIH HHS R01 HL128468NHLBI NIH HHS RO1 HL 128468NHLBI NIH HHS T32 HL 139439NHLBI NIH HHS T32 HL139439
6 · The paper itself

Abstract

Alterations in the coronary vascular system are likely associated with a mismatch between energy demand and energy supply and critical in triggering the cascade of events that leads to symptomatic hypertrophic cardiomyopathy. Targeting the early events, particularly vascular remodeling, may be a key approach to developing effective treatments. Improvement in our understanding of hypertrophic cardiomyopathy began with the results of early biophysical studies, proceeded to genetic analyses pinpointing the mutational origin, and now pertains to imaging of the metabolic and flow-related consequences of such mutations. Microvascular dysfunction has been an ongoing hot topic in the imaging of genetic cardiomyopathies marked by its histologically significant remodeling and has proven to be a powerful asset in determining prognosis for these patients as well as enlightening scientists on a potential pathophysiological cascade that may begin early during the developmental process. Here, we discuss questions that continue to remain on the mechanistic processes leading to microvascular dysfunction, its correlation to the morphological changes in the vessels, and its contribution to disease progression.

Indexed as

Cardiac MyosinsCardiomyopathy, HypertrophicCoronary CirculationCoronary VesselsHumansCardiac MyosinsEnergeticsHypertrophic cardiomyopathyIschemiaMicrovascularPathogenesis

Identifiers

PMID30370501
PMCPMC6481925
OpenAlexW2899065058

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.