Evidence map›Paper›PMID 24308936›Full record

ArticleJournal of the American Heart Association2013

Mechanical dyssynchrony precedes QRS widening in ATP-sensitive K⁺ channel-deficient dilated cardiomyopathy.

Satsuki Yamada, D Kent Arrell, Garvan C Kane, Timothy J Nelson, Carmen M Perez-Terzic, Atta Behfar, Saranya Purushothaman, Frits W Prinzen, Angelo Auricchio, Andre Terzic

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Brachyury engineers cardiac repair competent stem cells.Stem cells translational medicine · 2021
    Article
  5. Deletion of cardiac polycystin 2/PC2 results in increased SR calcium release and blunted adrenergic reserve.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Rad-deletion Phenocopies Tonic Sympathetic Stimulation of the Heart.Journal of cardiovascular translational research · 2016
    Article
  12. Observational
  13. Article
  14. Article
  15. Article
  16. [Nuclear medicine and biology
    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

10 authors at 4 institutions in 3 countries.

Satsuki YamadaCenter for Regenerative Medicine, Marriott Heart Disease Research Program, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN.
D Kent Arrell
Garvan C Kane
Timothy J Nelson
Carmen M Perez-Terzic
Atta Behfar
Saranya Purushothaman
Frits W Prinzen
Angelo Auricchio
Andre Terzic
Mayo Clinic · USMayo Clinic in Arizona · USEpatocentro Ticino · CHMaastricht University · NL

Funding

Medical Scientist Traning Program at Mayo ClinicT32GM065841 · NIGMS · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H, SCHIMMENTI, LISA A · 2003 to 2022
$5.8M
NIGMS NIH HHS T32 GM065841NIGMS NIH HHS T32GM065841
6 · The paper itself

Abstract

backgroundContractile discordance exacerbates cardiac dysfunction, aggravating heart failure outcome. Dissecting the genesis of mechanical dyssynchrony would enable an early diagnosis before advanced disease. METHODS AND

resultsHigh-resolution speckle-tracking echocardiography was applied in a knockout murine surrogate of adult-onset human cardiomyopathy caused by mutations in cardioprotective ATP-sensitive K(+) (K(ATP)) channels. Preceding the established criteria of cardiac dyssynchrony, multiparametric speckle-based strain resolved nascent erosion of dysfunctional regions within cardiomyopathic ventricles of the K(ATP) channel-null mutant exposed to hemodynamic stress. Not observed in wild-type counterparts, intraventricular disparity in wall motion, validated by the degree, direction, and delay of myocardial speckle patterns, unmasked the disease substrate from asymptomatic to overt heart failure. Mechanical dyssynchrony preceded widening of the QRS complex and exercise intolerance and progressed into global myocardial discoordination and decompensated cardiac pump function, precipitating a low output syndrome.

conclusionsThe present study, with the use of high-resolution imaging, prospectively resolved the origin and extent of intraventricular motion disparity in a K(ATP) channel-knockout model of dilated cardiomyopathy. Mechanical dyssynchrony established as an early marker of cardiomyopathic disease offers novel insight into the pathodynamics of dyssynchronous heart failure.

Indexed as

Myocardial ContractionVentricular Function, LeftAnimalsCardiac Output, LowCardiomyopathy, DilatedDisease Models, AnimalDisease ProgressionEchocardiography, DopplerHeart FailureHeart VentriclesHemodynamicsKATP ChannelsKcnj11 ChannelMaleMiceMice, KnockoutKATP ChannelsKcnj11 ChannelPotassium Channels, Inwardly RectifyingATP‐sensitive K+ channelheart failureKir6.2QRS complexspeckle‐tracking

Identifiers

PMID24308936
PMCPMC3886734
OpenAlexW2166877777

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.