Evidence map›Paper›PMID 22253411›Full record

ArticleCirculation research2012

Subcellular structures and function of myocytes impaired during heart failure are restored by cardiac resynchronization therapy.

Frank B Sachse, Natalia S Torres, Eleonora Savio-Galimberti, Takeshi Aiba, David A Kass, Gordon F Tomaselli, John H Bridge

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 131 citations in OpenAlex.

  1. Trial
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  8. Concepts of Cardiac Dyssynchrony and Dynamic Approach.Diagnostics (Basel, Switzerland) · 2024
    Review
  9. Review
  10. Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023
    Article
  11. Review
  12. Serial block face scanning electron microscopy reveals region-dependent remodelling of transverse tubules post-myocardial infarction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
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  18. Review
  19. The mechanism of osmotically induced sealing of cardiac t tubules.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  20. Article

22 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Frank B SachseNora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, 95 South 2000 East, Salt Lake City, UT 84112-5000, USA. fs@cvrti.utah.edu
Natalia S Torres
Eleonora Savio-Galimberti
Takeshi Aiba
David A Kass
Gordon F Tomaselli
John H Bridge
Johns Hopkins University · US

Funding

Pathobiology of Cardiac Dyssynchrony &ResynchronizationP01HL077180 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2004 to 2014
$22.8M
Remodeling of the Transverse Tubular System and Ryanodine Receptor Clusters in DyR01HL094464 · NHLBI · UNIVERSITY OF UTAH · PI SACHSE, FRANK BERND · 2010 to 2014
$1.9M
NHLBI NIH HHS P01 HL077180NHLBI NIH HHS R01 HL094464
6 · The paper itself

Abstract

rationaleCardiac resynchronization therapy (CRT) is an established treatment for patients with chronic heart failure. However, CRT-associated structural and functional remodeling at cellular and subcellular levels is only partly understood.

objectiveTo investigate the effects of CRT on subcellular structures and protein distributions associated with excitation-contraction coupling of ventricular cardiomyocytes. METHODS AND

resultsOur studies revealed remodeling of the transverse tubular system (t-system) and the spatial association of ryanodine receptor (RyR) clusters in a canine model of dyssynchronous heart failure (DHF). We did not find this remodeling in a synchronous heart failure model based on atrial tachypacing. Remodeling in DHF ranged from minor alterations in anterior left ventricular myocytes to nearly complete loss of the t-system and dissociation of RyRs from sarcolemmal structures in lateral cells. After CRT, we found a remarkable and almost complete reverse remodeling of these structures despite persistent left ventricular dysfunction. Studies of whole-cell Ca(2+) transients showed that the structural remodeling and restoration were accompanied with remodeling and restoration of Ca(2+) signaling.

conclusionsDHF is associated with regional remodeling of the t-system. Myocytes undergo substantial structural and functional restoration after only 3 weeks of CRT. The finding suggests that t-system status can provide an early marker of the success of this therapy. The results could also guide us to an understanding of the loss and remodeling of proteins associated with the t-system. The steep relationship between free Ca(2+) and contraction suggests that some restoration of Ca(2+) release units will have a disproportionately large effect on contractility.

Indexed as

Cardiac Resynchronization TherapyExcitation Contraction CouplingVentricular Function, LeftVentricular RemodelingAnimalsCalciumDisease Models, AnimalDogsHeart FailureMaleMembrane PotentialsMyocardial ContractionMyocytes, CardiacRecovery of FunctionRyanodine Receptor Calcium Release ChannelSarcolemmaCalciumRyanodine Receptor Calcium Release Channel

Identifiers

PMID22253411
PMCPMC3299196
OpenAlexW1996841780

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.