Evidence map›Paper›PMID 19907317›Full record

ReviewCurrent opinion in cardiology2010

Electrical remodeling in the failing heart.

Takeshi Aiba, Gordon F Tomaselli

Abstract readReview
In one paragraph

Review in Current opinion in cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
8.5field-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

76 citing papers in PubMed, 155 citations in OpenAlex.

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  15. Electroimmunology and cardiac arrhythmia.Nature reviews. Cardiology · 2021
    Review
  16. Modelling sudden cardiac death risks factors in patients with coronavirus disease of 2019: the hydroxychloroquine and azithromycin case.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2021
    Article
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  18. Cardioprotection of an IAmerican journal of translational research · 2021
    Article
  19. Article
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16 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

2 authors at 1 institution in 1 country.

Takeshi AibaDepartment of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Gordon F Tomaselli
Johns Hopkins Medicine · US

Funding

Pathobiology of Cardiac Dyssynchrony &ResynchronizationP01HL077180 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2004 to 2014
$22.8M
Expression Profiling in Canine Models of Human DiseaseR01HL072488 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TOMASELLI, GORDON FRANK · 2002 to 2005
$3.2M
The System Biology of Sudden Cardiac DeathR33HL087363 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TOMASELLI, GORDON FRANK · 2007 to 2009
$997k
NHLBI NIH HHS P01 HL077180NHLBI NIH HHS R01 HL072488NHLBI NIH HHS R33 HL087363
6 · The paper itself

Abstract

purpose of reviewWe focus on the molecular and cellular basis of excitability, conduction and electrical remodeling in heart failure with dyssynchronous left ventricular contraction (DHF) and its restoration by cardiac resynchronization therapy (CRT) using a canine tachy-pacing heart failure model. RECENT

findingsThe electrophysiological hallmark of cells and tissues isolated from failing hearts is prolongation of action potential duration (APD) and conduction slowing. In human studies and a number of animal models of heart failure, functional downregulation of K currents and alterations in depolarizing Na and Ca currents and transporters are demonstrated. Alterations in intercellular ion channels and extracellular matrix contribute to heterogeneity of APD and conduction slowing. The changes in cellular and tissue function are regionally heterogeneous, particularly in the DHF. Furthermore, beta-adrenergic signaling and modulation of ionic currents is blunted in heart failure. CRT partially reverses the DHF-induced downregulation of K current and improves Na channel gating. CRT significantly improves Ca homeostasis, especially in lateral myocytes, and restores the DHF-induced blunted beta-adrenergic receptor responsiveness. CRT abbreviates DHF-induced prolongation of APD in the lateral myocytes, reduces the left ventricular regional gradient of APD and suppresses development of early afterdepolarizations. SUMMARY: CRT partially restores DHF-induced electrophysiological remodeling, abnormal Ca homeostasis, blunted beta-adrenergic responsiveness, and regional heterogeneity of APD, and thus may suppress ventricular arrhythmias and contribute to the mortality benefit of CRT as well as improving mechanical performance of the heart.

Indexed as

Action PotentialsAnimalsCalciumCardiac Pacing, ArtificialConnexinsGene ExpressionHeart Conduction SystemHeart FailureHumansPotassiumSodiumCalciumConnexinsPotassiumSodium

Identifiers

PMID19907317
PMCPMC2855498
OpenAlexW1988452782

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.