Evidence map›Paper›PMID 21502574›Full record

ArticleCirculation2011

Transmural heterogeneity and remodeling of ventricular excitation-contraction coupling in human heart failure.

Qing Lou, Vadim V Fedorov, Alexey V Glukhov, Nader Moazami, Vladimir G Fast, Igor R Efimov

Abstract readComparative Study
In one paragraph

Article in Circulation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
–field-weighted citation impact
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

92 citing papers in PubMed.

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  14. Heart Slices to Model Cardiac Physiology.Frontiers in pharmacology · 2021
    Review
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32 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

6 authors.

Qing LouDepartment of Biomedical Engineering, Washington University, St. Louis, MO, USA.
Vadim V Fedorov
Alexey V Glukhov
Nader Moazami
Vladimir G Fast
Igor R Efimov

Funding

Virtual Electrode Polarization Hypothesis of DefibrillationR01HL067322 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2001 to 2010
$3.7M
The role of electroporation in defibrillationR01HL074283 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2004 to 2007
$2.3M
ARRHYTHMOGENIC REMODELING IN HUMAN HEART FAILURER01HL114395 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2012 to 2015
$2.1M
STRUCTURE/FUNCTION OF THE PACEMAKING AND CONDUCTION SYSTEM OF THE HEARTR01HL085369 · NHLBI · WASHINGTON UNIVERSITY · PI EFIMOV, IGOR R · 2008 to 2011
$1.5M
NHLBI NIH HHS HL067322NHLBI NIH HHS HL074283NHLBI NIH HHS HL085369NHLBI NIH HHS R01 HL067322NHLBI NIH HHS R01 HL074283NHLBI NIH HHS R01 HL085369NHLBI NIH HHS R01 HL114395
6 · The paper itself

Abstract

backgroundExcitation-contraction (EC) coupling is altered in end-stage heart failure. However, spatial heterogeneity of this remodeling has not been established at the tissue level in failing human heart. The objective of this article was to study functional remodeling of excitation-contraction coupling and calcium handling in failing and nonfailing human hearts. METHODS AND

resultsWe simultaneously optically mapped action potentials and calcium transients in coronary perfused left ventricular wedge preparations from nonfailing (n=6) and failing (n=5) human hearts. Our major findings are the following. First, calcium transient duration minus action potential duration was longer at subendocardium in failing compared with nonfailing hearts during bradycardia (40 bpm). Second, the transmural gradient of calcium transient duration was significantly smaller in failing hearts compared with nonfailing hearts at fast pacing rates (100 bpm). Third, calcium transient in failing hearts had a flattened plateau at the midmyocardium and exhibited a 2-component slow rise at the subendocardium in 3 failing hearts. Fourth, calcium transient relaxation was slower at the subendocardium than at the subepicardium in both groups. Protein expression of sarcoplasmic reticulum Ca(2+)-ATPase 2a was lower at the subendocardium than the subepicardium in both nonfailing and failing hearts. Sarcoplasmic reticulum Ca(2+)-ATPase 2a protein expression at subendocardium was lower in hearts with ischemic cardiomyopathy compared with those with nonischemic cardiomyopathy.

conclusionsFor the first time, we present direct experimental evidence of transmural heterogeneity of excitation-contraction coupling and calcium handling in human hearts. End-stage heart failure is associated with the heterogeneous remodeling of excitation-contraction coupling and calcium handling.

Indexed as

Action PotentialsAdultAgedCalciumCalcium-Binding ProteinsCalcium ChannelsCardiomyopathiesFemaleHeart FailureHumansMaleMiddle AgedMyocardial ContractionMyocardial IschemiaPhospholambanSarcoplasmic Reticulum Calcium-Transporting ATPasesCalciumCalcium-Binding ProteinsCalcium ChannelsPhospholambanSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID21502574
PMCPMC3100201

What OpenQuestion holds

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Registered trials

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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.