Evidence map›Paper›PMID 22268104›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Intramural optical mapping of V(m) and Ca(i)2+ during long-duration ventricular fibrillation in canine hearts.

Wei Kong, Raymond E Ideker, Vladimir G Fast

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. A century of optocardiography.IEEE reviews in biomedical engineering · 2014
    Review
  7. Cardiac optogenetics.American journal of physiology. Heart and circulatory physiology · 2013
    Review
  8. Mapping cardiac surface mechanics with structured light imaging.American journal of physiology. Heart and circulatory physiology · 2012
    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.

Wei KongDepartment of Biomedical Engineering, University of Alabama, Birmingham, 35294, USA.
Raymond E Ideker
Vladimir G Fast

Funding

Mechanisms of Long Duration Fibrillation, Defibrillation and RefibrillationR01HL085370 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI IDEKER, RAYMOND E. · 2007 to 2014
$2.9M
Mechanisms of Defibrillation &Shock-Induced ArrhythmiasR01HL067748 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FAST, VLADIMIR G · 2001 to 2012
$2.1M
NHLBI NIH HHS HL-067748NHLBI NIH HHS HL-85370NHLBI NIH HHS R01 HL085370
6 · The paper itself

Abstract

Intramural gradients of intracellular Ca(2+) (Ca(i)(2+)) Ca(i)(2+) handling, Ca(i)(2+) oscillations, and Ca(i)(2+) transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Ca(i)(2+) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Ca(i)(2+) handling contribute to LDVF, we measured membrane voltage (V(m)) and Ca(i)(2+) during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, V(m) and Ca(i)(2+) progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed V(m) upstrokes during pacing and LDVF. In conclusion, the fact that V(m) upstrokes always preceded CaTs indicates that spontaneous Ca(i)(2+) oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong V(m)-Ca(i)(2+) desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Ca(i)(2+) handling and may potentially contribute to LDVF maintenance.

Indexed as

Calcium SignalingVoltage-Sensitive Dye ImagingAction PotentialsAnimalsCalciumCardiac Pacing, ArtificialDogsEndocardiumHeart RateHeart VentriclesIn Vitro TechniquesMaleMyocardiumPerfusionPericardiumTime FactorsCalcium

Identifiers

PMID22268104
PMCPMC3311483

What OpenQuestion holds

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Read underepoch 390

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.