Evidence map›Paper›PMID 21586291›Full record

ArticleJournal of molecular and cellular cardiology2011

Effects of KATP channel openers diazoxide and pinacidil in coronary-perfused atria and ventricles from failing and non-failing human hearts.

Vadim V Fedorov, Alexey V Glukhov, Christina M Ambrosi, Geran Kostecki, Roger Chang, Deborah Janks, Richard B Schuessler, Nader Moazami, Colin G Nichols, Igor R Efimov

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
8.1field-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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Bayliss-Starling Prize Lecture: KThe Journal of physiology · 2025
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  7. KArhiv za farmaciju · 2024
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  8. Article
  9. Article
  10. Personalized Therapeutics for KAnnual review of pharmacology and toxicology · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Chemical science · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

4 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

10 authors at 1 institution in 1 country.

Vadim V FedorovDepartment of Biomedical Engineering, Washington University, St. Louis, MO 63130, USA.
Alexey V Glukhov
Christina M Ambrosi
Geran Kostecki
Roger Chang
Deborah Janks
Richard B Schuessler
Nader Moazami
Colin G Nichols
Igor R Efimov
Washington University in St. Louis · US

Funding

SUR1 (ABCC8) AND ATRIAL KATP CHANNELSR01HL095010 · NHLBI · WASHINGTON UNIVERSITY · PI NICHOLS, COLIN G · 2009 to 2017
$3.4M
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 R01 HL085369NHLBI NIH HHS R01 HL114395NHLBI NIH HHS R01 HL95010
6 · The paper itself

Abstract

This study compared the effects of ATP-regulated potassium channel (K(ATP)) openers, diazoxide and pinacidil, on diseased and normal human atria and ventricles. We optically mapped the endocardium of coronary-perfused right (n=11) or left (n=2) posterior atrial-ventricular free wall preparations from human hearts with congestive heart failure (CHF, n=8) and non-failing human hearts without (NF, n=3) or with (INF, n=2) infarction. We also analyzed the mRNA expression of the K(ATP) targets K(ir)6.1, K(ir)6.2, SUR1, and SUR2 in the left atria and ventricles of NF (n=8) and CHF (n=4) hearts. In both CHF and INF hearts, diazoxide significantly decreased action potential durations (APDs) in atria (by -21±3% and -27±13%, p<0.01) and ventricles (by -28±7% and -28±4%, p<0.01). Diazoxide did not change APD (0±5%) in NF atria. Pinacidil significantly decreased APDs in both atria (-46 to -80%, p<0.01) and ventricles (-65 to -93%, p<0.01) in all hearts studied. The effect of pinacidil on APD was significantly higher than that of diazoxide in both atria and ventricles of all groups (p<0.05). During pinacidil perfusion, burst pacing induced flutter/fibrillation in all atrial and ventricular preparations with dominant frequencies of 14.4±6.1 Hz and 17.5±5.1 Hz, respectively. Glibenclamide (10 μM) terminated these arrhythmias and restored APDs to control values. Relative mRNA expression levels of K(ATP) targets were correlated to functional observations. Remodeling in response to CHF and/or previous infarct potentiated diazoxide-induced APD shortening. The activation of atrial and ventricular K(ATP) channels enhances arrhythmogenicity, suggesting that such activation may contribute to reentrant arrhythmias in ischemic hearts.

Indexed as

Action PotentialsAdolescentAdultArrhythmias, CardiacCoronary VesselsDiazoxideFemaleGene Expression RegulationHeart AtriaHeart FailureHeart VentriclesHumansKATP ChannelsMaleMiddle AgedMyocardial IschemiaDiazoxideKATP ChannelsPinacidilRNA, MessengerVasodilator Agents

Identifiers

PMID21586291
PMCPMC3124600
OpenAlexW2056622908

What OpenQuestion holds

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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.