Evidence map›Paper›PMID 24163078›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2013

Increased inducibility of ventricular tachycardia and decreased heart rate variability in a mouse model for type 1 diabetes: effect of pravastatin.

Mohammad Rajab, Hongwei Jin, Charles M Welzig, Alfred Albano, Mark Aronovitz, Yali Zhang, Ho-Jin Park, Mark S Link, Sami F Noujaim, Jonas B Galper

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Metabolic stress exacerbates CaExperimental physiology · 2026
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  4. Bioengineered peptibodies as blockers of ion channels.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. In vitro and in vivo cardiac toxicity of flavored electronic nicotine delivery systems.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Pulmonary Vein Ganglia Are Remodeled in the Diabetic Heart.Journal of the American Heart Association · 2018
    Article
  13. Article
  14. Article
  15. Observational
  16. Hyperglycemia induces defective Ca2+ homeostasis in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  17. Review
  18. Review
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 2 institutions in 1 country.

Mohammad RajabTufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts;
Hongwei Jin
Charles M Welzig
Alfred Albano
Mark Aronovitz
Yali Zhang
Ho-Jin Park
Mark S Link
Sami F Noujaim
Jonas B Galper
Tufts Medical Center · USTufts University · US

Funding

Training Program in Cardiovascular ResearchT32HL069770 · NHLBI · TUFTS MEDICAL CENTER · PI KARAS, RICHARD H · 2003 to 2013
$4.7M
Role of Sterols &Insulin in Cardiac Autonomic ResponseR01HL074876 · NHLBI · TUFTS MEDICAL CENTER · PI GALPER, JONAS BERNARD · 2004 to 2013
$3.2M
Structural and molecular basis of drug-induced IKACh reductionR00HL105574 · NHLBI · TUFTS MEDICAL CENTER · PI NOUJAIM, SAMI FOUAD · 2012 to 2014
$715k
A Molecular Marker for Cardiac Autonomic DysfunctionR21DK079622 · NIDDK · TUFTS MEDICAL CENTER · PI PARK, HO-JIN · 2007 to 2008
$403k
NHLBI NIH HHS HL-069770NHLBI NIH HHS R00 HL105574NHLBI NIH HHS R00-HL-105574NHLBI NIH HHS R01-HL-074876NIDDK NIH HHS R21-DK 079622
6 · The paper itself

Abstract

Although a reduction in the high-frequency (HF) component of heart rate variability (HRV) is a major complication of diabetes and a risk factor for sudden death, its relationship to ventricular tachycardia (VT) is unknown. We developed a mouse model for the study of VT and its relationship to changes in HRV in the Akita type 1 diabetic mouse. Programmed ventricular stimulation of anesthetized mice demonstrated that Akita mice were more inducible for VT compared with wild-type mice: 78.6% versus 28.6% (P = 0.007). Optical mapping of perfused hearts demonstrated multifocal breakthroughs that occasionally gave rise to short-lived rotors consistent with focal initiation and maintenance of VT. Treatment of Akita mice with pravastatin, which had been previously shown clinically to decrease ventricular ectopy and to increase HRV, decreased the inducibility of VT: 36.8% compared with 75.0% with placebo treatment (P = 0.022). The HF fraction of HRV was reduced in Akita mice (48.6 ± 5.2% vs. 70.9 ± 4.8% in wild-type mice, P = 0.005) and was increased compared with placebo treatment in pravastatin-treated mice. Pretreatment of Akita mice with the muscarinic agonist carbamylcholine or the β-adrenergic receptor blocker propranolol decreased the inducibility of VT (P = 0.001). In conclusion, the increased inducibility of focally initiated VT and reduced HF fraction in Akita mice were partially reversed by both pravastatin treatment and pharmacologic reversal of parasympathetic dysfunction. In this new animal model for the study of the pathogenesis of VT in type 1 diabetes, pravastatin may play a role in the prevention of VT by attenuating parasympathetic dysfunction.

Indexed as

AnimalsDiabetes Mellitus, Type 1Disease Models, AnimalHeart RateHydroxymethylglutaryl-CoA Reductase InhibitorsMicePravastatinTachycardia, VentricularHydroxymethylglutaryl-CoA Reductase InhibitorsPravastatinsecondary effects of diabetesstatinstype 1 diabetesventricular tachycardia

Identifiers

PMID24163078
PMCPMC3882547
OpenAlexW2108671364

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.