Evidence map›Paper›PMID 23056390›Full record

ArticlePloS one2012

Longstanding hyperthyroidism is associated with normal or enhanced intrinsic cardiomyocyte function despite decline in global cardiac function.

Nathan Y Weltman, Dajun Wang, Rebecca A Redetzke, A Martin Gerdes

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cardiac manifestations in hyperthyroidism.Reviews in cardiovascular medicine · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
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  13. U-shaped association between serum free triiodothyronine and recurrence of atrial fibrillation after catheter ablation.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2018
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Isolation and physiological analysis of mouse cardiomyocytes.Journal of visualized experiments : JoVE · 2014
    Article
  20. 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

4 authors at 3 institutions in 1 country.

Nathan Y WeltmanDepartment of Basic Biomedical Sciences, Sanford School of Medicine at the University of South Dakota, Sioux Falls, South Dakota, United States of America.
Dajun Wang
Rebecca A Redetzke
A Martin Gerdes
University of South Dakota · USNew York Institute of Technology · USSanford Research · US

Funding

The ubiquitin-proteasome system in cardiac remodelingP20RR017662 · NCRR · UNIVERSITY OF SOUTH DAKOTA · PI HARMON, ERIN B · 2002 to 2011
$18.7M
Thyroid hormone regulation of vasculature in adult myocardiumR01HL093160 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI GERDES, ANTHONY MARTIN · 2009 to 2010
$814k
NCRR NIH HHS 2P20RR017662-06A1NCRR NIH HHS P20 RR017662NHLBI NIH HHS R01 HL093160NHLBI NIH HHS R01 HL093160-01A1
6 · The paper itself

Abstract

Thyroid hormones (THs) play a pivotal role in cardiac homeostasis. TH imbalances alter cardiac performance and ultimately cause cardiac dysfunction. Although short-term hyperthyroidism typically leads to heightened left ventricular (LV) contractility and improved hemodynamic parameters, chronic hyperthyroidism is associated with deleterious cardiac consequences including increased risk of arrhythmia, impaired cardiac reserve and exercise capacity, myocardial remodeling, and occasionally heart failure. To evaluate the long-term consequences of chronic hyperthyroidism on LV remodeling and function, we examined LV isolated myocyte function, chamber function, and whole tissue remodeling in a hamster model. Three-month-old F1b hamsters were randomized to control or 10 months TH treatment (0.1% grade I desiccated TH). LV chamber remodeling and function was assessed by echocardiography at 1, 2, 4, 6, 8, and 10 months of treatment. After 10 months, terminal cardiac function was assessed by echocardiography and LV hemodynamics. Hyperthyroid hamsters exhibited significant cardiac hypertrophy and deleterious cardiac remodeling characterized by myocyte lengthening, chamber dilatation, decreased relative wall thickness, increased wall stress, and increased LV interstitial fibrotic deposition. Importantly, hyperthyroid hamsters demonstrated significant LV systolic and diastolic dysfunction. Despite the aforementioned remodeling and global cardiac decline, individual isolated cardiac myocytes from chronically hyperthyroid hamsters had enhanced function when compared with myocytes from untreated age-matched controls. Thus, it appears that long-term hyperthyroidism may impair global LV function, at least in part by increasing interstitial ventricular fibrosis, in spite of normal or enhanced intrinsic cardiomyocyte function.

Indexed as

AnimalsCardiomegalyCells, CulturedCricetinaeEchocardiographyHyperthyroidismMyocytes, CardiacThyroid HormonesVentricular RemodelingThyroid Hormones

Identifiers

PMID23056390
PMCPMC3464244
OpenAlexW2059786731

What OpenQuestion holds

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LicenceCC BY
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.