Evidence map›Paper›PMID 26254335›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Long-term physiological T3 supplementation in hypertensive heart disease in rats.

Nathan Y Weltman, Christine J Pol, Youhua Zhang, Yibo Wang, Adrienne Koder, Sarah Raza, Riccardo Zucchi, Alessandro Saba, Daria Colligiani, A Martin Gerdes

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

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  11. Review
  12. Cardioprotection and thyroid hormones.Heart failure reviews · 2016
    Review
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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 3 institutions in 2 countries.

Nathan Y WeltmanDepartment of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota;
Christine J PolDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and.
Youhua ZhangDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and.
Yibo WangDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and.
Adrienne KoderDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and.
Sarah RazaDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and.
Riccardo ZucchiUniversity of Pisa, Dipartimento di Scienze dell'Uomo e dell'Ambiente, University of Pisa, Pisa, Italy.
Alessandro SabaUniversity of Pisa, Dipartimento di Scienze dell'Uomo e dell'Ambiente, University of Pisa, Pisa, Italy.
Daria ColligianiUniversity of Pisa, Dipartimento di Scienze dell'Uomo e dell'Ambiente, University of Pisa, Pisa, Italy.
A Martin GerdesDepartment of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, New York; and agerdes@nyit.edu.
New York Institute of Technology · USUniversity of Pisa · ITUniversity of South Dakota · US

Funding

Low Thyroid function and myocardial infarctionR01HL103671 · NHLBI · NEW YORK INST OF TECHNOLOGY · PI GERDES, ANTHONY MARTIN · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL103671NHLBI NIH HHS R01-HL-103671
6 · The paper itself

Abstract

Animal studies suggest that hypertension leads to cardiac tissue hypothyroidism, a condition that can by itself lead to heart failure. We have previously shown that short-term thyroid hormone treatment in Spontaneously Hypertensive Heart Failure (SHHF) rats near heart failure is beneficial. This study tested the hypothesis that therapeutic, long-term T3 treatment in SHHF rats can prevent or attenuate cardiac dysfunction. Female SHHF rats were treated orally with a physiological T3 dose (0.04 μg/ml) from 12 to 24 mo of age. Age-matched female SHHF and Wistar-Kyoto rats served as hypertensive and normotensive controls, respectively. SHHF rats had reduced serum free thyroid hormone levels and cardiac tissue T3 levels, LV dysfunction, and elevated LV collagen content compared with normotensive controls. Restoration of serum and cardiac tissue thyroid hormone levels in T3-treated rats was associated with no change in heart rate, but strong trends for improvement in LV systolic function and collagen levels. For instance, end-systolic diameter, fractional shortening, systolic wall stress, and LV collagen levels were no longer significantly different from controls. In conclusion, longstanding hypertension in rats led to chronic low serum and cardiac tissue thyroid hormone levels. Long-term treatment with low-dose T3 was safe. While cardiac dysfunction could not be completely prevented in the absence of antihypertensive treatment, T3 may offer additional benefits as an adjunct therapy with possible improvement in diastolic function.

Indexed as

AnimalsCollagenFemaleHeartHeart FailureHeart VentriclesHypertensionHypothyroidismMyosinsRandom AllocationRatsRats, Inbred SHRRats, Inbred WKYThyroxineTriiodothyronineVentricular Dysfunction, LeftCollagenMyosinsThyroxineTriiodothyroninefibrosisheart failurehypertensionleft ventriclethyroid hormone

Identifiers

PMID26254335
PMCPMC4591362
OpenAlexW2343460128

What OpenQuestion holds

Textmetadata
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.