Evidence map›Paper›PMID 25164124›Full record

ArticleAnnals of biomedical engineering2014

Structural and mechanical adaptations of right ventricle free wall myocardium to pressure overload.

Michael R Hill, Marc A Simon, Daniela Valdez-Jasso, Will Zhang, Hunter C Champion, Michael S Sacks

Abstract read
In one paragraph

Article in Annals of biomedical engineering, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing 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

59 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Sex-dependent remodeling of right ventricular function in a rat model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

6 authors.

Michael R HillCenter for Cardiovascular Simulation, Institute for Computational Engineering and Sciences, Department of Biomedical Engineering, The University of Texas at Austin, 201 East 24th Street, University Station, C0200, POB 5.236, Austin, TX, 78712-0027, USA.
Marc A Simon
Daniela Valdez-Jasso
Will Zhang
Hunter C Champion
Michael S Sacks

Funding

Vascular Subphenotypes of Lung DiseaseP01HL103455 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHIVA, SRUTI · 2011 to 2020
$26.1M
Gene networks beyond organ boundaries; heart, lung and pulmonary vascular diseaseU01HL108642 · NHLBI · YALE UNIVERSITY · PI AHMAD, FERHAAN, BENOS, PANAGIOTIS V · 2011 to 2014
$2.2M
"A new computational model of right ventricular hypertrophy"F32HL117535 · NHLBI · UNIVERSITY OF TEXAS AT AUSTIN · PI HILL, MICHAEL R · 2013 to 2014
$76k
NHLBI NIH HHS 1F32 HL117535NHLBI NIH HHS F32 HL117535NHLBI NIH HHS P01 HL103455NHLBI NIH HHS P01HL103455NHLBI NIH HHS U01 HL108642NHLBI NIH HHS U01 HL108642-01
6 · The paper itself

Abstract

Right ventricular (RV) failure in response to pulmonary hypertension (PH) is a severe disease that remains poorly understood. PH-induced pressure overload leads to changes in the RV free wall (RVFW) that eventually results in RV failure. While the development of computational models can benefit our understanding of the onset and progression of PH-induced pressure overload, detailed knowledge of the underlying structural and biomechanical events remains limited. The goal of the present study was to elucidate the structural and biomechanical adaptations of RV myocardium subjected to sustained pressure overload in a rat model. Hemodynamically confirmed severe chronic RV pressure overload was induced in Sprague-Dawley rats via pulmonary artery banding. Extensive tissue-level biaxial mechanical and histomorphological analyses were conducted to assess the remodeling response in the RV free wall. Simultaneous myofiber hypertrophy and longitudinal re-orientation of myo- and collagen fibers were observed, with both fiber types becoming more highly aligned. Transmural myo- and collagen fiber orientations were co-aligned in both the normal and diseased state. The overall tissue stiffness increased, with larger increases in longitudinal vs. circumferential stiffness. The latter was attributed to longitudinal fiber re-orientation, which increased the degree of anisotropy. Increased mechanical coupling between the two axes was attributed to the increased fiber alignment. Interestingly, estimated myofiber stiffness increased while the collagen fiber stiffness remained unchanged. The increased myofiber stiffness was consistent with clinical results showing titin-associated increased sarcomeric stiffening observed in PH patients. These results further our understanding of the underlying adaptive and maladaptive remodeling mechanisms and may lead to improved techniques for prognosis, diagnosis, and treatment for PH.

Indexed as

AnimalsHeart VentriclesHypertension, PulmonaryMaleModels, CardiovascularMyocardiumPulmonary ArteryRats, Sprague-DawleyVentricular Pressure

Identifiers

PMID25164124
PMCPMC4241140

What OpenQuestion holds

Textmetadata
LicenceTDM
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.