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Related Experiment Video

Updated: Feb 9, 2026

A Pulmonary Trunk Banding Model of Pressure Overload Induced Right Ventricular Hypertrophy and Failure
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Multiscale structure-function relationships in right ventricular failure due to pressure overload.

Tik-Chee Cheng1, Jennifer L Philip1,2, Diana M Tabima1

  • 1Department of Biomedical Engineering, University of Wisconsin-Madison College of Engineering , Madison, Wisconsin.

American Journal of Physiology. Heart and Circulatory Physiology
|June 9, 2018
PubMed
Summary
This summary is machine-generated.

Right ventricular failure (RVF) involves structural changes like hypertrophy and fibrosis, impacting heart function. This study links mitochondrial abnormalities to increased oxygen consumption and reduced efficiency in RVF.

Keywords:
mitochondriamyocardial energeticspressure-volume loopspulmonary artery bandingright ventricular failure

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Area of Science:

  • Cardiology
  • Physiology
  • Pathology

Background:

  • Right ventricular failure (RVF) is a primary cause of mortality in pulmonary hypertension.
  • RVF is characterized by structural changes including hypertrophy, fibrosis, and mitochondrial abnormalities.
  • The relationship between multiscale structural and functional changes in RVF remains underexplored.

Purpose of the Study:

  • To investigate the functional consequences of multiscale structural remodeling in RVF.
  • To explore the correlations between organ, tissue, and organelle level changes and RV function.
  • To elucidate the impact of mitochondrial alterations on ventricular energetics in RVF.

Main Methods:

  • Induction of RVF in male rats via pulmonary artery banding (PAB).
  • Invasive hemodynamic measurements to assess RV ejection fraction and cardiac output.
  • Histological analysis for fibrosis quantification and transmission electron microscopy for mitochondrial ultrastructure.

Main Results:

  • PAB induced RVF with significantly reduced ejection fraction and cardiac output.
  • RV hypertrophy correlated with increased contractility, while fibrosis was linked to diastolic dysfunction.
  • Mitochondrial abnormalities were associated with increased oxygen consumption and reduced mechanical efficiency.

Conclusions:

  • Multiscale RV remodeling, including mitochondrial alterations and fibrosis, significantly impacts RV function in pressure-overload-induced RVF.
  • Fibrosis is directly correlated with diastolic dysfunction, and mitochondrial changes are linked to impaired ventricular energetics.
  • This study provides critical insights into the mechanisms underlying RVF, connecting organelle-level changes to organ-level dysfunction.