Related Experiment Video
Updated: May 11, 2026

A Murine Model of Pressure Overload-Induced Right Ventricular Hypertrophy and Failure by Pulmonary Trunk Banding
Published on: June 14, 2024
Acute right ventricular pressure overload compromises left ventricular function by altering septal strain and
Jason Chua1, Wei Zhou, Jonathan K Ho
1Department of Anesthesiology, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California.
Acute right ventricular pressure overload impairs left ventricular function by altering septal strain and apical rotation. This study reveals key mechanisms linking right ventricular dysfunction to reduced cardiac performance.
Area of Science:
- Cardiology
- Physiology
- Echocardiography
Background:
- Right ventricular (RV) dysfunction is known to impact left ventricular (LV) performance, but underlying mechanisms are unclear.
- Speckle-tracking echocardiography highlights the importance of strain and rotational dynamics for LV function.
Purpose of the Study:
- To investigate alterations in septal strain and LV rotational dynamics during acute RV pressure overload (RVPO).
- To determine the impact of these changes on overall cardiac performance.
Main Methods:
- Anesthetized pigs underwent pulmonary artery banding to induce RVPO.
- Intraventricular pressure-volume loops and 2D echocardiography were used to assess LV and RV function at baseline and during RVPO.
- Speckle-tracking analysis evaluated LV global circumferential strain, septal strain, and rotational dynamics.
Main Results:
- RVPO significantly decreased LV end-systolic elastance, systolic pressure change, end-diastolic volume, and cardiac output.
- These functional declines correlated with reduced LV global circumferential strain, apical rotation, and peak untwisting rate.
- RVPO specifically impaired septal radial and circumferential strain on both the LV and RV sides of the septum.
Conclusions:
- Acute RVPO primarily impairs LV performance by altering septal strain and apical rotation.
- These findings elucidate mechanisms connecting RV dysfunction to compromised LV function and overall cardiac output.
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