Related Experiment Video
Updated: Mar 1, 2026
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
Published on: March 1, 2022
Left Ventricular Fibrosis and Systolic Hypertension Persist in a Repaired Aortic Coarctation Model
Jie Liu1, Douglas Drak2, Anish Krishnan1
1Department of Physiology, The University of Sydney, Camperdown, Australia.
Insights
Even after successful coarctation of the aorta (CoA) repair, rats showed persistent hypertension and left ventricular (LV) fibrosis. These cardiovascular issues developed without significant changes in LV hemodynamics or gene expression.
Area of Science:
- Cardiovascular Research
- Animal Models
- Medical Science
Background:
- Coarctation of the aorta (CoA) repair in early life does not prevent later cardiovascular complications.
- Systemic hypertension and left ventricular (LV) dysfunction are common in patients with repaired CoA.
- The underlying pathogenesis of these late complications remains unclear.
Purpose of the Study:
- To investigate the long-term cardiovascular consequences of repaired coarctation of the aorta (CoA) in an animal model.
- To determine if repaired CoA leads to persistent hypertension and LV dysfunction.
- To explore the molecular and histological changes in the left ventricle after CoA repair.
Main Methods:
- Three-week-old rats underwent transverse aortic constriction (TAC) or sham operation, with constriction release after 3 weeks.
- Hemodynamic assessment, LV gene profiling, and histologic analysis were performed 25 weeks post-repair.
- Key parameters measured included central systolic pressure, LV pressure, LV mass, myocyte size, and collagen deposition.
Main Results:
- Repaired CoA rats exhibited significantly elevated central systolic pressure compared to shams (p < 0.05).
- A significant 2-fold increase in LV collagen deposition was observed in repaired CoA rats (p < 0.001).
- No significant differences were found in maximum LV pressure, LV mass, or myocyte size between groups.
Conclusions:
- Repaired coarctation of the aorta (CoA) leads to persistent relative hypertension and LV fibrosis in this animal model.
- These late cardiovascular consequences occur despite successful early relief of the aortic constriction.
- Abnormal LV fibrosis persists even without significant alterations in LV hemodynamics or gene expression.
Background:
Despite successful repair in early life, patients with coarctation of the aorta (CoA) are predisposed to several cardiovascular complications in later life related to systemic hypertension or left ventricular (LV) dysfunction, or both, the pathogenesis of which is unclear.
Methods:
Three-week-old Sprague-Dawley rats underwent transverse aortic constriction (TAC) or a sham operation, with release of the constriction 3 weeks later. Twenty-five weeks after the repair operation, animals underwent hemodynamic assessment, LV gene profiling, and histologic analysis.
Results:
Animals with repaired aortic constriction exhibited a significantly elevated central systolic pressure (116 ± 5 mm Hg vs 103 ± 4 mm Hg; p < 0.05) despite the absence of any significant pressure gradient across the former constriction site compared with shams (5 ± 4 mm Hg vs 0 ± 2 mm Hg; p = 0.2). They also had more than a 2-fold increase in LV collagen deposition (4.86% ± 0.24% vs 2.40% ± 0.18%; p < 0.001). However, no significant differences were noted between the groups in maximum LV pressure (116 ± 3 mm Hg vs 107 ± 3 mm Hg; p = 0.1), LV mass indexed to tibial length (p = 0.07), or myocyte size. There was no significant differential expression of hypertrophy or fibrosis-related genes in the left ventricles of the repaired animals compared with shams.
Conclusions:
Despite successful early relief of simulated CoA in early life, relative hypertension and LV fibrosis were demonstrable late consequences in this animal model. This abnormal fibrosis persists in the absence of altered LV hemodynamics and gene expression.
Related Concept Videos
01:29Heart Failure II: Pathophysiology
01:15Aortic Regurgitation I: Introduction