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Updated: Feb 25, 2026
Rat Model of Right-Sided Cardiac Remodeling and Arrhythmia Using Pulmonary Artery Banding
Published on: August 30, 2024
Cardiac Progenitor Cells Enhance Neonatal Right Ventricular Function After Pulmonary Artery Banding
Brody Wehman1, Nicholas Pietris2, Grace Bigham1
1Division of Cardiac Surgery, University of Maryland School of Medicine, Baltimore, Maryland.
Insights
Cardiac progenitor cells (CPCs) improved right ventricular (RV) function in a preclinical model of RV dysfunction. This study demonstrates the potential of CPCs for treating congenital heart disease involving RV issues.
Area of Science:
- Regenerative Medicine
- Cardiovascular Research
- Congenital Heart Disease
Background:
- C-kit+ cardiac progenitor cells (CPCs) show promise in adult heart disease.
- CPCs have not been studied in preclinical models of right ventricular (RV) dysfunction, common in congenital heart disease.
Purpose of the Study:
- To evaluate the efficacy of human c-kit+ CPCs in a preclinical model of RV dysfunction.
- To assess the impact of CPCs on RV performance and myocardial structure in neonatal pigs.
Main Methods:
- Human c-kit+ CPCs were generated from atrial appendage biopsies.
- Pulmonary artery banding induced RV dysfunction in immunosuppressed swine.
- CPCs or control were injected into the RV free wall; animals were studied for 30 days.
Main Results:
- CPC treatment led to less RV dilatation and improved RV fractional area of change.
- Enhanced RV myocardial strain (longitudinal strain and strain rate) was observed in the CPC group.
- CPC injection increased arteriole formation and reduced fibrosis in the RV free wall.
Conclusions:
- Intramyocardial CPC injection improved RV performance in a neonatal pig model of RV dysfunction.
- This preclinical model is valuable for further investigating CPCs for congenital heart disease.
Background:
C-kit+ cardiac progenitor cells (CPCs) have been shown to be safe and effective in large-animal models and in an early-phase clinical trial for adult patients with ischemic heart disease. However, CPCs have not yet been evaluated in a preclinical model of right ventricular (RV) dysfunction, which is a salient feature of many forms of congenital heart disease.
Methods:
Human c-kit+ CPCs were generated from right atrial appendage biopsy specimens obtained during routine congenital cardiac operations. Immunosuppressed Yorkshire swine (6 to 9 kg) underwent pulmonary artery banding to induce RV dysfunction. Thirty minutes after banding, pigs received intramyocardial injection into the RV free wall with c-kit+ CPCs (1 million cells, n = 5) or control (phosphate-buffered saline, n = 5). Pigs were euthanized at 30 days postbanding.
Results:
Banding was calibrated to a consistent rise in the RV-to-systemic pressure ratio across both groups (postbanding: CPCs = 0.76 ± 0.06, control = 0.75 ± 0.03). At 30 days postbanding, the CPCs group demonstrated less RV dilatation and a significantly greater RV fractional area of change than the control group (p = 0.002). In addition, measures of RV myocardial strain, including global longitudinal strain and strain rate, were significantly greater in the CPCs group at 4 weeks relative to control (p = 0.004 and p = 0.01, respectively). The RV free wall in the CPCs group demonstrated increased arteriole formation (p < 0.0001) and less myocardial fibrosis compared with the control group (p = 0.02).
Conclusions:
Intramyocardial injection of c-kit+ CPCs results in enhanced RV performance relative to control at 30 days postbanding in neonatal pigs. This model is important for further evaluation of c-kit+ CPCs, including long-term efficacy.
