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Updated: Feb 1, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Cardio-omentopexy Reduces Cardiac Fibrosis and Heart Failure After Experimental Pressure Overload
Jian Wang1, Qing-Jun Zhang2, Timothy J Pirolli1
1Department of Thoracic and Cardiovascular Surgery, University of Texas Southwestern Medical Center, Dallas, Texas.
Insights
Cardio-omentopexy significantly improved heart function in a rat model of left ventricular hypertrophy (LVH). This procedure reduced cardiac dilation, improved contractility, and decreased fibrosis, offering a potential therapeutic strategy for heart disease.
Area of Science:
- Cardiovascular Surgery
- Regenerative Medicine
- Cardiac Physiology
Background:
- The pedicled greater omentum shows promise in treating ischemic heart disease.
- The efficacy of cardio-omentopexy in pressure overload-induced left ventricular hypertrophy (LVH) remains unexplored.
Purpose of the Study:
- To investigate the impact of cardio-omentopexy on a rat model of LVH.
- To assess the effects of omentopexy on cardiac structure, function, and molecular markers in LVH.
Main Methods:
- Left ventricular hypertrophy (LVH) was induced in rats by ascending aortic banding.
- Survivors underwent either cardio-omentopexy or sham surgery.
- Echocardiography, gene expression, and histological analyses were performed 10 weeks post-procedure.
Main Results:
- Cardio-omentopexy significantly reduced LV end-systolic diameter, cardiomyocyte size, and myocardial fibrosis compared to controls.
- LV ejection fraction was preserved in the cardio-omentopexy group.
- Myocardial capillary density was increased, and fibrotic markers were decreased post-omentopexy.
Conclusions:
- Cardio-omentopexy effectively mitigated cardiac dilation, contractile dysfunction, and fibrosis in a pressure overload LVH model.
- The procedure maintained molecular indicators of cardiac contractile function.
- Omentopexy presents a potential therapeutic approach for managing LVH.
Background:
The pedicled greater omentum has been shown to offer benefit in ischemic heart disease for both animal models and human patients. The impact of cardio-omentopexy in a pressure overload model of left ventricular hypertrophy (LVH) is unknown.
Methods:
LVH was created in rats by banding the ascending aorta after right thoracotomy (n = 23). Sham surgery was performed in 12 additional rats. Six weeks after banding, surviving LVH rats were assigned to cardio-omentopexy by left thoracotomy (LVH+Om, n = 8) or sham left thoracotomy (LVH, n = 8). Sham rats also underwent left thoracotomy for cardio-omentopexy (Sham+Om, n = 6); the remaining rats underwent sham left thoracotomy (Sham, n = 6).
Results:
Echocardiography 10 weeks after cardio-omentopexy revealed LV end-systolic diameter, cardiomyocyte diamter, and myocardial fibrosis in the LVH group were significantly increased compared with the LVH+Om, Sham+Om, and Sham groups (p < 0.01). LV ejection fraction of the LVH group was lower than the LVH+Om group (p < 0.01). Gene expression analysis revealed significantly lower levels of sarcoendoplasmic reticulum calcium adenosine triphosphatase 2b in LVH rats than in the LVH+Om, Sham+Om, and Sham groups (p < 0.01). In contrast, collagen type 1 α 1 chain, lysyl oxidase-like protein 1, nuclear protein-1, and transforming growth factor- β1 in the LVH group were significantly higher than in the LVH+Om cohort (p < 0.01), consistent with a reduced fibrotic phenotype after omentopexy. Lectin staining showed myocardial capillary density of the LVH group was significantly lower than all other groups (p < 0.01).
Conclusions:
Cardio-omentopexy reduced cardiac dilation, contractile dysfunction, cardiomyocyte hypertrophy, and myocardial fibrosis, while maintaining other molecular indicators of contractile function in this LVH model.
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