Cardio-omentopexy Reduces Cardiac Fibrosis and Heart Failure After Experimental Pressure Overload.

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.