Background: This study was designed to determine whether tissue engineering could be used to reduce ventricular remodeling in a rat model of non-transmural, non-ST-elevation myocardial infarction. Methods: We grafted an acellular 3-dimensional (3D) collagen type 1 scaffold (solid porous foam) onto infarcted myocardium in rats. Three weeks after grafting, the scaffold was integrated into the myocardium and retarded cardiac remodeling by reducing left ventricular (LV) dilation. The LV inner and outer diameters, measured at the equator at zero LV pressure, decreased (p < 0.05) from 11,040 ± 212 to 9,144 ± 135 μm, and 13,469 ± 187 to 11,673 ± 104 μm (N = 12), after scaffold transplantation onto infarcted myocardium. The scaffold also shifted the LV pressure-volume curve to the left toward control and induced neo-angiogenesis (700 ± 25 vs 75 ± 11 neo-vessels/cm2, N = 5, p < 0.05). These vessels (75 ± 11%) ranged in diameter from 25 to 100 μm and connected to the native coronary vasculature. Systemic treatment with granulocyte-colony stimulating factor (G-CSF), 50 μg/kg/day for 5 days immediately after myocardial injury, increased (p < 0.05) neo-vascular density from 700 ± 25 to 978 ± 57 neo-vessels/cm2. Conclusions: A 3D collagen type 1 scaffold grafted onto an injured myocardium induced neo-vessel formation and reduced LV remodeling. Treatment with G-CSF further increased the number of vessels in the myocardium, possibly due to mobilization of bone marrow cells.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Cardiology and Cardiovascular Medicine