Abstract 11715: The Effect of Cell Therapy versus Noncellular Biomaterial Implantation on Cardiac Structure and Function Following Myocardial Infarction
Background: Although numerous studies demonstrated that localized delivery of either cells or biomaterials improved post-infarction cardiac function, underlying mechanisms for this effect remain unclear. We performed a comparison in our laboratory of the effect of fetal/neonatal cardiac cell transplantation, versus biomaterial (collagen/extracellular matrix) implantation therapy in rat myocardial infarction model, specifically comparing effects on cardiac structure and function.
METHODS: Rats with one-week-old myocardial infarction were used in 5 studies. The rats received intramyocardial injection of immature (fetal/neonatal) cardiac cells (n=43), biomaterial (n=29), or control vehicle (n=81), and were followed for 4 weeks to 10 months. The end points included infarct wall thickness, neovascularization, infarct wall motion and left ventricular (LV) ejection fraction.
RESULTS: Transplanted immature cardiac cells increased infarct wall thickness by 0.28 mm on average and increased LV ejection fraction by 5.8 (absolute percentage points) compared to controls (p<0.05 in all studies). Biomaterial implantation also increased infarct wall thickness by 0.20 mm and LV ejection fraction by 6 compared to controls (p<0.05 in all studies). Both cell and biomaterial treatment prevented paradoxical LV systolic bulging. They both decreased LV expansion index (1.48 for controls; 0.91 for cells; 0.92 for biomaterials; p<0.05 vs controls for all studies). Both cells and biomaterials reduced LV volume compared to vehicle (by 14% and 5%, respectively). Cell transplantation significantly improved neo-angiogenesis at 4 weeks after treatment, however, neovascularization was not detected within the implanted biomaterials.
CONCLUSIONS: Both cell and biomaterial treatment had similar beneficial effects on cardiac structure (increasing of infarct wall thickness and preventing of infarct expansion) and function (preventing paradoxical LV systolic bulging and improving LV ejection fraction). However, only cells appeared to benefit neovascularization within the infarct area. The mechanism for improvement of cardiac structure and function may largely be a passive mechanical phenomenon, which is not dependent upon enhanced angiogenesis.
- © 2012 by American Heart Association, Inc.