| dc.description.abstract | Despite the many advances in medicine, bronchopulmonary dysplasia (BPD) remains a major obstacle for survival in neonates. Recent studies have fostered interests in the effects of hemodynamics on the disease’s progression and in potential treatment strategies to optimize those effects on pulmonary vascular development. We proposed the application of a stent to alter wave phenomena in the pulmonary vasculature and utilized a monocroatiline porcine model of another pulmonary vascular disease, pulmonary arterial hypertension (PAH), to identify the hemodynamic attributes which could be altered to ameliorate the progression of these diseases. We then simulated blood flow through five, simple finite element vessel models to determine the effects of stents on wave propagation. Our porcine model showed a significant increase in the impedance moduli (|Z|), a 200% increase in the characteristic impedance (ZC), and a 30% decrease in pulmonary vascular resistance (PVR) in the diseased subjects (n=4) compared to the controls (n=3). In our simulations, we noticed a large decrease in the |Z| and a 50-70% decrease in ZC with the deployment of a stent. We also noticed an increased difference in |Z| and ZC between the upstream and downstream ends of the vessel indicating that stiffened regions of a vessel created by a stent do alter wave propagation within the vessel. In our porcine models, we concluded that the changes in the ZC could reflect the remodeling of the pulmonary vasculature in response to the disease’s progression, and, since the PVR was lower than the controls in these subjects, we hypothesized that the remodeling of the vasculature has not progressed enough to see the increase in mean pressure and PVR yet. This observation could have indicated that the disease was in an earlier stage that is synonymous with the early, undetected stages of PAH in humans. We also concluded that the small observed changes in the pressure and flow in our simulations, small size of the stent, and the current stent complications would prevent them from provoking an adequate global response to mediate the disease state and its progression. | en |
