Abstract:
This study provides new model of pulsatile flow in the pulmonary circulation in health and pulmonary hypertensive disease. Structural vascular remodeling typical of pulmonary hypertensive disease was implemented in the model by progressively altering the mechanical properties of the arterial geometry and progressively increasing the inlet pulse pressure (PP). The transmission of PP throughout the tree was shown to increase in advanced stages of disease, creating the potential for a `vicious-cycle' of damage to vasculature. Wall shear stress (WSS) was shown to be highest in the terminal arteries of the model and increased significantly with disease. A further trend observed in WSS results was that high WSS values began to `climb' the arterial tree towards the proximal vessels as disease progressed. This suggests a link between WSS and distal remodeling in pulmonary hypertensive disease, which initiates in the small muscular arteries and arterioles and spreads into larger arteries as the disease progresses.
