Date of Award

Spring 2010

Document Type

Thesis

Degree Name

Doctor of Philosophy (PhD)

Department

Mechanical Engineering

First Advisor

Robin Shandas

Second Advisor

Kendall S. Hunter

Third Advisor

Wei Tan

Abstract

Pulmonary arterial hypertension (PAH) is an important determinant of morbidity and mortality in children with congenital heart disease. Previous and current investigations on pulmonary vascular stiffness (PVS), input impedance and right ventricular (RV) power have found PVS to be an important contributor to flow energy power, and thus, afterload. However these investigations focus on the analysis of clinical data, which requires long term observation and inspection of a great number of individuals, whose clinical pathogenesis may not be the same. It is difficult if not impossible to vary stiffness/resistance in an example system within clinical or animal studies, and it is difficult to separate the contributing effects of stiffness and flow from clinical results.

Here we proposed numerical artery models based on the clinically and experimentally measured parameters for children and calves, to determine if they could offer clinically relevant hemodynamic information on the circulation. With non-specific on pulmonary vascular structure information, we can create a realistic computational simulation environment, which can be used to test our theories regarding various associations between hemodynamic and mechanical variables in the human or animal pulmonary vasculature. These models could be useful in helping evaluate the efficacy of newly designed therapies that may target particular components of RV afterload such as proximal vascular stiffness or distal vasoconstriction, and as a tool to examine disease progression, and others.

Through these types of studies, we will obtain a better understanding of how structural adaptations that occur in pulmonary vascular disease affect hemodynamics, vascular function and subsequently impedance and right ventricular (RV) afterload. Several achievements are obtained: 1) effect of these experimental measurable parameters on hemodynamics when PAH progresses to worsen; 2) hemodynamics play an important role in progressing PAH; 3) provide possible prediction of WSS, impedance, RV power and pulsatility of hemodynamics based on easily obtained measurable parameters; 4) decreasing or reversing proximal vascular remodeling can provide treatment of PAH as well as decrease mean pressures (mPAP). Overall, these results suggest a close association between PVS, PVR and hemodynamics, that hemodynamics may play an important role in progressing PAH, and that treatments should target decreasing or reversing upstream vascular remodeling in addition to decreasing mean pressures.

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