Plaque rupture with superimposed thrombosis is the primary cause of acute coronary syndromes of unstable angina, myocardial infarction and sudden death. Although intensive studies in the past decade have shed light on the mechanism that causes unstable atheroma, none has directly addressed the clinical observation that most myocardial infarction (MI) patients have moderate stenoses (less than 50%). Considering the important role the arterial wall compliance and pulsitile blood flow play in atheroma rupture, fluid-structure interaction (FSI) phenomenon has been of interest in recent studies. In this thesis, the impact is investigated numerically of coupled blood flow and structural dynamics on coronary plaque rupture. The objective is to determine a unique index that can be used to characterize plaque rupture potential. The FSI index, developed in this study for the first time derives from the theory of buckling of thin-walled cylinder subjected to radial pressure. Several FSI indices are first defined by normalizing the predicted hemodynamic endothelial shear stress by the structural stresses, specifically, by the maximum principal stress (giving the ratio ), and the Von Mises stress (giving the ratio ). The predicted at the location of maximum (i.e { }) denoted , is then chosen to characterize plaque rupture through systematic investigation of a variety of plaque characteristics and simulated patient conditions. The conditions investigated include varying stenosis levels ranging from 20% to 70%, blood pressure drop ranging from 3125 Pa/m to 9375 Pa/m, fibrous cap thickness ranging from to , lipid pool location ranging from the leading to the trailing edge of plaque, lipid pool volume relative to stenosis volume ranging from 24% to 80%, Calcium volume relative to stenosis volume ranging from 24% to 80% and arterial remodeling. The predicted varies with the stenosis severity and indicates that the plaques investigated are prone to rupture at approximately 40-45% stenosis levels. It predicts that high pressure significantly lowers the threshold stenosis rate for plaque rupture. In addition, the plaque potential to rupture increases for relatively thin fibrous cap, lipid core located near the leading plaque shoulder, and dramatically for relative lipid pool volume above 60%. However, calcium deposit has marginal effect on plaque rupture. Overall, the predicted results are consistent with clinical observations, indicating that the has the potential to characterize plaque rupture when properly established. In the appendix, the unsteady flow in a collapsible tube model of a diseased artery is solved analytically. The novelty of our approach is that the set of governing equations is reduced to a single integro-differential equation in the transient state. The equation was solved using the finite difference method to obtain the pressure and compliant wall behavior. The analytical approach is less computer-intensive than solving the full set of governing equations. The predicted membrane deflection is quite large at low inlet velocity, suggesting possible approach to breakdown in equilibrium. As the transmural pressure increases with wall deflection, bulges appear at the ends of the membrane indicating critical stage of stability, consistent with previous studies. An increase in wall thickness reduces the wall deflection and ultimately results in its collapse. The collapse is due to breakdown in the balance of wall governing equation. An increase in internal pressure is required to maintain membrane stability.
| Identifer | oai:union.ndltd.org:ucf.edu/oai:stars.library.ucf.edu:etd-2071 |
| Date | 01 January 2006 |
| Creators | Teuma-Melago, Eric |
| Publisher | STARS |
| Source Sets | University of Central Florida |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | Electronic Theses and Dissertations |
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