Patient-Specific Mechanical Analysis of Atherosclerotic Arteries with Resolved Pre- and Post-Rupture Intraplaque Composition
- Author(s): Leach, Joseph R.
- Advisor(s): Saloner, David
- et al.
Atherosclerotic plaque rupture at the carotid bifurcation is a major cause of stroke. While plaques vulnerable to rupture progress under significant influence from the local biochemical environment, and often experience a chronic or acute inflammatory process, mechanical forces are also of importance. Finite element studies have been conducted on models of diseased vessels to elucidate the effects of lesion characteristics on the stresses within plaque materials. Ultimately, it is hoped that patient-specific biomechanical analyses may serve as a robust clinical tool to assess the rupture potential for any particular lesion, allowing better stratification of patients into the most appropriate treatment plans.
The relationship between various mechanical descriptors such as stresses or strains and rupture vulnerability is incompletely known, however, and the patient-specific utility of biomechanical analyses is thus unclear. Progress on this front has been impeded by several distinct challenges. First, data on in vivo plaque rupture, under normal physiologic conditions, is unfortunately sparse. Second, methods for building highly realistic patient-specific finite element models of diseased vessels are lacking, and the simplifications common in the literature may render current analyses inadequate. Third, the time and computational resource demands of realistic analyses including fluid-structure interaction prohibit large-scale investigation.
In this dissertation, a strategy for accurate and efficient patient-specific modeling of the atherosclerotic carotid bifurcation is developed. We present surface-based methods for rapid yet detailed geometric discretization of image-derived vessel features, allowing for highly resolved stress calculations. A two-stage solution method is also introduced to compliment the unstructured meshes representing different tissues, allowing sizeable reductions in the time and computing resources needed for arterial fluid-structure interaction simulations.
Using these methods, we present a fluid-structure interaction analysis of a patient for whom pre- and post-rupture imaging data is available. The effects of image imprecision on the calculated stress fields are characterized to further elucidate challenges of image-based modeling. We find that plaque rupture location and extent, derived from post-rupture imaging data, correspond well to a region of elevation in first principal stress within the fibrous plaque layer of the lesion.