Vulnerability of atherosclerotic plaques: risk analysis using computational mechanics

  • Kiousis, Dimitrios, (Teilnehmer (Co-Investigator))
  • Holzapfel, Gerhard (Teilnehmer (Co-Investigator))

Projekt: Arbeitsgebiet

Beschreibung

Cardiovascular diseases are one of the leading causes of mortality in the developed world. Most of them are caused by atherosclerosis, a common disorder of the arteries. Fat, cholesterol and other substances accumulate in the arterial walls and form atheromas and plaques. Eventually, this fatty tissue can erode the wall of the artery, diminish its elasticity and interfere with the blood flow. Atherosclerosis is triggered by a number of risk factors. These include smoking, diabetes, obesity, high blood cholesterol, a diet high in fats and having a personal or family history record of heart disease. Two of the key early stages in the development of atherosclerosis are: lipoprotein oxidation and inflammation. Inflammation plays an important role, since it can lead to an early atheroma. From this point on, the stenosis can either progress to a stabilized or vulnerable plaque. There are treatments available that may stabilize a vulnerable plaque. If they are not successful though, the plaque may fracture, leading to thrombosis. This may consequently cause debris to migrate downstream within an artery, which is a common cause of myocardial infarction and stroke. Debris can also form around the plaque deposits, further interfering with blood flow and posing added danger if they rupture and travel towards the heart, lungs or brain. However, the plaque may heal again, thereby leaving a severely narrow lumen with a thick fibrous intima. When blood flow in the arteries to the heart muscle becomes severely restricted, it leads to symptoms like chest pain.
There is general agreement that the majority of acute cardiovascular syndromes is caused by vulnerable plaques. Hence, identification of high-risk plaques is considered a primary objective of vascular diagnostics. Earlier studies showed that plaque cap thickness and lipid core size are essential determinants of plaque stability. Considering the rapid developments in arterial wall imaging, based mainly on magnetic resonance imaging and intravascular ultrasound, detection of these micro-morphological characteristics appears to be a promising diagnostic strategy. Yet, restriction to morphological criteria is not an approach likely to provide a highly predictive basis for the diagnosis of vulnerable plaques. The reason for this is that, in general, it is impossible to assess the stability of a structure solely by considering its geometry. Stability analysis requires additional information of mechanical loads applied, mechanical properties of involved materials, and the associated mechanical stresses occurring in the structural components.
Previous mechanical studies have demonstrated the coincidence of plaque rupture sites and regions of circumferential stress concentrations. These landmark studies supported the intuitive hypothesis that the acute process of plaque fracture is caused by high mechanical stresses, which exceed the ultimate tensile strength of the fibrous cap. Consequently, computational mechanics may provide significant contributions for the understanding, identification and treatment of vulnerable plaques.
The objective of the project is to design realistic three-dimensional (3D) morpho-mechanical models of diseased arteries, which are based on (i) high-resolution MR imaging of human atherosclerotic lesions and (ii) mechanical testing of their isolated tissue components, and to present a computational methodology to identify high-risk plaques. Nonlinear finite element methods are used for the analysis of plaque mechanics. The potential of the proposed approach for the assessment of plaque stability is demonstrated by means of computational case studies for one human diseased artery. The present approach allows detailed studies of the mechanical effects of blood pressure elevations and variations of the stiffness of the individual plaque components on the mechanical behavior of the atherosclerotic lesion.
StatusAbschlussdatum
Tatsächlicher Beginn/ -es Ende1/02/0731/12/09