Investigation of factors influencing pathological tortuosity of the carotid artery

Pathological tortuosity, coiling, and kinking of blood vessels are frequently associated with chronic diseases such as atherosclerosis, diabetes, and hypertension. In the carotid arteries, which supply blood to the brain, these structural abnormalities are linked to disturbances of cerebral circulation and an increased risk of ischemic stroke. A stroke is a sudden disruption of blood flow to the brain that can result in severe neurological deficits or death. Despite their clear clinical relevance, the mechanisms responsible for the initiation and progression of these vessel deformations remain largely unknown, limiting the ability to predict risk or guide treatment.

The aim of this project is to study the origin and temporal progression of pathological tortuosity at the carotid bifurcation. A deeper understanding of this pathology is expected to improve diagnostic strategies and help reduce ischemic stroke risk. Central to the project is the hypothesis that pathological vessel deformation develops through mechanisms similar to those underlying atherosclerosis. Specifically, patient-specific vessel geometry is assumed to induce local disturbances in blood flow, leading to endothelial cell dysfunction and pathological remodeling of the vessel wall. Over time, these processes may promote the formation of atherosclerotic deposits and blood clots, further impairing cerebral blood flow.

To address this hypothesis, the project adopts an interdisciplinary approach integrating medical imaging, patient-specific computational modeling, experimental biomechanics, and advanced numerical simulations. First, a digital database of patient-specific carotid geometries will be established using medical imaging data. These geometries will be analyzed using statistical shape modeling to identify characteristic variations associated with pathological deformation. Second, mechanical testing of vessel wall samples will characterize tissue properties and support realistic material modeling, while also improving our understanding of the underlying mechanobiological processes. Third, computational simulations of blood flow and vessel wall deformation will quantify hemodynamic and biomechanical factors and their interaction. Finally, an iterative modeling framework will describe the temporal evolution and progression of the pathology.

Partners

Institute of Biomechanics, Graz University of Technology, Austria (lead)
Institute of Computer-assisted Cardiovascular Medicine, Deutsches Herzzentrum der Charité, Germany