target menu
... / ... / ... / ... / Plaque Mechanics / Rupture risk map for carotid plaques

Rupture risk map for carotid plaques

Rupture risk map for carotid plaques

Investigators: Dr. Ir. F.J.Gijsen(EMC), Dr. A AKyildiz (EMC), Prof. Dr. Ir. A.F.W. van der Steen (EMC), Prof. Dr. Ir. F.N. van de Vosse (TU/e), Prof. Dr. A. van der Lugt (EMC), Prof. Dr. M.A. van Buchem (LUMC)

Rupture of atherosclerotic plaques in the carotid artery is the main cause for stroke. Rupture prone plaques are characterized by the presence of a lipid pool covered by a thin fibrous cap, infiltrated by inflammatory cells. Plaque rupture occurs when mechanical stress in the cap of a plaque exceeds cap strength. We introduce a new concept –the rupture risk map- which enables us to quantify cap stress and cap strength combining magnetic resonance imaging (MRI) data with biomechanical models. The rupture risk map can be used to separate rupture prone from stable plaques and clinical application potentially reduces the large number of patients that are currently subjected to unnecessary surgical removal of carotid plaques.

To construct and validate the rupture risk map, we defined three main objectives. Since reliable experimental data on carotid plaque properties are currently not available, we will first develop a new experimental technique. This ex vivo technique relies on the combination of an inflation experiment and optical deformation measurements, and will allow us to determine local plaque properties and cap strength, and how cap strength is influenced by the presence of inflammatory cells. The second objective focuses on generating the rupture risk map of human carotid plaques in vivo, using the results from the ex vivo experiments. The geometrical plaque features from in vivo MRI will be combined with plaque properties to determine peak cap stress with advanced biomechanical models. Cap strength will be obtained from combining in vivo MRI data on inflammatory cells. The ratio between computed stresses and strength defines the rupture risk map, which will be validated against histology. The third objective deals with the clinical evaluation of the rupture risk map. Symptomatic and asymptomatic patients will be imaged with MRI and plaque specific rupture risk maps will be constructed. We expect to find more locations with a high rupture risk in the plaques of the symptomatic patients. We will also investigate whether we can use geometrical surrogate markers for cap stress to determine the geometrical rupture risk map.