Measurement of the blood flow rate as well as the distribution of the flow rates in the patient's feeding arteries may be needed for numerical simulations to accurately reproduce the intraaneurysmal hemodynamics in a specific aneurysm in the clinical setting.

A method for the determination of the contrast-agent propagation in vessel trees is presented. A standard three-dimensional (3-D) rotational angiography procedure is performed to reconstruct the morphology of the contrast-filled vessel tree in a 3-D volume. An additional fluoroscopy projection series acquired with a fixed projection angle delivers the temporal information of the bolus propagating. The mapping of the propagation information from the two-dimensional projections to the 3-D image data set is the topic of this paper. A symbolic tree structure is built up that represents the vessel tree including bifurcations. Neighborhood relations between vessel pieces are given in three dimensions. This facilitates filtering procedures and plausibility controls of the resulting time dependent 3-D data set. The presented method proved to be accurate with phantom data and gives novel insight in the feeding structure of arterio-venous malformations and aneurysms.

Abstract. We propose a parametric lumped model (LM) for fast patientspecific computational fluid dynamic simulations of blood flow in elongated vessel networks to alleviate the computational burden of 3D finite element (FE) simulations. We learn the coefficients balancing the local nonlinear hydraulic effects from a training set of precomputed FE simulations. Our LM yields pressure predictions accurate up to 2.76mmHg on 35 coronary trees obtained from 32 coronary computed tomography angiograms. We also observe a very good predictive performance on a validation set of 59 physiological measurements suggesting that FE simulations can be replaced by our LM. As LM predictions can be computed extremely fast, our approach paves the way to use a personalised interactive biophysical model with realtime feedback in clinical practice.

It has been shown recently that in Alzheimer''s disease the degree of dementia is strongly correlated with a reduction of the synaptophysin reactivity of the cortical neuropil as a measure of synapse density, while counts of neuritic plaques showed a weak correlation. This suggests that mechanisms acting at the synaptic level, finally resulting in a numerical decline of synapses, may represent an important factor in the pathogenesis of dementia. Under these aspects, we wanted to examine whether changes of synaptophysin immunoreactivity may also occur in dementia of vascular origin such as Binswanger''s disease, where the white matter atrophy is usually conceived to be the main morphologic correlate of dementia. However, infrequently patients with morphologically typical Binswanger''s subcortical encephalopathy including white matter atrophy are not demented. We found in 9 cases of vascular dementia of Binswanger type a significant reduction in synaptophysin immunoreactivity of the cortical neuropil (9.1 %), the magnitude of which was not much less than in Alzheimer type dementia (10.9 %). These results suggest that a reduction in cortical synaptic population density may also play a significant role in the pathogenesis of dementia in Binswanger''s disease. In view of the fact that similar conditions have been shown to occur in neurodegenerative disorders with dementia other than Alzheimer type dementia, there seems to be evidence for a possible common pathogenetic link between these forms of dementia at the synaptic level, where different etiologic factors may result in similar changes.

Accounting for the partial volume effects in automatic coronary lumen segmentation algorithms has the potential to improve the accuracy of CCTA-based hemodynamic assessment of coronary artery lesions.