Computational haemodynamics in stenotic IJVs

[Cece]

This was posted today on Facebook:
http://www.ncbi.nlm.nih.gov/m/pubmed/24671429/

Computational haemodynamics in stenotic internal jugular veins.

Authors Caiazzo A, et al.
J Math Biol. 2014 Mar 27. [Epub ahead of print]

Affiliation
Abstract
An association of stenotic internal jugular veins (IJVs) to anomalous cerebral venous hemodynamics and Multiple Sclerosis has been recently hypothesized. In this work, we set up a computational framework to assess the relevance of IJV stenoses through numerical simulation, combining medical imaging, patient-specific data and a mathematical model for venous occlusions. Coupling a three-dimensional description of blood flow in IJVs with a reduced one-dimensional model for major intracranial veins, we are able to model different anatomical configurations, an aspect of importance to understand the impact of IJV stenosis in intracranial venous haemodynamics. We investigate several stenotic configurations in a physiologic patient-specific regime, quantifying the effect of the stenosis in terms of venous pressure increase and wall shear stress patterns. Simulation results are in qualitative agreement with reported pressure anomalies in pathological cases. Moreover, they demonstrate the potential of the proposed multiscale framework for individual-based studies and computer-aided diagnosis.

'Simulation results are in qualitative agreement with reported pressure anomalies in pathological cases.'
Are there pressure anomalies? I thought that point was in contention. Wasn't it Dr. Beggs at ISNVD this year who said there was only a negligible effect on pressure? But this work here is being done using patient data. Regardless this is further exploration of the physics and equations and mathematical model aspect of CCSVI. It's excellent as always to see the work continuing and progress being made.

[1eye]

I just hope they didn't get their cerebral BP measurements from an arm cuff...

[ttucker3]

Thanks for posting this Cece. This research seems pretty significant to me. Note it is co-authored by Toro and Haacke. Bear in mind that there is always an average non-fluctuating pressure and a systolic/diastolic fluctuating pressure to consideration. The literature tends to blur these a bit. My view is that the systolic peak of an outflow pulse is repetitively combining with that of a reflux pulse in the fine vein structure causing localized high pressure at select venous points on the outflow side of the cerebral capillary bed. This localized pressure is, again my view, likely to be substantially greater than if there were no obstruction to cause the reflux.
Trev. Tucker