This research was recently published in the journal Blood Coagulation & Fibrinolysis:

Endovascular treatment of CCSVI modifies circulating markers of endothelial dysfunction & coagulation activation http://journals.lww.com/bloodcoagulation/pages/articleviewer.aspx?mobile=0&year=9000&issue=00000&article=99197&type=Abstract&desktopMode=true

Here are comments from Dr. Bernhard Juurlink and his suggestions for further reading on this topic:

One effect of obstructed venous return is decreased intracranial compliance that will result in more pulsatility in blood flow. I did a pubmed search for arterial compliance and inflammatory markers and came up with this one:

Li M, Scott DE, Shandas R, Stenmark KR, Tan W: High pulsatility flow induces adhesion molecule and cytokine mRNA expression in distal pulmonary artery endothelial cells. Ann Biomed Eng 2009, 37:1082-1092.

I could not find any literature on arterial compliance and coagulability.

Elevated homocysteine is correlated with arterial stiffness, i.e., decreased compliance - but we do not know whether it is a cause or an effect.

Refer to the following 2 articles:

Vyssoulis G, Karpanou E, Kyvelou SM, Adamopoulos D, Gialernios T, Gymnopoulou E, Cokkinos D, Stefanadis C: Associations between plasma homocysteine levels, aortic stiffness and wave reflection in patients with arterial hypertension, isolated office hypertension and normotensive controls. J Hum Hypertens 2010, 24:183-189.

van Dijk SC, Smulders YM, Enneman AW, Swart KM, van Wijngaarden JP, Ham AC, van Schoor NM, Dhonukshe-Rutten RA, de Groot LC, Lips P, et al: Homocysteine level is associated with aortic stiffness in elderly: cross-sectional results from the B-PROOF study. J Hypertens 2013, 31:952-959.

I want to add that angioplasty will increase intracranial compliance (this has beeb reported) and, thus, decrease pulsatility, and thereby, inflammation.

Dr. Bernhard Juurlink
Professor Emeritus
University of Saskatchewan