Wow, Jugular! Thank you!
The Venous Valve and Primary Chronic Venous Disease Journal, a French publication, is a
must-read for all IRs doing valvuloplasty procedures. Unfortunately, some articles are written in French and need to be translated (I use Google-Translate, fwiw).
The Editorial to the Journal is titled,
"Venous valve incompetence: the first culprit in the pathophysiology of primary chronic venous insufficiency" and was written by Dr. John Bergan of The Vein Institute of La Jolla Department of Surgery
UCSD School of Medicine which is
the same institution that conducted the Daflon 500 valve remodeling animal study (that I linked to) in which Dr. Bergan just so happens to be a named author.
I wonder if Dr. Bergan is still at UCSD? His email address is listed in the Journal as
jbergan@ucsd.edu We need to find out if he's heard about CCSVI, and if not, we need to enlighten him. Perhaps someone from CCSVI Alliance could initiate contact with him? Maybe Dr. Hubbard (of San Diego, U.S.) might be interested in talking with him or with other doctors in the University of California at San Diego School of Medicine.
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ALL THE ARTICLES in the Journal are terrific and provide a very thorough overview of venous valves. Articles from embryology to venous disease in childhood to triggering mechanisms of venous valve incompetence to Daflon 500 to more areas of this research are covered. Read the Table of Contents -- it's extraordinarily comprehensive.
Dr. Françoise Pitsch of France wrote the terrific article,
"DAFLON 500 MG: PROTECTIVE AGAINST VENOUS VALVE FAILURE" from which the below paragraph was taken:
Dr. Françoise Pitsch wrote:
In most cases, venous hypertension is caused by reflux through incompetent venous valves.7 Examination of surgical specimens removed from limbs with chronic venous insufficiency and, more recently, the direct observation offered by angioscopy, has revealed lesions involving the venous wall, the valvular annulus, and the valve cusps.8,9 Failure of the valve and its annulus is responsible for progression of the disease via maintenance and further increase of venous hypertension. Immunohistochemical studies using monoclonal antibodies specific for monocytes and macrophages have demonstrated monocyte/macrophage infiltration into the valve leaflets and venous wall of patients with varicose veins (CEAP Class 2).10 Monoclonal antibody studies have found that leukocyte infiltration is greater within the base of the valve leaflets and in the proximal venous wall. Venous valves have been found to be prominent in regions of low shear stress with venous eddies and recirculation.11 It may be that these phenomena explain how the leukocytes are preferentially deposited in these regions.
I wonder if the "venous eddies" are the same as Dr. Sclafani's "funnels."
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Dr. G. W. Schmid-Schönbein of the U.S. (UCSD School of Medicine) wrote the terrific article,
"Triggering mechanisms of venous valve incompetence" from which the below paragraph was taken:
G. W. Schmid-Schönbein wrote:
A key event in CVD is the loss of the ability to properly close venous valves. Failure of valves may be brought about by dilation of the venous wall and the valvular annulus with remodeling of the valve leaflets, bulging and stretching of valve leaflets, commissural dilation, shortening, tearing and perforation of leaflets and, finally, complete destruction of the valve.31,32 Furthermore, ultrastructural and immunohistochemical studies of valves and the venous wall have revealed the presence of leukocytes adhering and transmigrating into the venous wall.17,33 The leukocyte infiltration of the venous parenchyma is accompanied by remodeling of the extracellular matrix, a process that may in part be responsible for the destruction of venous valves.
I could continue copying important sections from the Journal articles, but I'll stop here with the hope that everyone will read all the articles.
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