"This is the first wave of research that has been presented that is beyond just the observational," Michael Dake, MD, professor of cardiothoracic surgery at Stanford University in Palo Alto, California, told Medscape Medical News. "It's a nice experience with a large group of patients."
I like that he adds on the part about it not being completely characterized. It's true and it leaves room for a vascular explanation of what's triggering the autoimmune process.Most practitioners view multiple sclerosis as an autoimmune disease and treat it with drugs that suppress the immune response. "The generally held view is that this is an autoimmune process that's not completely characterized," explained Dr. Dake, who was not involved with either of the studies.
I might borrow that phrasing for future use....
From a discussion in the article about Dr. Farrel's study at Rush:
5% is actually higher than I expect for patients with MS who are not found to have CCSVI.In 5 of the patients (5.2%), venography and ultrasound were normal; in 89 (94.9%), there was evidence of stenosis.
2.8% is a nice low percentage, for percentage of patients who get stents.The surgeons performed angioplasty in all the abnormal veins and put stents in 5 of 179 (2.8%).
I think 3 instances of thrombosis is 3 instances too many. I usually say the use of IVUS could reduce the numbers of thrombosis but Dr. Farrel uses IVUS. Perhaps the patients should be maintained on anticoagulants longer?Complications included 3 instances of jugular vein thrombosis and 3 instances of bleeding at the puncture site.
Clopidogrel is Plavix, which is an antiplatelet, and Dr. Arata shared a pdf showing no benefit from the use of Plavix in venous disease. http://atvb.ahajournals.org/content/28/3/413.full.pdfThey administered anticoagulants for 10 days and clopidogrel bisulfate for 6 weeks.