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It's been eight months now! It may be the usual thanks but it is an unusual commitment, well worth acknowledging as often as we do.1eye wrote:Dr. Sclafani: the usual thanks and all for sticking with us all this time.
annad, if it helps, here is the link to the post from when he came back from Italy and we all first learned about right vs. left entry:annad wrote:Dr. Sclafani,
Could you explain R versus L entry for CCSVI treatment? I understand L is preferred for catching MT Syndrome but are there other reasons and is it more dangerous than going in through the R side?
thank you in advance!
Someone with a similar name asked a similar question once beforeCCSVIhusband wrote:Do you think there could be potentially any IVC issues, or have you seen any, related to CCSVI? (I know that's not part of the theory, but has anyone looked?) I have no reason to suggest there may be ... I just wonder.
http://www.thisisms.com/ftopicp-117982.html#117982drsclafani wrote:i do not think that the inferior vena cava plays a role in ccsvi unless the usualy suspected veins are involved. Then alterations of flow within other structures can make it worse.mshusband wrote:Dr. Sclafani ... what role do you suspect the inferior vena cava could play in issues in the legs?
nigelNZer1 wrote:Have to agree with Cece on the graphic, but its real!
I have recently watched a very good forum by Dr. George Jelinek the writer of several books on MS and a research publisher from Australia, he also has MS.
See the talk at http://www.msakl.org.nz/.
"Professor Jelinek was invited to present the Keynote Address to the Focus on MS Conference run by the MS Society of New Zealand on Saturday 18th September 2010. He chose to discuss the value of medical evidence, what weight researchers put on various trials, and how bias and conflict of interest can influence the results of these studies. The talk particularly focuses on drug-company sponsored research, and the often hidden or unreported flaws in clinical trials that raise questions about the real efficacy of some of the currently used disease-modifying medications. This is an important talk for those of us wishing to get a really balanced perspective on the treatment options for MS, rather than blindly following a drug-only approach."
The whole video is worth looking at, it is 1.5 hour long. I think it is valuable information if you are to design studies for CCSVI treatments.
Most of the video is about the flaws and biases in RCT research, mostly by Pharmaceutic Industry to sell there products. Very, very good content.
The very end has a comment he made about CCSVI angio problems from stretching veins that in his words has been known about for some time as a problem in angio treatments having restenosis.
Can you comment on the 'known' complication of restenosis after angio that he speaks briefly about please.
Dear Dr Sclafani,Dr. Rubin said ...Last week, he treated a woman who had the vein procedure in Mexico.
"We found extensive clotting in the left arm reaching into the chest veins, and some of the clots had broken off and travelled to her lungs, which is called a pulmonary embolus, which is life threatening, potentially life-threatening complication."
The purpose of the valve is to allow one way flow of the vein toward the heart. It prevents backup of the blood in the wrong direction.Johnson wrote:Dear Doctor,
I am wondering, but have been reticent to ask - lest I have missed a previous Q & A - what is an "incompetent valve"? Is it a generic term that would cover inverted valves, fused leaflets, etc., or is it a more specific pathology?
you could have either of the causes of insufficiency i described above. For one you may have had such stretching that the valve does not prevent reflux of blood from the heart up the neck.In my second round, a Doppler US revealed "incompetent valves" and the venogram suggested stent (declined), then a cutting balloon, but cutting balloons apparently don't come as large as the 18 mm required for my LIJV. What, if anything, might I infer from this limited information? Would an incompetent valve fall into congenital malformation, or could there be another antagonist?
Thank you, sir.
To be honest with you, that question is not yet defined. First we have to agree on a measurement of stenosis. is it diameter or area? Is the pressure relevant? 70% is considered significant stenosis in most arteries, but they have a lot more pressure to push the blood through. So if pressure is low and volume of flow is high, will lower degress of stenosis overwhelm the ability of blood to pass through stenoses.CCSVIhusband wrote:
My question results from that (and, again, I'm sure it's one that has been asked and answered several times).
What constitutes a clinical narrowing? (maybe those are the wrong words) ... but if a vein is narrowed 20% ... would you balloon it if there was potential reversed flow?
Yes, yes.Are valves the main issue? - and if so, does running a guide wire through the veins pose any issues with moving them and not being able to see accurately what is happening then?
i have not seen it, just the may thurner syndromeDo you think there could be potentially any IVC issues, or have you seen any, related to CCSVI? (I know that's not part of the theory, but has anyone looked?) I have no reason to suggest there may be ... I just wonder.
megansmomMegansMom wrote:Hello Dr Sclafani, Thanks for being such a rebel!
Its not an easy place to be... but it will get better.
My question concerns Endothelin 1. I am an RN ( x 38 years) with a good handle on anatomy and physiology. My interest is in the function of Endothelin 1.
It is my undertsnading that Endothelin 1 is made by all people to maintain the health of the lining of our vessels. It is also my understading that increased shear stress and hypoxia are triggers that increase production of Endothelin 1- I am guessing its the bodies way to reinforce the vessel intergrity.
I have learned that Endothelin 1 in high levels can increase fibrosis( fibrotic changes) and hypertrophy (thickening) of the vessels/valves. So IF the person is born with this congenital condition , say at a minor blockage in early life and then over time, with shear stress and hypoxia as triggers the Endothelin levels soar and the CCSVI lesions/vessel get worse.......then the shear stress and hypoxia get worse etc etc
Its sort of a cycle....over many years the vessels would be stiffer, stenosis could be worsening and valves could be thickened and more of a blockage. Of course all of this would cause more iron to be laid down in the parenchyma too doing its own bit to contribute to damage. The iron and hypoxemia and hypogylcemia in the brain leading to axonal and oligodendrocyte damage and maybe even cell death. Could the extremely high Endothelin levels cause the venocentric MS lesion formation ( sort of like sandbagging the walls?) And the WBCs be chrochically activated as the "clean up crew"?
Its my undertsnading that pwMS have a much higher ( hundred times higher)than normal Endothelin 1 level. After successful PTA would the Endothelin level 1 drop because their triggers are gone?? How long does that take? Would the fibrotic and hypertrophic changes decrease? Are there people studying this?
Sorry to blast you with so many questions but I don't know who to ask these questions of.
Thanks in advance and I will totally understand if the answer is "we don't know yet"
The Mom that got her daughter liberated 1 month after CIS diagnosis
sorry to disappoint you, cece.Cece wrote:MegansMom, I am happy to see you in here, I think you're onto something with your endothelin research. Can't wait for the "iconoclast from Brooklyn" to weigh in on it.
its really difficult to do a catheterization in someone with hip contraction. It is a really challenging piece of work, so much so, that i would think of other ways to go about the taskbluesky63 wrote:
Does it have to be done on a flat table? Is there any way to use something like an angled bed or even something like a procedure "chair" that could accommodate a person who had trouble being flat? Thinking creatively here. I guess that wouldn't work with the specialized equipment?
that depends on the sequence and the use of the contrast agent.cah wrote:Dear Dr. Sclafani, I've got a simple question and I think I know the answer, but I'm not completely sure. What do these 3D videos from Dr. Haacke actually show, the vein walls or the blood (as if it were frozen and everything else removed)?
I think the blood disolves because enzymes allow it to liquify. Cooling an alive body actually makes the blood clot less well1eye wrote:I hope, I hope... This question is ignored as being too foolish for further discussion:
Dr. Sclafani: One of the most simple rules of chemistry is that heat speeds up reactions. A cold dead body will tell you that heat liquifies blood. I have had the liberation procedure and feel much better.
you are not kidding there. We know exercise improved muscle tone, flexibility and general health. You have been restricted a long time by MS. Now you feel some improvements. You better get out there an exercise. you never know if, whether or when your symptoms might return. Dont wast the opportunity.But heat continues to be my enemy. The solution, I know, is to get up off my kiester and get some exercise,
I think that your nerves are damaged and have not or may not heal sufficiently for symptoms like this to resolve.but the problem is, I spend a lot of time with my computer on my lap *heating* it up. My legs will twitch and complain if I do not have an insulating device between it and them.
They also complain when I am in bed. I believe (possibly wrongly) that reflux is happening when I am lying down. I can get my legs tolerable if I put them out from under the covers. I think maybe being under covers and retaining heat makes my blood thinner, and reflux happens more easily with the jugulars wide open and the blood moving well. The reference at http://www.thisisms.com/ftopict-14541.html says arm position seems to make a difference (but does not say what position). I guess all of this may resolve when I am off Plavix, but is this hyperactive imagining, or ongoing brain damage (or both )? Do you think that having so much heat on my legs when sitting can thin my blood and allow reflux, which then makes my legs twitch? Can you comment at all?
well you guys have been reading this stuff for eight months, that is well worth acknoledging. You cannot imagine how many comments (most positive) i receive for doing this from physicians. I think there are more than a few lurking MDs there.Cece wrote:It's been eight months now! It may be the usual thanks but it is an unusual commitment, well worth acknowledging as often as we do.1eye wrote:Dr. Sclafani: the usual thanks and all for sticking with us all this time.