DrSclafani answers some questions

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cah
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Post by cah »

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)?
"There is only one good, knowledge, and one evil, ignorance." Socrates
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Post by 1eye »

I hope, I hope... This question is ignored as being too foolish for further discussion:

Dr. Sclafani: the usual thanks and all for sticking with us all this time. Does this have any relevance? It recently occurred to me. 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. But heat continues to be my enemy. The solution, I know, is to get up off my kiester and get some exercise, 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?

Thanks again.
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Post by Cece »

1eye wrote:Dr. Sclafani: the usual thanks and all for sticking with us all this time.
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. :)
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Post by annad »

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!
a
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Post by Cece »

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!
a
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:

http://www.thisisms.com/ftopicp-117268.html#117268

CCSVIhusband,
CCSVIhusband 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.
Someone with a similar name asked a similar question once before :D :D
drsclafani wrote:
mshusband wrote:Dr. Sclafani ... what role do you suspect the inferior vena cava could play in issues in the legs?
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.
http://www.thisisms.com/ftopicp-117982.html#117982
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Post by drsclafani »

NZer1 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.
Regards Nigel
nigel
thank you for that gift. It was very illuminating. I have suggested to my residents that they view it and have shared it with other academics becoming interested in MS research and treatments.

Know complications of restenosis:
veins have an inherent increased restenosis rate, thought to be related to greater elastic recoil. Vein stenoses are usually secondary to fibrotic strictures and restenosis is often related to persistence or recurrence of the fibrosis. Stretching or tearing of the wall occurs with dilatation and healing of that stretch injury can also lead to restenosis of a fibrotic sense. Finally, underdilatation of a narrowing can result in transient dilatation. with time the stenosis recurs.

In CCSVI it is believed my me and others that this is a congenital problem resulting from inelastic collagen and malformed veins and valves. Dilatation of these problems is different. Perhaps the restenosis comes from inadequate venodilatation. or perhaps it is secondary to a new fibrotic reaction.

Fibrotic strictures are very difficult. I treat a man with an esophageal stricture who after many surgeries ended up in my procedure room because the surgeons felt they had nothing to offer him. He was unable to swallow anything and he was emaciated. I started dilatation. , in the past ten years i have dilated him more than fifty times. We seem to be prolonging the interval between dilatations of his esophagus. whether we have made a real change in the scar or whether he has just gotten to better adapt to his tragic situation is unknown to me. However he and I know that he is better for the dilatations, however painful and repetitively frustrating it may be.

We expect patients who get venous angioplasty to restenose. I am looking for a better mousetrap that will result in less frequent restenoses. I do not consider restenosis a failure of the technique but a component of the treatment.


we continue to go to dentists even though we get cavities, gum disease and other problems between visits. the fact that we get cavities after visiting hem, right?


The day that is is shown that the risks outweigh the benefits of this procedure, I will announce to you all my regrets and announce my retirement. in the meantime, i will continue to try to figure out how to reduce the rate of restenosis, be it by medications, or techniques .
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Post by PCakes »

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."
Dear Dr Sclafani,
What would cause clotting in the arm?
Thank you,
pc
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Post by drsclafani »

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?
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.

The more common form of incompetence of the valve is when the valve functions inadequately. thus blood backup from the heart toward the vein. We call this venous insufficiency. In such situations the valve does not close properly because it is unable to close, or cannot withstand the pressures trying to push it open or because it has been scarred open.

CCSVI seems to be different. The valves are upside down,, coming off the side wall, formed single barriers, etc. The valve leaflets might be fused or the valves are stiff. This leads to insufficiency in which the flow refluxes back up into the head or spine, not because the valve does not stop blood from flowing up beyond it from the heart, but because the blood from above must find alternate pathways back to the heart.


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.
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.
But more likely, you have had an underdilation. I say this because you are being advised to consider stents. Stents would not be used to counteract a wide open incompetent valve.
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Post by drsclafani »

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?
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.

So what do i do? I use Doppler to give me hemodynamic data, looking for reflux, I use venography and IVUS to find veins that are narrowed enough to explain that hemodynamic problem. I look at the xray dye to see if it washes out quickly, or stagnates and doesnt was away. I look for lots of collaterals as a reflection of inability to get all that blood out of the vein.
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?
Yes, yes.

if i do not see anything on the venogram, i pull the catheter to an area just next to the valve to avoid this and repeat the angiogram. I will show a case that illustrates that sometime.
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.
i have not seen it, just the may thurner syndrome
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Re: Endothelin 1 and its effects

Post by drsclafani »

MegansMom 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"

Cat

The Mom that got her daughter liberated 1 month after CIS diagnosis
megansmom

i am not going to say, we dont know yet, just I dont know yet. You bring up some very interesting concepts. perhaps this can explain the apparent increase in stenoses with age described recently

unfortunately for me, my training is elsewhere and I am trying to learn more than i can teach
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Post by drsclafani »

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.
sorry to disappoint you, cece.
i wont comment on something i dont know
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Post by drsclafani »

bluesky63 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?
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 task
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Post by drsclafani »

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)?
that depends on the sequence and the use of the contrast agent.
The contrast is sometimes subtracted and this leaves a cast of the vessel.

If no contrast is used, we see the wall of the vessel

your analogy is quite accurate.
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drsclafani
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Post by drsclafani »

1eye 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.
I think the blood disolves because enzymes allow it to liquify. Cooling an alive body actually makes the blood clot less well
But heat continues to be my enemy. The solution, I know, is to get up off my kiester and get some exercise,
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 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?

Thanks again.
I think that your nerves are damaged and have not or may not heal sufficiently for symptoms like this to resolve.
It is quite possible that sitting with a computer on your legs is causing a response that includes twitching.
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drsclafani
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Post by drsclafani »

Cece wrote:
1eye wrote:Dr. Sclafani: the usual thanks and all for sticking with us all this time.
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. :)
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.
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