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Brainteaser wrote:Thank you Dr Sclafani for your response re arixtra and aftercare. I suppose the jury's out regarding whether this protocol is optimal, but at least there is a reasonable plan in place which presumably you will tweak as you go along.

I'd like to enquire if you see the arixtra as sufficient to address the expected added level of intimal injury resulting from the use of larger balloons and longer ballooning times or is intimal damage something you will address, if and when observed at the set ultrsound points? Thanks.

I believe that three weeks should be sufficient, but as yhou say, the jury is out

drsclafani wrote:

Brainteaser wrote:Thank you Dr Sclafani for your response re arixtra and aftercare. I suppose the jury's out regarding whether this protocol is optimal, but at least there is a reasonable plan in place which presumably you will tweak as you go along.

I'd like to enquire if you see the arixtra as sufficient to address the expected added level of intimal injury resulting from the use of larger balloons and longer ballooning times or is intimal damage something you will address, if and when observed at the set ultrsound points? Thanks.

I believe that three weeks should be sufficient, but as yhou say, the jury is out

I am usually quick at finding past drsclafani quotes, but this time I am at a loss! I believe Brainteaser is referring to intimal hyperplasia, not clotting.

Here are some general mentions of intimal hyperplasia by Dr. Sclafani in the past, but I know there are better ones.
http://www.thisisms.com/ftopicp-144690.html#144690
http://www.thisisms.com/ftopicp-144874.html#144874
http://www.thisisms.com/ftopicp-105219.html#105219

My own question:
When there's a duplication, does it always cause compression of the main IJV or can it exist benignly?

Thank you drsclafani
I want to know your opinion , what is the major factor, is it the narrow stimulates vascular endothelial growth factor (VEGF ) , or vascular endothelial growth factor (VEGF ) is causing the narrow ?

Is there any chance that in a few cases the problem is in the arteries rather than the veins. Maybe that could diminish the blood flow to the extent that the veins collapse. If that were the case you could balloon the veins "til the cows come home" but they would not stay open. That might explain why some patient's veins seem so determined to close up. Just wondering.

Thank you Dr Sclafani and Cece regarding your responses concerning restenosis. If I understand the situation clearly, problems can be addressed, in a nutshell as follows -

a. elastic recoil - by using larger balloons and longer balloon times
b. thrombosis/clotting - by 3 weeks of arixtra, post angioplasty
c. intimal hyperplasia - by monitoring and perhaps using cryoplasty, but also drug eluting stents are starting to be used.

Am I correct in assuming that a. and b. can be better managed than c? Intimal hyperplasia seems very problematic and is likely to show up several months after CCSVI treatment and hence the need for an active aftercare program. Some docs are not using larger balloons in order to reduce the risk of intimal hyperplasia at the expense of better short term results. Arixtra can't be used with aspirin and therefore seems to be a better option than aspirin.

Is this all about right in terms of the current state of play?

Dr S.

How would a patient know if "restenosis" is due to elastic recoil, thrombosis (blood clots), or intimal hyperplasia?

Would there be any way to differentiate one from the other without a doctor?

Brainteaser wrote:Thank you Dr Sclafani and Cece regarding your responses concerning restenosis. If I understand the situation clearly, problems can be addressed, in a nutshell as follows -

a. elastic recoil - by using larger balloons and longer balloon times

conjecture, no evidence yet

b. thrombosis/clotting - by 3 weeks of arixtra, post angioplasty

extrapolated from data from other indications and used in CCSVI. Fondaparinux has no increase in risk, better anticoagulation, longer half life, better safety profile, but is more expensive and not universally available and not well known by many physicians.

c. intimal hyperplasia - by monitoring and perhaps using cryoplasty, but also drug eluting stents are starting to be used.

Almost all the evidence for intimal hyperplasia both clinical and experimental is from vein to artery grafts where pressure differentials and high flow lead to intimal hyperplasia. There is little written about pure vein intimal hyperplasia. Angioplasty alone of Budd Chiari venous stenosis has mid term and long term patency. vein to vein anastomoses in liver transplants may have stenosis from a different cause.

Also venous stenosis from intimal hyperplasia should occur later than we are seeing restenosis after ccsvi angioplasty. Thus, i am unclear about the role of intimal hyperplasia right now and have not added antiplatelet drugs such as aspirin or clopidogrel (plavix) to my post procedure regimen

But i am surely no expert in all of this.

Am I correct in assuming that a. and b. can be better managed than c? Intimal hyperplasia seems very problematic and is likely to show up several months after CCSVI treatment and hence the need for an active aftercare program. Some docs are not using larger balloons in order to reduce the risk of intimal hyperplasia at the expense of better short term results.

big assumptions. we dont have these answers yet.

Arixtra can't be used with aspirin and therefore seems to be a better option than aspirin.

This is not accurate. It can be used with aspirin. Pharmacological studies have shown that the antiplatelet effects of aspirin and the anti-thrombin activities of fondaparinux are not altered by simultaneous use.

Fondaparinux should not be used by patients who:
weigh less than 110 pounds (50 kilograms); have kidney disease; have active bleeding; have a low level of platelets in the blood; or have bacterial endocarditis (infection of the heart).

Fondaparinux may be risky in patients with high blood pressure; a bleeding or blood clotting disorder; a prosthetic heart valve; need to have (or have recently had) surgery or another invasive procedure; stomach bleeding or ulcers; eye problems due to diabetes; a history of a low level of platelets in the blood during treatment with heparin; or liver disease.

Individual judgments must be made in such circumstances.

Is this all about right in terms of the current state of play?

The game is still on

David1949 wrote:Is there any chance that in a few cases the problem is in the arteries rather than the veins. Maybe that could diminish the blood flow to the extent that the veins collapse. If that were the case you could balloon the veins "til the cows come home" but they would not stay open. That might explain why some patient's veins seem so determined to close up. Just wondering.

i dont think so. in order for the brain to survive significant blood flow is required. if arterial inflow were a problem, patients would not be so damn intelligent to ask such tough questions

Dr. Sclafani,

I am behind on reading up here.. perhaps you've already talked about this.
What kind of results are you seeing? Similar to Dr. Siskin perhaps? 1/3 great, 1/3 moderate, 1/3 no change?
Are you seeing any patterns emerge regarding impact of venoplasty? type of ms, location of stenosis, initial treatment vs re-treatment etc?

thanks

sara-sama wrote:Thank you drsclafani
I want to know your opinion , what is the major factor, is it the narrow stimulates vascular endothelial growth factor (VEGF ) , or vascular endothelial growth factor (VEGF ) is causing the narrow ?

This is surely not my expertise.

The roles of VEGF are many as there are many VEGF types now recognized. migration and proliferation of endothelial cells, enhance vascular permeability, induction of neovascularity are all noted. Some VEGF cause neovascular development in the adventitia of the vessel which results in hyperplasia of the intima,

Its pretty confusing right now

VEGF coated stents or bolus injection within the vasculature seem to accelerate endothelial growth and recovery after angioplasty has denuded the blood vessel of its inner lining of intima. As long as the intimal surface is denuded, smooth muscle proliferation from the media of the blood vessel will result in intimal hyperplasia and risk thrombosis.

So i dont think i can give you a simple answer to your question.

drsclafani wrote:

Brainteaser wrote:Is this all about right in terms of the current state of play?

The game is still on

Lots of fans in the stadium shouting the name "Sclafani"!

Cece wrote:

drsclafani wrote:

Brainteaser wrote:Thank you Dr Sclafani for your response re arixtra and aftercare. I suppose the jury's out regarding whether this protocol is optimal, but at least there is a reasonable plan in place which presumably you will tweak as you go along.

I'd like to enquire if you see the arixtra as sufficient to address the expected added level of intimal injury resulting from the use of larger balloons and longer ballooning times or is intimal damage something you will address, if and when observed at the set ultrsound points? Thanks.

I believe that three weeks should be sufficient, but as yhou say, the jury is out

I am usually quick at finding past drsclafani quotes, but this time I am at a loss! I believe Brainteaser is referring to intimal hyperplasia, not clotting.

Here are some general mentions of intimal hyperplasia by Dr. Sclafani in the past, but I know there are better ones.
http://www.thisisms.com/ftopicp-144690.html#144690
http://www.thisisms.com/ftopicp-144874.html#144874
http://www.thisisms.com/ftopicp-105219.html#105219

My own question:
When there's a duplication, does it always cause compression of the main IJV or can it exist benignly?

what is this? stump the professor day by asking about this stump of a vein?


It was less than one year ago that i recognized my first "duplication" My questions have been:
1. is this normal or abnormal?
2.if its abnormal, is it related to ccsvi?
3.if it causes ccsvi, how does it do it
4. if it does it, is there an effective treatment.

1. Without looking for this in patients without ccsvi, i cannot answer #1
2. and 3. Regarding 2&3, I look at that duplication as a windsock. When one increases intravenous pressure, the duplication distends with blood. At it distends it presses up against the wall of the jugular vein. I have seen that with IVUS. Is this a form of outlet obstruction? I believe it is.
4. How to treat it effectively.....good question.
possibilities that come to mind, include:
fenestration of the common wall?
stent?
close the lumen of the duplication?
surgery?

any other simple questions today

CCSVIhusband wrote:Dr S.

How would a patient know if "restenosis" is due to elastic recoil, thrombosis (blood clots), or intimal hyperplasia?

Would there be any way to differentiate one from the other without a doctor?

a few weeks ago, we were educating about narrowings, now you want to know how to diagnose them without a doctor

you guys are amazing.

allof them may be associated with recurrent neuro symptoms

thrombosis tends to hurt and be tender to touch
ER occurs relatively early
IH occurs later

ultrasound is helpful with thrombosis, other two can be virtually identical in appearance, although IVUS and US might show thickening of the inner lining layer in cases of IH.

pklittle wrote:Dr. Sclafani,

I am behind on reading up here.. perhaps you've already talked about this.
What kind of results are you seeing? Similar to Dr. Siskin perhaps? 1/3 great, 1/3 moderate, 1/3 no change?
Are you seeing any patterns emerge regarding impact of venoplasty? type of ms, location of stenosis, initial treatment vs re-treatment etc?

thanks

i have only been back in action about two months. too early to tell

drsclafani wrote:what is this? stump the professor day by asking about this stump of a vein?

Nah, it was the other IR who was stumped. You were the one who saw the duplication in hwebb's image! Altogether impressive.