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drsclafani wrote:this is still a work in progress, and i have not vetted this by anyone yet, but IVUS is informative to me.



This image shows IVUS interrogating three areas of the right jugular vein (IVUS images on the left corresponding to the normal areas of the vein (red arrows). In the J1 segment, one notes on venography a narrowing. The ivus shows the valve edges as bright signals (yellow curved arrows). One can see that the valve is the problem.

It is not that it is opening normally; on the contrary, it is failing to open normally and has created a funnel that restricts flow into the inominate vein.

The goal of treatment is not to stretch a normal annulus, but to tear the annulus and disrupt the funnel effect.

In this case i used high pressure large 18 mm balloons to disrupt the annulus and to tear the funnel apart. As you can see from the post procedure image, flow is excellent and the diameter is now normal

We really haven't discussed this yet. With the third IVUS image, were the valve leaflets fixed and always as they are in the image or was there some small movement? If it were a healthy valve, how would it look different, would there still be bright signals showing the valve edge?

If you were looking at it with the IVUS that didn't work for this, how would it look different? Would the valve not be as easily seen? How can two IVUSes differ like that!

In the first of the three IVUS images, it's corresponding to an area on the venogram that looks suspicious, with the darker contrast above the light area. Could this be misinterpreted as a stenosis in need of treating? You can really see how both of the first two IVUS images look so similar but so different on the venogram.

The post-venography images are always the beauty shots, it is wonderful seeing all the various tortuosities turned into straightforward flow.

Dr Sclafani,

You have provided a wealth of information and some beautiful pictures.
Now that you have treated a number of MS patients, can I enquire as to your protocol for blood thinners and aftercare. Thanks.

Dr S,

I stand corrected. I just reviewed an old venogram file - and the treating doctor did take images of the right jugular (which was deemed to be flowing well..not sure if you agree).

Here are some images from that venogram:

[img][img]http://farm6.static.flickr.com/5001/531 ... ee6598.jpg[/img]
right venogram1 by anatomical, on Flickr[/img]
[img][img]http://farm6.static.flickr.com/5166/531 ... 9d4daa.jpg[/img]
right venogram2 by anatomical, on Flickr[/img]
To remind you - here are some images from my MRV. The right internal jugular looks obstructed in the axial image.

[img][img]http://farm6.static.flickr.com/5290/530 ... 89fe48.jpg[/img]
axial jugular image by anatomical, on Flickr[/img]


Helen

Dr. Sclafani,

Could you give us your thoughts of follow up after a venogram? Who orders the tests and acts on any problems found? Is it the IR? If not, what kind of doctor should also be involved in our treatment? Who recommends and follows up on any medications prescribed, and how often should that happen?

I was treated at Georgetown in July and got no results. I also got no follow up tests of any kind. I met with the neurologist after three months (and he's wonderful, by the way), but it seems that, assuming I don't have some sort of relapse, I'm on my own.

As you help write the procedures that others will follow, will you include a section on after-care?

Thanks!

Happy New Year, Dr. Sclafani!

hwebb wrote:Dr S,

I stand corrected. I just reviewed an old venogram file - and the treating doctor did take images of the right jugular (which was deemed to be flowing well..not sure if you agree).

Here are some images from that venogram:


right venogram1 by anatomical, on Flickr[/img]

right venogram2 by anatomical, on Flickr[/img]
To remind you - here are some images from my MRV. The right internal jugular looks obstructed in the axial image.


axial jugular image by anatomical, on Flickr[/img]


Helen

Helen
iteresting...from my view of that venogram, it looks like a stenosis to me with the stenosis hidden by filling of a jugular duplication
look at the closeup

notice how the contrast media seems, as illustrated by the curved orange lines, to extend beyond the margins of the IJV (red straight arrows). I made this same mistake in one of my patients and only accidentally detected it up by doing a third view.

Helen, was this the area of the stenosis?

Rosegirl wrote:Dr. Sclafani,

Could you give us your thoughts of follow up after a venogram? Who orders the tests and acts on any problems found? Is it the IR? If not, what kind of doctor should also be involved in our treatment? Who recommends and follows up on any medications prescribed, and how often should that happen?

I was treated at Georgetown in July and got no results. I also got no follow up tests of any kind. I met with the neurologist after three months (and he's wonderful, by the way), but it seems that, assuming I don't have some sort of relapse, I'm on my own.

As you help write the procedures that others will follow, will you include a section on after-care?

Thanks!

Rosegirl, of course there must be followup, but how much is necessary.
Also until there is infrastructure near home, some of this followup is challenging.

my Canadian patients and I have learned the hard way about how difficult it is currently for patients to get cooparation between their primary physician and their cCSVI physician. Getting a Canadian doctor to order a simpoe blood test or to write a script for an anticoagulant is really challenge. Some just refuse.

my original thoughts were that the primary could take care of the patient's general needs and, with good collaboration the IR could see the patient only very occasionally. However this is not working out that well.

I use an anticoagulation profile that requires no testing. This is one of the reasons i picked it.

it appears that the IRs will have to take care of you....in many ways this is a new paradigm for us....we like it

Cece wrote:

drsclafani wrote:this is still a work in progress, and i have not vetted this by anyone yet, but IVUS is informative to me.



This image shows IVUS interrogating three areas of the right jugular vein (IVUS images on the left corresponding to the normal areas of the vein (red arrows). In the J1 segment, one notes on venography a narrowing. The ivus shows the valve edges as bright signals (yellow curved arrows). One can see that the valve is the problem.

It is not that it is opening normally; on the contrary, it is failing to open normally and has created a funnel that restricts flow into the inominate vein.

The goal of treatment is not to stretch a normal annulus, but to tear the annulus and disrupt the funnel effect.

In this case i used high pressure large 18 mm balloons to disrupt the annulus and to tear the funnel apart. As you can see from the post procedure image, flow is excellent and the diameter is now normal

We really haven't discussed this yet. With the third IVUS image, were the valve leaflets fixed and always as they are in the image or was there some small movement?

If it were a healthy valve, how would it look different, would there still be bright signals showing the valve edge?

cece,
my analogy for this problem is that there is a door with a mail slot. If the postal worker tries to put an envelope through it, there is no problem, but if that person tries to put a big box, it just isnt going to happen if the door is locked.

I see these fused valves in much the same way. The IJ vein is the door, but these fused valves are the mail slot. They just cannot open.

There is motion in these valves....they get smaller. but the valves just do not open all the way to the outer reaches of the vessel wall.

The signal on the edges of the valve are thicker in these valves than in normal valves.

If you were looking at it with the IVUS that didn't work for this, how would it look different? Would the valve not be as easily seen? How can two IVUSes differ like that!

There were so many artefacts in one IVUS. it had other problems that are too technical and not worth the discussion, IMHO

In the first of the three IVUS images, it's corresponding to an area on the venogram that looks suspicious, with the darker contrast above the light area. Could this be misinterpreted as a stenosis in need of treating? You can really see how both of the first two IVUS images look so similar but so different on the venogram.

i thought that the upper venogram looked pretty normal. I think you might be misinterpreting because you did not see all images created or because the density is so different where the dye is overlying the jaw bone.

The post-venography images are always the beauty shots, it is wonderful seeing all the various tortuosities turned into straightforward flow. [/quote]

love it too.

Brainteaser wrote:Dr Sclafani,

You have provided a wealth of information and some beautiful pictures.
Now that you have treated a number of MS patients, can I enquire as to your protocol for blood thinners and aftercare. Thanks.

I prescribe for patients Fondaparinux (arixtra) 2.5-5.0 milligrams subcutaneously in the abdomen each evening for 2-3 weeks for prophylaxis against thrombosis of the treated veins. I have not given aspirin or plavix. I do not stent.

our followup is often remote and not desirable. We are initiating an online survey and sending patients for followup ultrasound several times in the first year, namely 1 month, 3 months, six months, nine months and twelve month. Then twice yearlyfor two years, then yearly thereafter. (unless symptoms recur, in which case we would do repeat ultrasound asap.

drsclafani wrote:cece,
my analogy for this problem is that there is a door with a mail slot. If the postal worker tries to put an envelope through it, there is no problem, but if that person tries to put a big box, it just isnt going to happen if the door is locked.

I see these fused valves in much the same way. The IJ vein is the door, but these fused valves are the mail slot. They just cannot open.

There is motion in these valves....they get smaller. but the valves just do not open all the way to the outer reaches of the vessel wall.

The signal on the edges of the valve are thicker in these valves than in normal valves.

It is always nice that, after all these months, there is still more to learn. Thank you.

drsclafani wrote:I prescribe for patients Fondaparinux (arixtra) 2.5-5.0 milligrams subcutaneously in the abdomen each evening for 2-3 weeks for prophylaxis against thrombosis of the treated veins. I have not given aspirin or plavix. I do not stent.

Does the Arixtra stay in the system for any length of time after the last shot? Are we really out of the danger zone for clotting once we're past those two-three weeks post procedure?

Dr. sclafani,

Does this abstract explain cause defects in the valves ?



Increased expression of platelet-derived growth factor receptor alpha and
beta and vascular endothelial growth factor in the skin of patients with chronic venous insufficiency.

Abstract

Growth factors produced by a variety of cells act as signalling peptides through specific cell surface receptor pathways. Functions such as cell proliferation, migration and differentiation have been assigned to each of them. Here, we report alterations of platelet-derived growth factor receptor alpha (PDGFR-alpha) and beta (PDGFR-beta) and vascular endothelial growth factor (VEGF) expression patterns in the progressive clinical stages of chronic venous insufficiency (CVI). A total of 30 punch biopsies were taken from patients with CVI, and VEGF and PDGFR were detected by indirect immunofluorescence and immunoperoxidase techniques. PDGFR-alpha and PDGFR-beta expression was strongly increased in endothelial cells of capillaries, pericapillary cells and connective tissue cells in the stroma of the skin of venous eczema and venous leg ulcer patients, and to a smaller extend in the dermis of those with lipodermatosclerosis. VEGF staining showed a similar expression pattern in the progressive CVI stages. However, staining of vessels in particular might simply reflect binding of VEGF, secreted by keratinocytes or fibroblasts, to its receptors. Growth factor and receptor expression in specimens from telangiectases and reticular veins, and from pigmented areas, resembled that of normal skin. We conclude that PDGFR-alpha, PDGFR-beta and VEGF play an important role in mediating inflammation and epithelial hyperproliferation in venous eczema, inducing connective tissue sclerosis in lipodermatosclerosis, and causing the reduced reepithelialization tendency in venous ulcers. We speculate that endothelial proliferation with chronic venous hypertension might be mediated by these growth factors.

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.

jugular duplication eh...interesting. This explains why it's quite tricky to detect using a venogram (unless you're really looking for this type of abnormality). Doc squirts in dye into the main chamber...and it flows through the main chamber without hindrance.

I'm still not sure what the doc did when he treated me, as haven't got the report yet. I do feel like the treatment was only partially successful though - I have more feeling in my face/lips.tongue...but my right hand still goes numb when I am flat. Interestingly, if I lie on my left side...I wake up with feeling in my right arm.

Is there a balloon angioplasty treatment for a duplicated vein?

Helen

Cece wrote:

drsclafani wrote:cece,
my analogy for this problem is that there is a door with a mail slot. If the postal worker tries to put an envelope through it, there is no problem, but if that person tries to put a big box, it just isnt going to happen if the door is locked.

I see these fused valves in much the same way. The IJ vein is the door, but these fused valves are the mail slot. They just cannot open.

There is motion in these valves....they get smaller. but the valves just do not open all the way to the outer reaches of the vessel wall.

The signal on the edges of the valve are thicker in these valves than in normal valves.

It is always nice that, after all these months, there is still more to learn. Thank you.

drsclafani wrote:I prescribe for patients Fondaparinux (arixtra) 2.5-5.0 milligrams subcutaneously in the abdomen each evening for 2-3 weeks for prophylaxis against thrombosis of the treated veins. I have not given aspirin or plavix. I do not stent.

Does the Arixtra stay in the system for any length of time after the last shot? Are we really out of the danger zone for clotting once we're past those two-three weeks post procedure?

In individuals with normal kidney function, fondaparinux is eliminated in urine mainly as unchanged drug. There really is no metabolism of it. The elimination half life of a single doese of the rug is 17-20 hours.

I would never say that there is no risk of thrombosis. However three weeks should be ample to reduce risk significantly

sara-sama wrote:Dr. sclafani,

Does this abstract explain cause defects in the valves ?



Increased expression of platelet-derived growth factor receptor alpha and
beta and vascular endothelial growth factor in the skin of patients with chronic venous insufficiency.

Abstract

Growth factors produced by a variety of cells act as signalling peptides through specific cell surface receptor pathways. Functions such as cell proliferation, migration and differentiation have been assigned to each of them. Here, we report alterations of platelet-derived growth factor receptor alpha (PDGFR-alpha) and beta (PDGFR-beta) and vascular endothelial growth factor (VEGF) expression patterns in the progressive clinical stages of chronic venous insufficiency (CVI). A total of 30 punch biopsies were taken from patients with CVI, and VEGF and PDGFR were detected by indirect immunofluorescence and immunoperoxidase techniques. PDGFR-alpha and PDGFR-beta expression was strongly increased in endothelial cells of capillaries, pericapillary cells and connective tissue cells in the stroma of the skin of venous eczema and venous leg ulcer patients, and to a smaller extend in the dermis of those with lipodermatosclerosis. VEGF staining showed a similar expression pattern in the progressive CVI stages. However, staining of vessels in particular might simply reflect binding of VEGF, secreted by keratinocytes or fibroblasts, to its receptors. Growth factor and receptor expression in specimens from telangiectases and reticular veins, and from pigmented areas, resembled that of normal skin. We conclude that PDGFR-alpha, PDGFR-beta and VEGF play an important role in mediating inflammation and epithelial hyperproliferation in venous eczema, inducing connective tissue sclerosis in lipodermatosclerosis, and causing the reduced reepithelialization tendency in venous ulcers. We speculate that endothelial proliferation with chronic venous hypertension might be mediated by these growth factors.

sama sama
i do not think that this is related to valve function or malformation