DrSclafani answers some questions

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Re: Is this stenosis in my deep cerebral vein?

Postby drsclafani » Tue Mar 22, 2011 7:27 pm

Perkele wrote:Hi Dr.Sclafani,

Could you give your opinion about my vein (deep cerebral?). These pictures are from my brain MRI and these pics represent the deep cerebral veins, if I'm correct.

I think I see clear stenosis there but your opinion would be highly valued.

To see all of the images click the picture.

Image

Thank you so much,
Perkele


perkele
that looks like the carotid artery to me. seems a bit irregular possibly due to some atherosclerosis

DrS
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Postby drsclafani » Tue Mar 22, 2011 7:29 pm

ozarkcanoer wrote:Dr Sclafani.... Sorry, I meant Dr Haskal performed both procedures not you.

I saw my neuro today, and he ordered an intracranial MRV for me because my left stent is completely occluded with scar tissue. When I asked him why, he said that this occlusion/scarring could cause damage higher up in the brain. This is quite scary to me. Do you also feel this could be a problem with stents high up in the jugulars : scarring, full occlusion and damage of some sort to the brain itself (aside from reflux) ?

ozarkcanoer

i think that any obstruction, including ccsvi, is a risk factor for dural sinus occlusion.
but we need to stay calm and evaluate the intracranial mrv before we react
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Postby Cece » Tue Mar 22, 2011 7:30 pm

drsclafani wrote:i am a bit more concerned about the hypercoagulability of the antiphospholipid syndrome (Hughes sydnrome) which can mimic MS to some degree.

If Hughes can mimic MS, wouldn't a misdiagnosed MS patient who really has Hughes most likely fail to show CCSVI on the doppler ultrasound or the venogram?
i am thinking to get a hematology consult on MS patients with a history of clotting problems like DVT before treatments to look for this syndrome

I approve. ;)
But what would you do differently if they turned out to have it? Or would this be as a differential diagnosis to MS and then they would not be very likely to need CCSVI treatment after all?
i really can only estimate it. It is only recently that i have seen any thromboses, much to my great upset. If I exclude the aggressive treatment of hypoplasias, I would see it at about 3but that incidence was clustered and may be a statistical chance occurence. But i was using 1181-20 mm balloons at that time so I am anxious to see if my new strategy of ballooning to precise diameter of the vein will reduce that incidence.

I am anxious/hopeful too.

I note that you used an 18 mm balloon on me, but that was the size of my vein, it was a match!
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Re: ccsvi

Postby Cece » Tue Mar 22, 2011 8:08 pm

drsclafani wrote: there is distinct differences between a healthy vein and a damaged vein.

if you injure the wall of the vein, the body sees it as a breach in the wall, even if there is no breach in the wall, only loss of the wallpaper. The body then sends its patchers(platelets) to the area to cover the hole and Aspirin makes them less sticky. Also signals go out to form clot to plug the hole. in other words thrombus is formed. Arixtra (fondaparinux) is an antithrombin drug. These medications are used to reduce the risk of thrombus caused by injury to the wall.

That is a helpful analogy.
Has anyone noticed that the increase in thrombosis came when larger balloons were used. Dr. Sinan first told us that he could use 18-22 mm balloons without any problems. This was encouraging in our battle to avoid restenosis. However i only had one thrombosis prior to the large balloons: this was in an hypoplasia. I had none is patients dilated to only 14 mm, although i did have restenosis.

but after using larger balloons i had several, and while some were in patients with hypoplasia, others were in patients with good old fashion valvular stenosis. .

:( I never connected the two. But if this turns out to be the explanation for the increase in thrombosis, at least balloon sizes can be lowered.

I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.

Its only been a few weeks so i cannot tell you that this works yet.

There, i am not lying low now.

You are not lying low at all. Much appreciated. :)
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Postby Robnl » Wed Mar 23, 2011 4:16 am

drsclafani wrote:
Robnl wrote:Dr Sclafani,

about OCT; In Poland (March 2010) i had an OCT scan, in Februari 2011 i had a GDX scan in Holland. Because of the difference in tests, the doctor would/could not 'speak out loud'....but she thinks she sees improvement in the status of the optic nerve (what would not be possible).

In December 2011 second GDX test.....i'm curious... 8)

Robert


robert, i cannot answer your question. Perhaps "phlebologist" could answer your question


Hi Doc,

Well it's not a real question...more trying to add info :D
Like i said...im waiting for December....2nd gdx

Robert
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Re: ccsvi

Postby fogdweller » Wed Mar 23, 2011 10:11 am

drsclafani wrote:I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.


I wonder if some longitudinal movment (i.e. pull the balloon) might also help, perhaps even with a balloon smaller than full vein diameter so it does not rub against the vessel wall"?
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Re: ccsvi

Postby pklittle » Wed Mar 23, 2011 10:33 am

drsclafani wrote:I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.


I think I read that Dr. Arata's approach is similar.

My question is, do you doctors that are performing most of the ccsvi treatments in the US compare notes and talk about your approaches? outside of formal conferences I mean.
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Re: ccsvi

Postby Liberation » Wed Mar 23, 2011 3:16 pm

drsclafani wrote:
Cece wrote:
drsclafani wrote:it is thought that stenoses beget stenoses. i am not so sure any longer

I am not entirely sure what you mean by this, but if restenosis makes clotting more likely, wouldn't just having the stenosis in the first place make clotting likely? If I had my 100% LIJV stenosis since birth, for example, so 35 years of stagnancy or turbulence on that side, shouldn't a clot have formed during those 35 years if those conditions make clot formation likely?

drsclafani wrote:AS you say restenosis could occur at any time but clotting tends to occur early unless stenosis recurs after which clotting could occur at any time. i have a theory about this that i cannot share yeet without appearing to shoot my mouth off so i will lay low for the time being

There is no judgment here, shooting off at the mouth is ok, being wrong is ok, sharing theories is very ok....and I suppose laying low is ok too. Sigh.


i have been laying low because i have been so busy. my, how active the board is now. like i said, it was mind candy at that meeting.

firstly, if you have a stenosis of a vein, it might not clot, it might form clots that dissolve, it might just send most of the blood on its merry way through the collaterals.

there is distinct differences between a healthy vein and a damaged vein.

if you injure the wall of the vein, the body sees it as a breach in the wall, even if there is no breach in the wall, only loss of the wallpaper. The body then sends its patchers(platelets) to the area to cover the hole and Aspirin makes them less sticky. Also signals go out to form clot to plug the hole. in other words thrombus is formed. Arixtra (fondaparinux) is an antithrombin drug. These medications are used to reduce the risk of thrombus caused by injury to the wall.

Has anyone noticed that the increase in thrombosis came when larger balloons were used. Dr. Sinan first told us that he could use 18-22 mm balloons without any problems. This was encouraging in our battle to avoid restenosis. However i only had one thrombosis prior to the large balloons: this was in an hypoplasia. I had none is patients dilated to only 14 mm, although i did have restenosis.

but after using larger balloons i had several, and while some were in patients with hypoplasia, others were in patients with good old fashion valvular stenosis. .

I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.

Its only been a few weeks so i cannot tell you that this works yet.

There, i am not lying low now.


Dr Sclafani, it is really good to have you back on board. :)
It seems very logical to me what you said about the use of larger balloons and thrombosis rate. It always impresses me that you try to find better and better ways to do the procedure.

You mentioned that you went back to using smaller ballons. Did I get it correctly that now you are dilating only the valves? Do you still break the annulus when it is too narrow? If I remember correctly,you told me earlier that the small balloon woulld not have a distinctive impact on veins.

I also contacted dr Sinan to find out more about his results as he uses large balloons and I also heard a lot of incidences of thrombosis and scarring recently.
He told me that they have been following their patients for 1 year now with close Doppler U/S, and never seen or heard of hyperplasia or scarring in the vein after angioplasty. He heard about such cases when stents have been used.
Out of 400 patients they had 4 patients with partial clotting of the vein after procedure (1%) all treated completely with anticoagulant. All of them in the first 100. With more experience, this did not happen. No patient with pulmonary embolism.

I am just wondering what is your opinion about this. Can the different anticougulant regimen make a difference as well? Is there a risk of thrombosis or scarring even 1 year after the procedure? What is the chance of scarring, intimal hyperplasia with angioplasty? With large balloons, what kind of risks do you see aside from thrombosis?

As for the missing valves, I just read some posts here that it caused pressure and pain behind the eyes for some people when they bend their heads. Could it be a problem for us? I am not sure if I remember correctly, but dr Sinan told me that as long as someone is breathing reflux does not happen even when the valves are permanently open. Did I get it correctly?

I would greatly appreciate your opinion
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Postby Cece » Wed Mar 23, 2011 4:54 pm

Liberation, of those 400 patients, would some be patients who he did not see again and who received no follow-up? Or is that 400 patients who have had successful doppler ultrasounds showing flow some weeks or months post-procedure?

He does use a strong anticoagulant regimen imo (Lovenox for one week, Plavix for...not sure how long, plus aspirin). There were also a few patients of Dr. Sinan's in December who clotted. That would not be in the first 100. I look forward to seeing publications out of Kuwait! Dr. Sinan made a very good impression at the Brooklyn symposium, he comes across as dynamic and intelligent.
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Postby sara-sama » Wed Mar 23, 2011 5:56 pm

Dr Sclafani, My sister had amyotrophic lateral sclerosis, she had conducted a catheter and dealt aspirin for eight months, but she died a month ago ..
I found this research about the impact of aspirin on Als patients ..
Do you think that aspirin harmed my sister ?


Abstract

We sought to examine the influence of medication usage and laboratory measurements on disease progression in amyotrophic lateral sclerosis (ALS). A database of 596 volunteers with ALS was generated from three clinical trials and one observational study. Disease course was measured by survival and three functional measures: the ALS Functional Rating Scale (ALSFRS), Vital Capacity (VC) and Maximum Voluntary Isometric Contraction (MVIC). Survival modeling was performed using Cox proportional hazards regression. The association of medication or laboratory measurements with disease progression was determined using a random effects model. In the multivariate analysis, survival was shorter in participants who took aspirin (HR =1.93, p =0.046); NSAIDs (HR =1.51, p =0.054); had low blood chloride (HR =0.76, p =0.020) or high bicarbonate levels (HR =1.37, p =0.006). Individuals who took calcium had better survival (HR =0.37, p =0.008) and a slower rate of decline of MVIC arm megascore (p =0.033). Vital capacity declined faster in individuals with lower serum chloride (p<0.0001), or higher bicarbonate (p =0.002) levels and those taking paracetamol (acetaminophen) (p =0.035). We conclude that aspirin or NSAID use may shorten survival in ALS, while calcium use may prolong survival. Our results support a need to further explore the role of neuroinflammation in the pathogenesis of ALS.

PMID: 18608098 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/18608098
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Postby drsclafani » Wed Mar 23, 2011 11:12 pm

MaggieMae wrote:Dr. Sclafani: "i am a bit more concerned about the hypercoagulability of the antiphospholipid syndrome (Hughes sydnrome) which can mimic MS to some degree.
i am thinking to get a hematology consult on MS patients with a history of clotting problems like DVT before treatments to look for this syndrome"



Dr. Sclafani,

My husband is scheduled to have the procedure with you at the end of this month. I had talked to my husband's PCP regarding testing for Hughes Syndrome for my husband since his niece has it. His PCP said it does not run in families. That was the end of the conversation. My husband also has two sisters with MS (one is mother of niece with Hughes). None have had any blood clotting issues in the past (except niece).


Read this:

Antiphospholipid syndrome (APS) is a heterogenous disorder in terms of clinical manifestations and range of autoantibodies. In 2006, revised criteria for the diagnosis of APS were published in an international consensus statement.5 At least one clinical criterion and one laboratory criterion (discussed further in Lab Studies) must be present for a patient to be classified as having APS.

•The clinical criteria are as follows:
◦Vascular thrombosis
■One or more clinical episodes of arterial, venous, or small-vessel thrombosis in any tissue or organ confirmed by findings from imaging studies, Doppler studies, or histopathology (see Histologic Findings).
■Thrombosis may involve the cerebral vascular system, coronary arteries, pulmonary system (emboli or thromboses), arterial or venous system in the extremities, hepatic veins, renal veins, ocular arteries or veins, or adrenal glands. Investigation is warranted if a history of DVT, PE, acute ischemia, MI, or CVA (especially when recurrent) is present in a younger individual (males <55 y; females <65 y) or in the absence of other risk factors.
◦Pregnancy morbidity
■One or more late-term (>10 weeks' gestation) spontaneous abortions
■One or more premature births of a morphologically healthy neonate at or before 34 weeks’ gestation because of severe preeclampsia or eclampsia or severe placental insufficiency
■Three or more unexplained, consecutive, spontaneous abortions before 10 weeks’ gestation
•Laboratory criteria: Patients must have (1) medium to high levels of immunoglobulin G (IgG) or immunoglobulin M (IgM) anticardiolipin (aCL), (2) anti–beta-2 glycoprotein I, or (3) LA on at least 2 occasions at least 12 weeks apart. (See also Lab Studies.)
Other antiphospholipid (aPL)–associated clinical features recognized by the 2006 consensus statement but not included in the criteria include cardiac valve disease, livedo reticularis, thrombocytopenia, nephropathy, and neurologic manifestations.

Thus, history of any of the following should raise the examiner's suspicion for APS:

•Thrombosis (eg, DVT/PE, MI, transient ischemic attack [TIA], or CVA, especially if recurrent, at an earlier age, or in the absence of other known risk factors)
•Miscarriage (especially late trimester or recurrent) or premature birth
•History of heart murmur or cardiac valvular vegetations
•History of hematologic abnormalities, such as thrombocytopenia or hemolytic anemia
•History of nephropathy
•Nonthrombotic neurologic symptoms, such as migraine headaches, chorea, seizures, transverse myelitis, Guillain-Barré syndrome, or dementia (rare)
•Unexplained adrenal insufficiency
•Avascular necrosis of bone in the absence of other risk factors
•Pulmonary hypertension


So, i do not think that we can propose that we work up patients simpoly because they have MS. I am considering working up patients who have a history of blood clotting

i will keep working on this
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Re: ccsvi

Postby drsclafani » Wed Mar 23, 2011 11:17 pm

fogdweller wrote:
drsclafani wrote:I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.


I wonder if some longitudinal movment (i.e. pull the balloon) might also help, perhaps even with a balloon smaller than full vein diameter so it does not rub against the vessel wall"?

it would have to be smaller than the wall diameter. if it were larger it would scrape the intimal cells off the wall. ouch
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Re: ccsvi

Postby drsclafani » Wed Mar 23, 2011 11:19 pm

pklittle wrote:
drsclafani wrote:I have been thinking of how to reduce this thrombosis rate. part of the strategy should be to reduce the injury to the vein wall.

from IVUS i have noted that the vein wall is not narrowed at all. The valve elements INSIDE the vein are malformed and this malformation leads to stenosis because the valves that do not open, they may be stuck to each other, or may be fused to each other. That said, i have been focused on trying to treat the valvular malformations with a balloon that does not dilate the normal vein. So I measure the vein diameter and use balloons that do not exceed that diameter.


I think I read that Dr. Arata's approach is similar.

My question is, do you doctors that are performing most of the ccsvi treatments in the US compare notes and talk about your approaches? outside of formal conferences I mean.


yes we do. sometimes it turns out that advice is bad, so we are skeptical of what we do not have experience with. But we do compare notes a lot

today i spoke with dr salvi, zamboni, arata, mcdonald, and mandato, and a few others unknown to this group.
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Re: ccsvi

Postby drsclafani » Wed Mar 23, 2011 11:38 pm

Dr Sclafani, it is really good to have you back on board. :)
It seems very logical to me what you said about the use of larger balloons and thrombosis rate. It always impresses me that you try to find better and better ways to do the procedure.


like i have said all along, we have to get some consensus on how to do this procedure before we can compare it to the gold standard, whatever we think that is.


You mentioned that you went back to using smaller ballons. Did I get it correctly that now you are dilating only the valves?


I said i am using balloons of a size similar to the vein itself. i still use large ballons but only large enough. with an accurate measurement of the vein diameter and cross sectional area, you can size the balloon appropriately. You can start with a smaller balloon and work your way up. I am using ivusto determine whether the valve is torn or stretched apart. Venography isnt particularly good at that

Do you still break the annulus when it is too narrow? If I remember correctly,you told me earlier that the small balloon woulld not have a distinctive impact on veins.


again, definition of small. if the vein wall measures 12 mm, then i am not going to dilate to 16. its kind of difficult to explain so far. balloon placement means a lot. balloon pressure is important, balloon length is important. precise diameter is very important for me.

I also contacted dr Sinan to find out more about his results as he uses large balloons and I also heard a lot of incidences of thrombosis and scarring recently.
He told me that they have been following their patients for 1 year now with close Doppler U/S, and never seen or heard of hyperplasia or scarring in the vein after angioplasty. He heard about such cases when stents have been used.
Out of 400 patients they had 4 patients with partial clotting of the vein after procedure (1%) all treated completely with anticoagulant. All of them in the first 100. With more experience, this did not happen. No patient with pulmonary embolism.


I do not want to disparage Tariq. If he is able to get that kind of followup i commend him, but i find it difficult to comprehend that his patients will come back to alexandria for followup ultrasounds. Maybe his patients in the kuwaiti trial are genetically different. Seriously, perhaps they do not have as much coagulopathy. perhaps different popoulations have jmore or less incidence of coagulation disorders.

I am just wondering what is your opinion about this. Can the different anticougulant regimen make a difference as well? Is there a risk of thrombosis or scarring even 1 year after the procedure? What is the chance of scarring, intimal hyperplasia with angioplasty? With large balloons, what kind of risks do you see aside from thrombosis?


definitely different regimens of anticoagulation can have different results. The real question is which is the best until wd standardize treatments, we will not be able to evaluate the incidence of thrombosis.

We have never treated by angioplasty a disease like this. pure valvular obstructionsi am not sure we need to continue to think that restenosis is an essential component of this. We just have to figure out how to do this properly.

As for the missing valves, I just read some posts here that it caused pressure and pain behind the eyes for some people when they bend their heads. Could it be a problem for us? I am not sure if I remember correctly, but dr Sinan told me that as long as someone is breathing reflux does not happen even when the valves are permanently open. Did I get it correctly?


i do not entirely agree with that statement. Some patients do consequences of incompetent valves. not all , some
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Postby drsclafani » Wed Mar 23, 2011 11:42 pm

sara-sama wrote:Dr Sclafani, My sister had amyotrophic lateral sclerosis, she had conducted a catheter and dealt aspirin for eight months, but she died a month ago ..
I found this research about the impact of aspirin on Als patients ..
Do you think that aspirin harmed my sister ?


Abstract

We sought to examine the influence of medication usage and laboratory measurements on disease progression in amyotrophic lateral sclerosis (ALS). A database of 596 volunteers with ALS was generated from three clinical trials and one observational study. Disease course was measured by survival and three functional measures: the ALS Functional Rating Scale (ALSFRS), Vital Capacity (VC) and Maximum Voluntary Isometric Contraction (MVIC). Survival modeling was performed using Cox proportional hazards regression. The association of medication or laboratory measurements with disease progression was determined using a random effects model. In the multivariate analysis, survival was shorter in participants who took aspirin (HR =1.93, p =0.046); NSAIDs (HR =1.51, p =0.054); had low blood chloride (HR =0.76, p =0.020) or high bicarbonate levels (HR =1.37, p =0.006). Individuals who took calcium had better survival (HR =0.37, p =0.008) and a slower rate of decline of MVIC arm megascore (p =0.033). Vital capacity declined faster in individuals with lower serum chloride (p<0.0001), or higher bicarbonate (p =0.002) levels and those taking paracetamol (acetaminophen) (p =0.035). We conclude that aspirin or NSAID use may shorten survival in ALS, while calcium use may prolong survival. Our results support a need to further explore the role of neuroinflammation in the pathogenesis of ALS.

PMID: 18608098 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/18608098


sara sama
the report does say that mortality was associated with aspirin and nsaid use. but does that mean that the aspirin caused the death? not necessarily. perhaps they were in more pain and perhaps more pain is associaed with death, as an example
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