Reason For Restenosis

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

Postby eric593 » Sat Nov 27, 2010 6:58 pm

Cheer, I'm just not clear that that info means MSer's are "most likely" to have high fibrin levels or hypercoagulation issues.

For all we know MSer's are responding in an appropriate manner to vasculature or other internal injuries (MS lesions ARE peri-venular). I don't see any strong indication that, but for a very few exceptions like bluesky, Jeff and dania, MSer's have reported anything but a healthy and appropriate coagulation response following angio or as a group at all. Jaundice is certainly not a traditional symptom of MS.

And I would think one of the treating CCSVI physicians would have made public this finding by now, given how significant this hypercoagulation issue would be to treatment risks (especially stent use and balloon size and corresponding vein injury) and aftercare medication regiments. I just don't think I've seen anything to suggest MSer's are "most likely" to have higher fibrin levels and hypercoagulation. I think that's a stretch not supported by how doctors are treating patients. My guess is fibrin levels are not due to hypercoagulation but instead are appropriate for venular or other internal injury that is occurring. And that is why doctors are not putting all MSer's who undergo angio on a stronger anti-coagulation protocol than other non-MSers who have had venous or arterial angio. I don't think that apirin would be given as the only follow up treatment at Albany for those just having ballooning if hypercoagulation was assumed to be the case for almost all MSer's. And I would think that coagulation ability would be a mandatory pre-test as well for the treating doctors to assess not only a proper treatment plan that did not put the patient at undue risk, but the aftercare as well.
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Postby cheerleader » Sat Nov 27, 2010 8:01 pm

Eric--Dr. Zamboni puts his angioplasty recipients on heparin for three weeks. Going home with low dose aspirin is not enough, not to me, but according to him and other IRs.

All patients were administered a prophylactic dose of low-molecular-weight heparin for the subsequent 3 weeks

link

I never said Jeff's jaundice or high liver enzymes was a typical response in MS...I said that his peculiar serum results were what clued me off that something was going on with his blood, and that's how I began reading about the vascular connection to MS and contacting Stanford. And I learned there is a sub-group of pwMS (mostly men/RRMS) that have high liver enzymes.

Abnormal liver test results found in people with multiple sclerosis in placebo arms of clinical trials
Risk factors for having an abnormal liver test were male gender and higher body mass index (BMI) over each time period (at the first recorded test as well as over the first year and the whole study). People with relapsing-remitting MS and a shorter disease duration were at an increased risk of an abnormal ALT test over the whole study period. Other liver tests found abnormal results associated with an older age and relapses in the previous 12 months.

http://mssociety.ca/en/research/medmmo- ... 061101.htm


You're right....Fibrin is an appropriate response to a break in the blood brain barrier and plays a large role in inflammation in MS. There is a connection to MS- and since fibrin is a systemic response, all of the body's blood is affected.

The association of tight junction abnormalities with increased fibrinogen leakage may have important implications for lesion initiation through interactions with microglia. Previous publications, including studies that correlate MRI with histology, find fibrinogen deposition to be one of the earliest events associated with MS lesion formation [13,14]. Experiments using fibrinogen-knockin mice have shown fibrinogen to be an activator of microglia, the resident immune cells of the CNS [15]. Activation of microglia appears to be sufficient to induce inflammatory demyelination, even in the absence of T-cells [16], and it has been suggested that focal areas of microglial activation represent an early stage of tissue injury in MS which precedes the formation of the hypoxia-like demyelinated plaques [14]. In our studies, the trend in MS NAWM for vessels with increasing TJ abnormality to show fibrinogen leakage could be suggested to be more important than first realized, as fibrinogen could function to mediate the initial activation of resting microglia leading to increased phagocytosis [17].

http://www.biochemsoctrans.org/bst/037/0329/0370329.pdf


Although fibrinogen has been primarily studied for its functions in blood coagulation, there is appreciable evidence that fibrinogen plays a pivotal role in the inflammatory response (12, 13) and host defense (14, 15). Fibrinogen is a classic acute-phase reactant, characterized by a unique molecular structure with binding sites for cellular receptors that regulate the inflammatory process (16, 17). Research in MS animal models shows that prophylactic fibrin depletion either by genetic depletion of fibrinogen (18) or by prophylactic administration of anti-coagulants (18, 19) ameliorates disease pathogenesis.

http://jem.rupress.org/content/204/3/571.full


My main concern is that there are people being treated who have no idea what their d-dimer or coagulation numbers are before treatment. And they are having problems. Patients need to know what questions to ask.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby blossom » Sun Nov 28, 2010 1:46 am

well, i didn't think i had to be a doctor to get this done right as far as getting the best suited blood thinner etc. i read as much as i could. knew some of the risks was willing to take the risk. depended on the dr. to know more than me which no doubt they do. that's why the more i read, the more that people are clotting up etc. i can't help but get feelings i can't write here or i'll be kicked off.

for sure as dania says look at her case the blood thinner she was on did not prevent clotting. so, this is very complicated and will vary.

yeah i read where zambonni used these certain blood thinners.

but, you go to a place here in the states. they have done a good many procedures. your life is in their hands. ok, they get your veins up and flowing. great, that is a real good thing they did. so you would think with all their knowledge and many experiences "see i only experienced this once." that more attention and individual health issues such as the patient having a clotting disorder that makes them more prone to clots would be looked at and considered more.

it's not like i did not let them know. i reminded that i had this issue even when the dr. came in before procedure. and, they were ready to take me in and i asked about when were they gonna do the blood work for the kidneys. oops!! then i got the blood work.

you think well, they know the circumstances. they're doctors they'll do what's best. well i was prescribed plavix, which i picked up that night at the hosp. drug store. got home on a fri. so any aftercare could not take place until the following week. some people are clotting within days. so, there goes your chances of improvement and then you got bigger problems.

from what i read now, plavix don't get it if you have blood disorders as well as other medicine may do to maybe make the odds a little better for success.

so, yeah it's very important to be tested and know. but it's worthless if the treating doctor don't act accordingly.
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Postby HappyPoet » Sun Nov 28, 2010 10:08 am

blossom, please know that you are not alone in how you feel. Thank you for being a voice for the poor, the tired, the huddled masses yearning to breathe free*

*Statue of Liberty... my brother is responsible for her safekeeping.
Last edited by HappyPoet on Sun Nov 28, 2010 10:40 am, edited 1 time in total.
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Postby Cece » Sun Nov 28, 2010 10:30 am

Hypercoaguability was not on the radar for Dr. Englander. She did not adjust treatment based on blossom's mthfr.

Hypercoaguability is on the radar for Dr. Sclafani. He would have adjusted what he did and not used a stent for Dania's case.

Hypercoaguability was not on the radar for Dania's original doc. (European, but who was it?) As far as we know, he did not adjust treatment when he knew his patient was already on Coumadin.

From what Cheerleader says of Dr. Dake and Marie, he took her hypercoaguability into consideration, it was on the radar.

What about the other docs? Hubbard's group, or Florida, or Sinan, do we know if any of them are taking hypercoaguability into consideration?

Right now if I had a known hypercoaguability disorder I would only go to a doctor who takes it into consideration. Right now that's Dr. Dake and Dr. Sclafani until we find out more about the others.

Mistakes may be being made and it's lifetime consequences if you're the one who gets the doc early in the learning curve or who doesn't provide full care before, during, after the procedure. :(
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Postby cheerleader » Sun Nov 28, 2010 10:40 am

Blossom....please, I hope you know this is not about blaming patients. No one expects the patients to be doctors. I'm so sorry for everything you've been thru. The real problem is that there is not a standardized means of care for pwMS and venous angioplasty. Each doctor has a different approach. When I started writing about this with Marie and others in 2009, we included many links on blood hypercoagulation and angioplasty because she got a clot in her leg. It's because of Marie that I knew to keep checking Jeff's INR and PT time and keep an eye on his blood. It's why he stayed on nattokinase, serrapeptase and bromelain even while on blood thinners. But it's over a year since Marie left to write her book, and the treatment has moved beyond Stanford's doors, around the world. And our threads are long gone...that's why I stick around...to hopefully keep what we learned out there.
I'm sorry-
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Cece » Sun Nov 28, 2010 10:56 am

cheerleader wrote:Eric--Dr. Zamboni puts his angioplasty recipients on heparin for three weeks. Going home with low dose aspirin is not enough, not to me, but according to him and other IRs.

All patients were administered a prophylactic dose of low-molecular-weight heparin for the subsequent 3 weeks

link

Cheer, do you have an opinion on the 3 weeks of heparin or heparin-like anticoagulant (say, Arixtra)? What could a person do after those three weeks if they were still concerned about possible clotting? If I were on your endothelial health program, as I've been since last January (except I went back to Diet Coke after two successful months without it), is there anything else to consider?
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Postby blossom » Sun Nov 28, 2010 8:14 pm

cheerleader, happypoet and cece, thanks for each individual input. cheer, i don't feel anyone is picking on me or i'm to blame as the patient nor should anyone feel they are to blame as a patient. we all have different circumstances from the degree of our illness, money factors, if we have a care giver such as spouse that can help us through this journey and if there is good after care when we get home etc. so, we that have been kinda on the front lines of this battle made the choices we thought best at the time.

with the way doctors are controlled by so many things it is hard for them to take the time some still want to give us. so, in many ways this is a trickle down effect of the times we live in. --but not an excuse.

so, i'm living with it as others are and we'll never know if our out comes would have different if we would have been prescribed different meds. or if we weren't so rushed. but it is hard wondering about it.
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Postby cheerleader » Sun Nov 28, 2010 9:57 pm

Cece wrote:Cheer, do you have an opinion on the 3 weeks of heparin or heparin-like anticoagulant (say, Arixtra)? What could a person do after those three weeks if they were still concerned about possible clotting? If I were on your endothelial health program, as I've been since last January (except I went back to Diet Coke after two successful months without it), is there anything else to consider?


Cece...no idea. I think Dr. Zamboni and Dr. Dake know what they're doing with anticoagulants, and Jeff trusted Dr. Dake. I think hydration, moderate exercise, a low fat diet and the supplements in the endo health program should keep blood flowing...but this will be for you and Dr. Sclafani to work out. I trust him, as well. And you'll be seeing him for aftercare, and check ups are essential too.
Blossom...I wish you peace and more answers. Again, I'm really sorry.
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby dania » Mon Nov 29, 2010 9:17 am

..Intimal hyperplasia is not a true disease, but a physiologic healing response to injury to the blood vessel wall. It is the bane of endovascular intervention and vascular surgery.

When the endothelium is injured, endothelial cells release inflammatory mediators that trigger platelet aggregation, fibrin deposition and recruitment of leukocytes to the area. These cells express growth factors that promote smooth muscle cells migration from the media to the intima. The smooth muscle cells proliferate in the intima and deposit extracellular matrix, in a process analogous to scar formation. This typically occurs over a period of a few months.

The result is formation of a neo-intima over the site of injury. An exuberant healing response leads to intimal hyperplasia (thickening) that encroaches on the vessel lumen and causes stenosis. This process is analogous to keloid formation in epithelial wounds. It seems to be accelerated by the presence of prosthetic material in the vessel.

Intimal hyperplasia may result from endovascular intervention, vascular surgical procedures, long term vascular catheters and devices, or turbulent flow. It is not infrequently seen after angioplasty, stent insertion, around long term venous catheters, and at surgical vascular and graft anastomoses. Re-stenosis occurring 3 to 12 months after angioplasty is typically due to intimal hyperplasia.
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Postby blossom » Mon Nov 29, 2010 12:33 pm

dania, very interesting. hope there is a way to treat this should it be found to be the reason for some not so good outcomes.
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Postby Cece » Mon Nov 29, 2010 1:10 pm

To corroborate what dania is saying, drsclafani has talked about intimal hyperplasia too. Here I am confused, because I thought intimal hyperplasia was the same as neointima but he lists them separately:
http://www.thisisms.com/ftopicp-99933.html#99933
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Postby magoo » Mon Nov 29, 2010 2:27 pm

but, you go to a place here in the states. they have done a good many procedures. your life is in their hands. ok, they get your veins up and flowing. great, that is a real good thing they did. so you would think with all their knowledge and many experiences "see i only experienced this once." that more attention and individual health issues such as the patient having a clotting disorder that makes them more prone to clots would be looked at and considered more.


This is a big problem. (no blame here, just discussion)
Yes, we think we should be able to trust that the doctor knows it all, but unfortunately they don't. The good one's will admit when they don't know something. :wink: There is a need to ask LOTS of questions of the physician we choose to work with. We have to be our own advocates.
I am so happy cheer is pointing us to the "old" discussions. They are so informative and need to be visited.
Rhonda~
Treated by Dake 10/19/09, McGuckin 4/25/11 and 3/9/12- blockages in both IJVs, azy, L-iliac, L-renal veins. CCSVI changed my life and disease.
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Postby TMrox » Mon Nov 29, 2010 3:23 pm

On my first appointment with my neuro he ran lots of tests. He found that I had a lesion in my spinal cord and elevated liver enzimes.

At that time I was not on medication so he thought that the liver was somehow connected to my transverse myelitis. He told me that there are no many coincidences in medicine.

I had fortnightly blood test monitoring my liver enzymes and they worsened over a six month period. I had liver ultrasounds and a liver biopsy which revealed nothing. No reason for the elevated enzymes.

My liver enzymes got back to normal two months after being treated for CCSVI. My liver docs don't know why either. Weird.
Diagnosed with Transverse Myelitis in December 2008. Inflammatory demyelination of the spinal cord (c3-c5). No MS, but still CCSVI.
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