Reason For Restenosis

[cheerleader]

We were talking about this in the summer of 2009...Marie, the 2nd treated at Stanford had serious hypercoagulation issues, and we'd been discussing this in relation to stent implantation. All of the Stanford patients were followed closely for INR and PT time.
This is why I've been so adamant about patients staying local and working with GPs to understand their blood numbers. This is a serious issue. Here are some threads--

http://www.thisisms.com/ftopicp-59511-h ... html#59511
http://www.thisisms.com/ftopicp-66244-h ... html#66244


Hypercoagulation from 2008
http://www.thisisms.com/ftopic-6192-0-d ... ation.html
cheer

[Cece]

Thanks for the links. Maybe we need to clean up and consolidate the stickies so that what to do if you have a hypercoaguability disorder can be included there as well.

Dr. Sclafani's advice, which everyone is free to take or leave but I admittedly tend to take, is here:
http://www.thisisms.com/ftopicp-138503.html#138503

If you have "a history of excessive clotting or clotting for no reasons" then a hematological work-up would be in order. But otherwise, he says it's not helpful or cost-effective.

[cheerleader]

If you have "a history of excessive clotting or clotting for no reasons" then a hematological work-up would be in order. But otherwise, he says it's not helpful or cost-effective.

Have to disagree...Jeff's hypercoagulation showed up in routine blood tests (CBC) ordered by his GP at his original diagnosis. He had never had a history of excessive clotting before his first MS flare. He never saw a hematologist, but after reading his results, I knew something was up. His high liver enzymes, SED rate (ESR) petechiae and jaundice were written off by his neuro at the time, who said Jeff should "stop drinking." Since he never drinks, I knew something was going on with his blood. Jeff's CBC and d-dimer numbers were normal before he was treated with angioplasty--he had been on the endothelial health program for about a year, and his SED rate and liver enzymes were down.

Too many pwMS are showing up with high d-dimer and hypercoagulation...this could be due to inflammation or the coagulation cascade which is initiated after an ischemic event. Patients need to know if they have hypercoagulation BEFORE being treated with angioplasty. These simple blood tests could help prevent thrombosis.
cheer

[Cece]

thanks, Cheer. If anyone investigated the right things, it was you. So you are saying that people with MS may have higher likelihood than normal people of having hypercoaguability. And we already know that if you have it, then it is a risk factor for increased clotting after the procecure.

I had a CBC done last winter, I'll have to go dig out the results and look it over again.

[Brainteaser]

From my CCSVI experiences, restenosis is a real issue. Both stenting and angioplasty appear problematic. It is a bit of a worry that professionals of the calibre of Dr Sclafani are playing it down.

[cheerleader]

thanks, Cheer. If anyone investigated the right things, it was you. So you are saying that people with MS may have higher likelihood than normal people of having hypercoaguability. And we already know that if you have it, then it is a risk factor for increased clotting after the procecure.

I had a CBC done last winter, I'll have to go dig out the results and look it over again.

Yup...that's what I'm saying, Cece. Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation. Dr. Dake commented to me that it took more coumadin than normal to get some MSers PT times into the "zone."

This concept of hypercoagulation in MS was the whole premise behind the endothelial health program...and why there are proteolytic enzymes like serrapeptase and nattokinase and anti-inflammatories like bromelain were included. (I believe hypercoagulation in pwCCSVI is due to the coagulation cascade initiated by diffuse cerebral hypoxia...but this is only a theory.)

In any case, it is imperative that pwMS have excellent aftercare if they are treated with angioplasty. Hypercoagulation mixed with additional inflammation in the endothelial lining of the veins due to angioplasty is a dangerous mix. The risk declines as time goes on, the lining of the vein incorporates a stent or calms down after ballooning. And I believe the EH program can help....but again, no research on this, only anecdotal. I closely followed Jeff's CBC results to keep an eye on inflammation and coagulation.
this is a very important piece of the puzzle,
cheer

[bluesky63]

I am traveling and don't have time to do this right but I want to jump in with a tid bit -- a huge "differential" for MS is antiphospholipid syndrome, which is rarely tested for and even more rarely tested for properly -- and many people don't really know the ins and out of coagulation weirdness.

Just had a fascinating discussion with my vascular guy about how many people with MS have a high d-dimer only during an MS flare-up. Why? Could they be throwing off clots that get caught in the stenosis and vcause symptoms but don't show up on the traditional CT screens because they test for pulmonary emoblism but not neck, etc?

Have to go but just throwing this out -- more later -- agree that MS probably includes idiosyncracies in the blood for at least some people!

Edited to add == during flare-ups my d-dimer has been high. I don't know about other people. I can thank the wonderful Marie for this insight, since it was her experience that I read about and made a connection with my own.

Edited again -- sorry! -- it's more than cbc -- I absolutely agree that there is something different with people who have MS and we may need a more specialized screen -- how could it hurt to be careful, especially when we don't know exactly what we're dealing with here?

Thanks for the thread!

[HappyPoet]

(I believe hypercoagulation in pwCCSVI is due to the coagulation cascade initiated by diffuse cerebral hypoxia...but this is only a theory.)

cheer, thanks for participating!

I didn't know that hypoxia causes a "coagulation cascade."
What other problems does hypoxia cause that we should know about, ask about, and/or test for?

Thank you!

[patientx]

Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.

My SED rate was completely normal.

[eric593]

Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.

My SED rate was completely normal.

Me too. Is there research that shows that MSer's 'most likely' have higher levels of fibrin? If this were so, it would increase the risks of angio and/or stenting for MSer's - if that were so - why aren't ALL MS angio patients being put on the likes of comoudin, heparin or warfarin? Wouldn't one of the treating doctors have reported this by now since it changes medications given after angio to prevent coagulation and the risk factors of the treatment itself? Wouldn't they be instituting pre-testing of levels beforehand if hypercoagulation is "most likely" in MSer's?

[dania]

Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.

My SED rate was completely normal.

Me too. Is there research that shows that MSer's 'most likely' have higher levels of fibrin? If this were so, it would increase the risks of angio and/or stenting for MSer's - if that were so - why aren't ALL MS angio patients being put on the likes of comoudin, heparin or warfarin? Wouldn't one of the treating doctors have reported this by now since it changes medications given after angio to prevent coagulation and the risk factors of the treatment itself? Wouldn't they be instituting pre-testing of levels beforehand if hypercoagulation is "most likely" in MSer's?

Coumadin did not prevent blood clots in my stent. I have been on 10mg of Coumadin for over 10 years. My INR is 2.7. Which means my blood should not be able to form clots. But it did. The answer is not a simple one. And my sed rate is normal.

[Cece]

Dania, I worry about generalizing from your situation to everyone's situation because you had known hypercoaguability issues going into the procedure.

If someone's norm is to be on Coumadin, after the procedure, maybe they need to be on something stronger?

I don't even know if there is anything stronger than Coumadin, that's already at the top of the pyramid. (With "Good luck, take an aspirin" at the bottom, when it comes to attention paid to anticoagulation after the treatment.)

[cheerleader]

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults. In this study, the coagulation status and biochemical and non-specific inflammatory markers in patients with MS were investigated. Plasma prothrombin time, activated partial thrombin time, fibrinogen, D-dimer, serum high sensitive C-reactive protein, homocysteine, blood urea nitrogen, creatinine, calcium, total protein, albumin, total cholesterol, vitamin B12, folate levels and erythrocyte sedimentation rate were measured in 42 patients with MS and 31 healthy subjects as a control group. There was a positive correlation between homocysteine and D-dimer levels (r=0.84, p<0.01). However, there was no significant correlation between homocysteine, vitamin B12 (r=0.18) and folate (r=0.23) levels. Serum total protein, albumin and calcium levels of MS patients were lower than the control group. There are some alterations in the coagulation and biochemical status in MS patients. These findings may contribute to better understanding of the etiopathogenesis and clinical characteristics of this disease.

http://www.ncbi.nlm.nih.gov/pubmed/18258432

D-dimer is a sign of fibrin degradation. These MS patients had higher d-dimer levels than controls. As Blue Sky mentioned...Marie has written about this on here. D-dimer levels are higher in pwMS during flares.

But all I really know for sure is Jeff's case. Jeff's blood numbers were taken at the time of his first exacerbation. He was jaundiced, had petechiae, high SED, high liver enzymes. His d-dimer wasn't taken. As Blue Sky and Cece have stated, everyone is different. MS is closely related to antiphospholipid syndrome, which became a differential diagnosis in the 1980s when Dr. Hughes detected APS.

Fibrin is elevated during the coagulation cascade after a break in the blood brain barrier.

Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium (lining of the vessel). Exposure of the blood to proteins such as tissue factor initiates changes to blood platelets and the plasma protein fibrinogen, a clotting factor. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Proteins in the blood plasma, called coagulation factors or clotting factors, respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.[1]

The association of fibrin in MS lesions has been noted-

Fibrin, as the final product of the coagulation cascade, plays a major role in blood clotting. However, the role of fibrin is not restricted to the blood, since components of the coagulation cascade reside within tissues and can stimulate extravascular fibrin formation (1). Studies of fibrin deposition in human diseases (2-5), in combination with experiments from gene-targeted mice deficient in fibrin (6), have shown that a wide range of pathological conditions, such as glomerulonephritis, lung ischemia, and rheumatoid arthritis, are exacerbated by fibrin deposition.

Compromised vasculature in the nervous tissue is a pathogenic manifestation apparent in traumatic injuries, such as spinal cord, optic nerve, and sciatic nerve injury, as well as in central nervous system (CNS) diseases with autoimmune characteristics, such as multiple sclerosis (MS) (7). Blood-brain barrier (BBB) disruption precedes clinical symptoms in MS patients , and fibrin is deposited in the lesions (9, 10), apparently before cerebral tissue injury and demyelination (11). Fibrin deposition also coincides with areas of demyelination (12), as well as with areas of axonal damage (13). In addition, in experimental autoimmune encephalomyelitis (EAE), an autoimmune animal model of MS, there is increased coagulation activation before symptom development (14). Pharmacologic depletion of fibrin in EAE ameliorates clinical symptoms, suggesting that fibrin plays a role in CNS inflammatory demyelination (15, 16). Furthermore, inhibition of fibrin formation by attenuation of thrombin activity is protective in the injured optic nerve (17).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC404108/

my larger point is that SOME patients may have a variety of coagulation issues, and the IRs and vascular surgeons should know the status before angioplasty. At least a d-dimer should be routine (it was at Stanford)
cheer

[MaggieMae]

MS is closely related to antiphospholipid syndrome, which became a differential diagnosis in the 1980s when Dr. Hughes detected APS.

My husband is on a list for treatment for CCSVI. He and his sister have MS. His niece was diagnosed with antiphospholipid syndrome. His neurologist doesn't believe in CCSVI. Should we see his GP and ask for specific tests before angioplasty treatment?

[Cece]

My husband is on a list for treatment for CCSVI. He and his sister have MS. His niece was diagnosed with antiphospholipid syndrome. His neurologist doesn't believe in CCSVI. Should we see his GP and ask for specific tests before angioplasty treatment?

From the sounds of it, yes, he might want to consider having a CBC and whatever they test to rule out antiphospholipid syndrome.