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PostPosted: Sun May 03, 2009 9:30 am 
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A note from Dr. Simka, regarding his impression of the difference in MS venous stenosis, after studying the veins with ultrasound:

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From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.

AC

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PostPosted: Sun May 03, 2009 9:51 am 
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Now that is an interesting comment. I wonder if Dr Zamboni has removed any tissue and sent it to pathology to see if it has the characteristic chages in these areas of our stenosis or if Dr Simka means to do that.

Here's an explanation of the syndrome:

Quote:
Endovascular venous stenting in May-Thurner syndrome.Heijmen RH, Bollen TL, Duyndam DA, Overtoom TT, Van Den Berg JC, Moll FL.
Departments of Vascular Surgery, St. Antonius Hospital, Nieuwegein, The Netherlands.

BACKGROUND: Chronic pulsatile compression of the left common iliac vein between the crossing right common iliac artery and the lowest lumbar vertebral body may induce focal intimal proliferation of the vein (May-Thurner syndrome), resulting in impaired venous return and left iliofemoral thrombosis. Corrective surgical treatment requires extensive dissection. In this report, we describe our experience with endovascular venous stenting in May-Thurner syndrome. METHODS: Six patients with symptomatic May-Thurner syndrome were treated with percutaneous transluminal angioplasty and implantation of self-expanding stents. RESULTS Postprocedure phlebography revealed patent iliofemoral veins with unimpeded venous outflow and disappearance of collaterals in all patients. No procedure-related complications occurred. At follow-up (median, 12 months), 5 of 6 patients were free of symptoms. In one patient lower extremity edema was aggravated despite a patent stented segment of the left iliac vein. The patient continues to wear support stockings to compensate for continuing venous insufficiency. Color coded duplex scanning revealed patency at regular intervals in 5 patients. In one patient, occlusion of the stented venous segment with return of symptoms was detected at one month. Patency could not be restored despite catheter-directed thrombolytic therapy. After angioplasty, however, adequate collateral circulation was restored and symptoms resolved completely. CONCLUSIONS: Endovascular venous stenting in May-Thurner syndrome is technically feasible, and leads to reduction of symptoms in the majority of patients with high patency rates in the medium-term. This approach may prove to be a percutaneous alternative to surgical treatment.

PMID: 11292912 [PubMed - indexed for MEDLINE]


cool that stenting seems to work at laeast in the shorter follow up they did here.

The vascular doc that did my dopplers mentioned that venous repairs tend to need re doing with time...........


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PostPosted: Sun May 03, 2009 10:25 am 
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WOW...more evidence of reduction of symptoms YIPPIE


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PostPosted: Sun May 03, 2009 11:01 am 
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It is interesting when new things fall into place, and as more time is spent on this model and more researchers get involved and more observations come out there will be more "Aha!" moments I believe.

but it may not be easy or straightforward notice this section of the abstract
Quote:
In one patient lower extremity edema was aggravated despite a patent stented segment of the left iliac vein. The patient continues to wear support stockings to compensate for continuing venous insufficiency. Color coded duplex scanning revealed patency at regular intervals in 5 patients. In one patient, occlusion of the stented venous segment with return of symptoms was detected at one month. Patency could not be restored despite catheter-directed thrombolytic therapy. After angioplasty, however, adequate collateral circulation was restored and symptoms resolved completely.


one person had to have surgery twice to get a good result and one person had an open corrected vein, but still had to wear compression stockings to keep the leg from swelling up. Notcie that they did rechecks very frequently also....

Protocols for these things are still to be illuminated for MS yet...


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PostPosted: Sun May 03, 2009 11:07 am 
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I've told Jeff he's still going to have to stick to his "good living" plan...no smoking (not that he ever did), drinking, red meat, heavy stress....and keep up the Swank diet, stress relief, cardiovascular exercise and healthy living. Everything he can do to keep his vascular system healthy and functioning after having the stent placed. He's more than happy to keep up his program. Two years now, and it's become habit. I think lifestyle might help keep things flowing-
AC

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PostPosted: Sun May 03, 2009 3:14 pm 
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I can't read that name without thinking of Latka and Simka on 'Taxi'.

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PostPosted: Sun May 03, 2009 4:21 pm 
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Funny- I loved Taxi!
More may-thurner stuff with repairs

Quote:
..... Four patients with May-Thurner syndrome underwent iliac vein angioplasty and stenting. Technical success was 100%. On clinical follow-up, the patients with May-Thurner syndrome have had improvement/resolution of their symptoms. There have been no complications from either therapy. May-Thurner syndrome is a clinical entity of left iliac vein compression by the right iliac artery, resulting in isolated left lower extremity swelling and may be a precipitating factor for iliofemoral deep venous thrombosis. Magnetic resonance imaging is the best modality for diagnosis of this entity as it can rule out the presence of pelvic masses and deep venous thrombosis while simultaneously demonstrating the anatomy characteristic of this syndrome.

from HERE


another one

Quote:
OBJECTIVE: May-Thurner syndrome is characterized by left common iliac obstruction secondary to compression of the left iliac vein by the right common iliac artery against the fifth-lumbar vertebra. This anatomic variant results in an increased incidence of left-sided deep venous thrombosis (DVT). Furthermore, while a preponderance of left-sided DVT has been demonstrated in women during pregnancy and oral contraceptive use, patients are not typically screened for this condition after developing a left-sided DVT. As anticoagulation alone is ineffective for DVT treatment in the setting of May-Thurner anatomy, more aggressive treatment is warranted. Failure to diagnosis this condition predisposes these women to the unnecessary risks of recurrent DVT and post-thrombotic syndrome. METHODS: We present the occurrence of 7 adolescent patients with previously undiagnosed May-Thurner syndrome who presented with DVT after the initiation of oral contraceptive steroids (OCP) use. All 7 patients elected to proceed with mechanical thrombolysis/catheter based thrombolysis followed by endovascular stenting and were postoperatively treated with 6 months of warfarin. RESULTS: Mean patient age was 18.3 +/- 3.3 years (range, 16-24 years). Mean time to presentation after initiation of OCP was 5 weeks (range, 2-10 weeks). Mean time to intervention was 16.8 days (range, 10-24 days). All patients were treated with mechanical thrombectomy. Our rate of intraoperative clot resolution was 100%. All 7 patients were treated with self expanding nitinol stents after angioplasty of the iliac vein stenosis with resolution of the stenotic segment. Primary stent patency is 100% (7/7). Mean follow-up time is 13 +/- 13.84 months (range, 6-42 months). There have been no long-term complications related to surgical treatment or anticoagulation. All 7 patients have experienced resolution of left leg swelling and pain and have no evidence of post-thrombotic syndrome or DVT recurrence to date. CONCLUSIONS: Women on OCPs presenting with left-sided iliofemoral DVT should be screened for hypercoagulable disorders and underlying May-Thurner anatomy. Treatment of May-Thurner syndrome should include thrombolysis/thrombectomy and anticoagulation for current DVT in addition to angioplasty and stenting of the underlying obstruction.

PMID: 19135831 [PubMed - indexed for MEDLINE]


from here

Interesting to note the association of women and coagulation. If MS endothelial changes reflect and are similar to May-Thurner, might we have a connection to the female hormones here? But it is good news that stents worked well.


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PostPosted: Wed May 06, 2009 8:36 pm 
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Quote:
A note from Dr. Simka, regarding his impression of the difference in MS venous stenosis, after studying the veins with ultrasound:

Quote:
From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.


Cheer,
Did Dr. Dake comment about the veins? I know you said they were small. Anything else?


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PostPosted: Wed May 06, 2009 8:58 pm 
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Terry wrote:

Cheer,
Did Dr. Dake comment about the veins? I know you said they were small. Anything else?


I need to talk to him more in depth...our recent conversations have been about post op care for Jeff, next appointments, etc.

What he said when we first looked at Jeff's MRV pics, and what we saw was venous stenosis...the veins look fine above and below, but at a certain point, parallel to each other at the base of Jeff's skull, the veins both tapered in really thin. One side (left) was completely blocked and lots of little veins had formed, trying to take the blood back. The other side (right) was almost closed all the way, very close to being shut off. Jeff has a cervical lesion at the same level of this narrowing. Dake thinks he was maybe born with this narrowing, and as he's gotten older, it's just gotten worse. The new stents are now pinching him a bit, because they are made to grow once they're in place, and the veins will stretch and grow around them. The thing I'm not sure of is if Dake thinks this is like a birth defect, of caused by something external...I don't know, and would love to hear his thoughts. I'll see if he'll send me a pic to post, or if he wants to save it for his research. He's been really cool about us talking about everything and sharing. This is all new to him, too!

AC

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PostPosted: Wed Jun 24, 2009 6:13 am 
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cheerleader wrote:
A note from Dr. Simka, regarding his impression of the difference in MS venous stenosis, after studying the veins with ultrasound:

Quote:
From my (still very limited) experience, the hallmark of venous lesions in MS patients is the stiffness of venous wall, it is not external compression. Neither is it alike varicose veins, thrombosis, atherosclerosis, or so. It is very strange, I am sitting in vascular sonography for years and I don't remember to see such a vein before scanning MS patients. Actually, the most similar pathology (as far as ultrasonographic picture is concerned) is May-Thurner syndrome in iliac veins.

AC


This text was most interesting! Where is from originally? I would like to read it, the whole text. Pleeaaseee..


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PostPosted: Wed Jun 24, 2009 6:59 am 
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Ernst, that is all of it. It was in private communication from Dr Simka to Cheer, and those were his comments with regards to this anomaly.

This is a new idea as to what causes MS and as such the research is in the works, not yet done. Dr Simka is one of the researchers. He generously has shared some of his observations with us here before it is in a paper.
marie

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PostPosted: Wed Jun 24, 2009 7:07 am 
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Thanks for answer. I have red Simka's texts, linked from here. But this text was something havent seen before. That Simka's comment was so, so interesting. Maybe it means that changes in veins found in ms.. are only typical with ms?


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PostPosted: Wed Jun 24, 2009 8:05 am 
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He is writing papers even now we will be seeing soon, perhaps he will comment on that particular aspect in the next paper. The researchers working on this are doing a lot of work even now and papers will come out soon. I think that perhaps someone will need to remove some tissue from a stenosis and send it to pathology to see what is involved with it.

So far, the only person approved for a study to actually do surgery on these lesions is Dr Zamboni and I have no idea if he has tried to see what kind of things might be different about the stenoses. Dr Dake is putting a stent into the area not trying to remove any tissue to look at. Dr Simka is in the process of getting approval to do a study.

The people who use antibiotics and how have had success there are interested in the idea that the stenoses might be caused by chlamydia pnemoniae. Time will tell the answer to these questions.
isn't it exciting?

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PostPosted: Wed Jun 24, 2009 8:11 am 
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This is so exiting that Im shivering :D


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PostPosted: Wed Jun 24, 2009 8:34 am 
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What is cool about it is that it is moving pretty fast really. We will have answers before too long I think. I am really having a good time watching this develop! It is like a big chess game with wonderful worldwide players.

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