Dr. Sullivan on the maturation of hypoplastic veins

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Dr. Sullivan on the maturation of hypoplastic veins

Postby Cece » Mon May 07, 2012 9:14 am


Maturation of hypoplastic veins

Dr. Sullivan has experience with maturation of veins in end stage renal disease.

Shows image of hypoplastic IJV. What to do? If dilated aggressively, it is likely to thrombose.

Gradually dilate. About 2-3 weeks apart for 6 weeks. Perfectly functional fistula. Working well.

These are 1-2 mm veins that are being matured into bigger veins. In the forearm.

If you have an alternative pathway, even if its collaterals, often the area which was angioplastied or stented with thrombose.

Fistula Maturation: Identify outflow vein in a superficial location. Try to achieve 6 mm lumen during first intervention (but it is painful.) Enlarge vein diameter every 3 weeks with angioplasty. Endpoint of a superficial fistula of 8 – 10 mm (6 mm sometimes adequate). Deep fistulae could require diameter up to 16 mm.

(Would going from a 2 mm vein to a 6-10 mm vein make a difference in a CCSVI patient? I would say yes. My second angioplasty took my left jugular from about those differences, and I had definite cogfog, numbness, and color saturation vision improvements, and that was the only vein treated at that time.) Every mm gained in diameter means a significant amount of cross-sectional area of the vein gained.

Patency is not fantastic. Secondary patency (after a second procedure) is 77% at 12 months, 61% at 24 months, and 32% at 36 months. This is for class 2 fistulas which start off small.

Because of high flow, there is a lot of intimal hyperplasia in these patients. In CCSVI, if you can get the vein open, you might not have that intimal hyperplasia and patency might actually be better.

These fistulas do require maintenance, with on-average intervention needed again at a year. (Not so good if patient is self-paying. But in the long run, we won't be self-paying, because CCSVI will be accepted across the medical community, and we need strategies like this in development if they can be made to work.)

Fistula Maturation: How Does It Occur?
* Up regulation of MMP-2 and 9, and reduction in TIMP-4 with creation of fistula probably involved in outward dilatation and thickening of vein wall.
* Increase in collagen I/III ratio also occurs and probably strengthens vein wall.
* This is probably flow, rather than pressure induced, as animal model studied low pressure.

(But again we're back to our veins having low flow. Does exercising increase that flow? Lying down does.)

It's remarkable that you can take these tiny veins and dilate them to the point that you are disrupting all three layers of the vein wall. (The intima or inner lining, the Media or smooth muscle middle layer, and the adventitia or strong outer covering.) Why does it work, why doesn't the vein tear or thrombose?

Based on animal models, all the changes are probably related to high flow (collagen changes etc listed above).

Overexpression of MMP-2 associated with dilatation and wall thinning in a mouse vein.

In patients, in a study of 20, AVF maturation was successful in 13 and failed in 7. Serum levels of MMP-2/TIMP-2 were significantly higher in patients with matured AVFs vs the levels in patients whose AVFs had failed.

Thrombus formation. There is a cascade after angioplasty damage that leads to deposition of fibrin, but it's somewhat limited in fistulas because high flow rates wash away the fibrin and components.

Would this technique work in CCSVI?

Would flow rates be adequate to initiate vein wall remodeling? Occluding collateral veins with coils might be necessary to achieve this but this would be detrimental to venous outflow from the central nervous system. (My thought: not all patients have good collateral routes, perhaps it would be possible to only select patients with fewer collaterals.)

It's not mentioned by Dr. Sullivan but it seems obvious that if a maturation attempt is to be made, and the other jugular is blocked, only the hypoplastic jugular should be worked on first in a series of planned procedures. By leaving the other jugular blocked, it would increase the blood flow in the hypoplastic jugular, giving it a higher chance of success. In the recent case in Dr. Sclafani's thread, where the patient had a 20 mm vein that was almost completely blocked and a hypoplastic vein on the other side, a strategy might have been to treat the hypoplastic vein first and then return within three months to treat the other jugular. There was a time when Dr. Sclafani used this strategy for an azygous vein, when the patient also had nutcracker syndrome; he treated the azygous vein first with plans for the patient to return for treatment of the renal vein, thereby taking advantage of the higher flow through the azygous vein created by the renal vein blockage.

To initiate vein wall remodeling in CCSVI, in addition to higher flow, Dr. Sullivan lists aggressive anticoagulation and multiple sessions needed both for the procedure itself and for follow-up for primary-assisted patency.

Dr. Sullivan says that sometimes treating CCSVI results in high flow rates and sometimes it does not. In patients with high enough flow rates, maturation might work. (Can you predict which patients will have a high flow after treatment?)

If a fistula fails, you just put a new one in. With CCSVI patients, this is a much-bigger problem if the vein fails a year or two out. Very close follow-up and a lot of interventions if needed to keep patency open. Potentially this could work. (!) On a limited basis, and perhaps interventionalists like Dr. Sullivan himself who have a lot of experience with maturation in dialysis patients could give it a try.

(Hope my notes were legible. I am encouraged by Dr. Sullivan's conclusion that this technique could potentially work. It would have to be the right IR and the right patient.)

(Would a hypoplasia higher in the jugular be more likely to be successfully matured? If it is high enough in the jugular, there is less opportunity for collaterals to divert the flow.)
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