Endofibrosis

[Jonathan Meredith]

I found the endofibrosis case interesting, in particular, the reduction in vessel calibre post exercise. This got me thinking. Could there be a haemodynamic explanation for this?

We know the iliac arteries undergo adaptive change from the repetitive stress on the vessel wall (flexion, shear stress, tethering) creating these long endofibrotic lesions.

My thought is endofibrosis changes vessel compliance. At peak performance (high cardiac output coupled with blood flow demand) the change in compliance further increases velocity across the lesion and reduces pressure.

I wonder then, could a reduction in vessel lumen post exercise be a result of the pressure drop across the lesion and system distally??

[Stephen Bird]

Hi Jonathan,

Yes, I am puzzled by this phenomenon also,

I have shared this case with many people and asked what the cause of the lumen diameter reduction could be.

The favoured theory is that it is a vessel wall muscle contraction, like you see with autonomic vasoconstriction, but in a larger vessel (If you like this stuff please watch the case of the week presentation “What makes you blush”) .

The theory is that the kinking of the vessel during the exercise is causing a high velocity jet and that is impacting the vessel wall and triggering the muscular contraction in the tunica media component of the vessel wall.

The pressure drop theory is another good possible explanation,

But do we see vessel diameter reduction during exercise in a normal athlete, I think not, so it is something to do with the localized vessel wall in the area where the kink is occurring.

These cases of iliac endofibrosis that I have seen are in cycling athletes where the postural changes of the cycling position cause a mechanical kink in the iliac vessel leading to a high velocity jet, like that caused by a stenosis, but the stenosis is caused by the kink, rather than any atheromatous process.

They are interesting cases!

Worth thinking outside the standard square of atherosclerosis as a cause of claudication.

Popliteal artery entrapment syndrome is another good topic in this conversation.

Also fibromuscular dysplasia.

Check out the case of the week presentations: Carotid artery kink as well.

Happy scanning,

Steve.

[Craig Cairns]

Hey Steve,
Another thought regarding endofibrosis, is that in a normal post-exercise status the arteries dilates, which can explain why with post exercise ABIs, it is normal to see up to 20% decrease in pressures pre verse post exercise ( which quickly normalises after cessation of exercise).
The diseased portion of the artery affected by endofibrosis losses this elastic capacity to dilate due to fibrosis, so in the post exercise state, it doesn’t dilate as much as the adjacent normal artery therefore becoming the post exercise functional stenosis.

They tend to be very sweaty cases, but very rewarding when you get a positive one.

Cheers
Craig

[Stephen Bird]

Hi Craig,

I was waiting for the big guns to wade into this!

So great you read the thread,

This is genius as always from you.

Just like the echogenicity of something is relative to the surrounding tissue, the diameter of this vessel segment must be seen as relative to the pre and post sections of artery.

It makes perfect sense.

Next time I do one of these I will measure the patent lumen diameter pre exercise and post exercise and I will not be surprised if that diameter remains the same, while the vessel diameter pre and post where the vessel wall is healthy will be increased post exercise causing a functional stenosis and associated rise in PSV in the diseased segment.

So great to hear form you Craig,

Steve.

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