I've just learned that our paper on carotid atherosclerosis has been accepted for publication in Ultrasound in Medicine and Biology.
In that paper, we describe our vision of the 3 stages leading to carotid stenosis.
We do not use the term "plaque" unless essential, (as in vasa plaquorum), but rather the term "atheroma" to emphasize the similarity between these atherosclerotic lesions and the cancerous tumors described by Judah Folkman [Folkman J, Merler E, Abernathy C, Williams G., Isolation of a tumor factor responsible for angiogenesis., J Exp Med. 1971 Feb 1;133(2):275-288.]
We assert that the 3 stages are:
1. Expansion of the media (thickening of the IMT).
2. Initiation and growth of the atheroma, beginning from a single location and expanding longitudinally and circumferentially.
3. Uncompensated reduction in lumen cross section and stenosis.
The living cells of the media are nourished and cleansed by diffusion. In this nearly planar structure, diffusion is sufficient as long as the thickness is less than 1.7 mm. (In the Folkman spherical tumor geometry, a tumor can grow to 3 mm diameter using diffusion for nourishment and cleansing). This 1.7 mm IMT limit is consistent with the highest Ultrasound IMT measurements (Paul L. Allan, Philip I. Mowbray, Amanda J. Lee, F. Gerald R. Fowkes, Relationship Between Carotid Intima-Media Thickness and Symptomatic and Asymptomatic Peripheral Arterial Disease, The Edinburgh Artery Study, Stroke. 1997 Feb;28(2):348-353.)
For an atheroma to grow in the media, angiogenic extensions from the vasa vasorum in the adventitia are required to transport solutes to and from the atheroma cells. As the atheroma increases in volume, occupying the within-adventitial cross-section, the lumen area is maintained by expansion of the adventitial circumference, this remodeling is stimulated by intrastenotic turbulence impinging on the portions of the media not obstructed by atheroma.
When the atheroma fully embraces the adventitial circumference, the factors driving remodeling are blocked; thus, increases in atheroma volume result in a reduction in residual lumen cross-section, a stenosis.
This, of course, is all speculation, but, I think, is consistent with all of the known information about atherosclerosis.
1. The maximum thickness for IMT is less than 2 mm, probably 1.7 mm.
2. Atheroma neovascularization (vasa plaquorum) is also known as intraplaque hemorrhage.
3. Intraplaque hemorrhage does not come from the arterial lumen, but from the vasa vasorum.
4. Like with breast tumors and other tumors, calcification is a late manifestation of atheroma development.
5. It is likely that the vasa venolum are more important than the vasa arteriolum in the eventual rupture (eruption) of the lesion.
For those with further interest, in a couple of months the paper will be posted to:
the "UMB Online First" section of UMB Online (http://www.umbjournal.org/)
and to Elsevier's Science Direct (http://www.sciencedirect.com/)
On Wed, 21 Oct 2015, Schneider, Joseph MD wrote:
> Ladies and gentlemen:
> I received the following query from a colleague and would appreciate hearing what people think about this
> Simple question for you- we are revising our vascular lab protocols and got into a debate about what actually defines the presence of plaque in the extracranial carotid system
> (which would mean the difference between calling the artery normal versus having 1-49% stenosis). Some techs say they were taught that if the IMT is > 1mm that they should
> consider this to indicate the presence of plaque, whereas others are using 3 mm as a cutoff- I am finding that there is a real issue with techs and reading physicians
> ‘eyeballing’ the carotid to determine plaque presence or not in cases where the artery wall is maybe a bit thick, but there is no real plaque (calcification, etc.) and I am
> wondering if we are over calling the presence of 1-49% stenosis in normal arteries. What is your understanding of the definition of plaque presence in the carotid when it comes
> to these cases of mildly thickened wall with no convincing plaque?
> Incidentally, my personal answer to her was as follows:
> I can tell you that we are set up to do IMT, but our Cardiologists have said that they think the bloom is off the rose for IMT and they don’t ask for it. I look for plaque
> primarily on the B-mode transverse loops and if I see anything I will call it <50% assuming there are no elevated velocities. As I recall the Grant articles about “consensus”
> standards don’t specifically address this and I’m not aware of any definitive literature on the topic. I will ask the Flownet (primarily sonographers) and I will ask John Gocke
> and Greg Moneta, both of them co-authors on the Grant papers, and get back to you.
> Thanks in advance
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