Congratulations Kirk!
Anne Moore
Supervisor Cerebrovascular Laboratory
Harborview Medical Center
206-744-3592, Box 359970

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On Wed, 4 Nov 2015, Kirk W Beach wrote:

>
>
> Dear Colleagues,
>
> 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.
>
> STAGE 1.
> 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.)
>
> STAGE 2
> 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.
>
> STAGE 3
> 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.
> NOTES:
> 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/)
>
> Kirk
>
>
>
>
> 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
>> 
>> 
>> Joe
>> 
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