Thank you for your thoughts. But why not utilize the contrast agents in those patients with >400cmsec velocities already knowing the probability of stroke. But that would not answer the question of athero versus throbotic.
However, we could probably study wall thickness or gather data on how the vasa vasorum reacts under certain situations, such as individuals with high carbon dioxide meaures, ie smokers, smokers with sleep apnea. Or how the vasa vasorum sonographically appears in high risk patient classifications, those in the high end NASCET classifications that is.
Rational would be to possibly look at lower end stenosis for instability in a patient with other comorbidities or cofactors. There is already much published material regarding severe velocity profiles. Heck we might be able to rule out intervention in the face of increased velocities, if all other cofactors are well controlled. But then again the disease process never stops, only slows .
Contrast sonography does have the advantage that you can see circulation
within a plaque.
Any wall greater than 1 or 2 mm in thickness must be nourished by vasa
vasorum from the outside of hte artery.
Intima up to 1 mm thick is nourished by diffusion from the main lumen.
So, if you use contrast to check for intraplaque circulation, which you
might want to call hemorrhage, then maybe it is useful. The only way to
tell is to study 2500 patients with severe stenosis for 5 years, without
CEA or STENT, and see if the natural history leads to atheroemboic stroke.
Thes are embolic strokes that are not improved by TPA (perhaps with TCU
((TCD)) augmentation). Transcranial Ultrasound wiht TPA wil dissolve
thrombus, but not atheroemboli.
Now compare the atheroembolic strokes in those with contrast enhanced
plaques to those without contrast enhanced plaques.
Personnally, I think that anybody who has a PSV > 400 cm/s (=
intrastenotic systolic Bernoulli pressure depression of 64 mmHg, which
rips the top of the plaque off) either persistently, or episodically
because of arrythmia or carbon dioxide cerebro vasodilation ((does sleep
apnea cause this??)), or thinking tooo hard, or looking at amazing
pictures, and perhaps with an incomplete circle of Willis (that cannot
provide the flow by collateralization), then these are the only folks that
are at high risk [[and they are likely to have an abnormal OPG test]].
Now test these patients to see if the ones with intraplaque contrast
blushing (either with ultarsound contrast or with MRI or X-ray contrast)
have a higher incidence of stroke over the 5 year period.
TIA does not count, who cares about TIA (except that it might be
predictive of stroke), and is TIA more likely to be thromboembolic than
So, that is my opinion.
On Sat, 20 Oct 2012, Vasc1 wrote:
> Kirk,Knowing these limitations, in your opinion, do you feel contrast sonography holds the key in future detection of such events?
> Probable versus stable?
> Sent from MARS
> -------- Original message --------
> Subject: Re: carotid correlations
> From: "K. Beach" <[log in to unmask]
> To: [log in to unmask]
> Dear Bill,
> Yes, this is the same Moniz that developed X-ray angiographic contrast
> agents for cerebral studies, and the frontal lobotomy
> (I'd rather have a bottle in front of me than a frontal lobotomy).
> He received the Nobel Prize for the Frontal Lobotomy in 1949, just a year
> prior to the introduction of the first drugs for the treatment of mental
> Regarding Doppler vs Angioigraphy.
> What we want to know is which patients will stroke from carotid
> atheroembolic events (not thromboembolic).
> Angiography does as poorly in predicting carotid atheroembolic stoke as
> the discarded Oculoplethysmography methods, but identifies different
> patients at risk. So, the correlation between anatomy and physiology does
> not completely resolve the question of who is at risk of stroke.
> That is why some talk about vulnerable plaque, which maybe neither Doppler
> nor Angiography identify.
> Logic does not always lead to truth.
> On Sat, 20 Oct 2012, Bill Johnson wrote:
> > Bill Johnson, Port Townsend, WA.
> > Kirk, Thanks as always for staying on this list and your continuing contributions.
> > Egaz Moniz? The same doctor that proposed lobotomy for mental illness? (Mine never worked. but how would I know?) ;-)
> > I do not entirely think Anatomy/Velocity Correlation is "futile" but would suggest that we still try to look at flow with multiple
> > and assume we can "pick" the correct angle to calculate velocities. What ever happened to the "infinitely gated Doppler"? Not sure
> > would help, but I have always been suspicious of spectrum analysis, and probably have less confidence than most. I have also been
> > suspicious regarding non-economic "gold standards". Ultrasound and angiography are such very different exams, that I am not very much
> > surprised that correlation is elusive.
> > I am not entirely a pessimist though, and do believe noninvasive vascular exams do provide useful information. As you wrote;
> > velocity criteria have been successfully used to classify the severity of stenosis...) Thanks again.
> > On Sat, Oct 20, 2012 at 9:01 AM, K. Beach <[log in to unmask]
> > Dear Ruth,
> > The question of how to classify carotid stenosis has been vexing us since Egaz Moniz.
> > Unfortunately, Anatomy/Velocity Correlation is futile, in spite of our confidence to the contrary.
> > ----------------------
> > Beach KW, Leotta DF, Zierler RE., Carotid Doppler velocity measurements and anatomic stenosis: correlation is futile., Vasc
> > Endovascular Surg. 2012 Aug;46(6):466-74.
> > from the Ultrasound Reading Center and the D.E. Strandness Jr. Vascular Laboratory at University of Washington Medical Center,
> > University of Washington, Seattle, WA 98195, USA.
> > Abstract
> > BACKGROUND: Duplex ultrasound with Doppler velocimetry is widely used to evaluate the presence and severity of internal
> > carotid artery stenosis; however, a variety of velocity criteria are currently being applied to classify stenosis severity.
> > The purpose of this study is to compare published Doppler velocity measurements to the severity of internal carotid artery
> > stenosis as assessed by x-ray angiography in order to clarify the relationship between these 2 widely used approaches to
> > assess carotid artery disease.
> > METHODS: Scatter diagrams or "scattergrams" of correlations between Doppler velocity measurements and stenosis severity as
> > assessed by x-ray contrast angiography were obtained from published articles for native and stented internal carotid arteries.
> > The scattergrams were graphically digitized, combined, and segmented into categories bounded by 50% and 70% diameter
> > reduction. These data were combined and divided into 3 sets representing different velocity parameters: (1) peak systolic
> > velocity, (2) end-diastolic velocity, and (3) the internal carotid artery to common carotid artery peak systolic velocity
> > ratio. The horizontal axis of each scattergram was transformed to form a cumulative distribution function, and thresholds were
> > established for the stenosis categories to assess data variability.
> > RESULTS: Nineteen publications with 22 data sets were identified and included in this analysis. Wide variability was apparent
> > between all 3 velocity parameters and angiographic percent stenosis. The optimal peak systolic velocity thresholds for
> > stenosis in stented carotid arteries were higher than those for native carotid arteries. Within each category of stenosis, the
> > variability of all 3 velocity parameters was significantly lower in stented arteries than in native arteries.
> > CONCLUSION: Although Doppler velocity criteria have been successfully used to classify the severity of stenosis in both native
> > and stented carotid arteries, the relationship to angiographic stenosis contains significant variability. This analysis of
> > published studies suggests that further refinements in Doppler velocity criteria will not lead to improved correlation with
> > carotid stenosis as demonstrated by angiography.
> > ------------------------
> > Kirk
> > -----------------------
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