Carotid Ultrasound: More than just a chart on the wall - HD

Introduction to Carotid Ultrasound

It is a true honor to be here,
and it's a pleasure to talk about my favorite topic,
which is in fact carotid ultrasound.
And I hope at the end of this to convince you
that if you do a good carotid ultrasound,
not only will it be great fun,
but you will realize
that doing it involves much more than just taping a chart
to the wall of your vascular lab.

Disclosures

I do have a couple of disclosures.
I give CME lectures for Philips healthcare,
and I will briefly discuss the use
of intravenous ultrasound contrast,
which is not FDA approved as of yet for vascular imaging.

Importance of the Chart and Pathophysiology

And while I think the chart on your wall
of your vascular lab is indeed very important
and where you really need to start,
it is also very important to understand the pathophysiology
of what you're looking at.
And vascular disease in the head is a little bit different
than vascular disease elsewhere, namely
that most strokes actually are embolic.
They are not due to a pressure or flow reducing lesion.
They're due to embolus.
And it's estimated that about 20% of these are due
to disease at the carotid bifurcation.
So basically, when you're thinking about stroke
and carotid disease, the primary bad actor is the plaque.
It's not actually the stenosis.
And so I encourage you all, as you start your examination
to begin by evaluating the plaque, ultimately you're going
to need to grade the stenosis.
And to do that, you are going to need a chart.
But it's very important
to know when those charts don't work.
And the things that you need
to be concerned about are the high
and low output states, tortuous vessels,
contralateral stenosis and occlusions, tandem long segment
and near occlusive lesions, as well
as the patient post intervention,
both endarterectomy and stent placement.
And because of these times when the chart doesn't work,
the way you're going to identify these situations is
by correlating your spectral Doppler findings
with a gray scale and color Doppler images, as well
as looking at the waveforms.
And if you see a discordance, you need
to find an explanation.
It's important to understand the carotid artery waveforms.
And the other thing that I think is very, very important,
which I'll talk about at the end, is that it is important
to continuously reevaluate your chart based on outcome
analysis because patient management does evolve over time.

Evaluating Plaque

So let's start with a plaque.
And I want to give a thanks to Dr.
Ed Bluth, who really is the plaque guru
I think, in our society.
And I thank him for these slides that he's lent me.
But basically what you're trying to do is
to identify vulnerable plaque
because it's the vulnerable plaque
that poses the increased risk of rupture and embolization.
And many studies have shown that this risk is related to,
several things, namely,
increased vascularity in the plaque, which causes hemorrhage
as you see in this schematic,
which causes the plaque to swell.
The presence of cholesterol
and lipid within the plaque also incites an
inflammatory response.
These two things contribute to forming a necrotic core
as well as swelling as the plaque.
And eventually the fibrous capsule over the plaque will thin
rupture will occur,
and that necrotic core will be exposed
to the circulating blood.
And it is very thrombogenic.
And what ends up happening is that thrombus forms on top
of the plaque, and it's actually not the plaque itself
typically, but the thrombus on top of the plaque
that is knocked off
by the high velocity jet coursing through the stenosis.
And that's what causes the distal embolus or the stroke.
And this is in contradistinction to stable plaque,
which is hyalinized, fibrous, fatty,
sometimes calcified that has many fewer vessels,
less inflammation in a very smooth surface.
And so there is nothing on top of this plaque
for the high velocity jet to knock off as it goes
through the stenosis caused by this very stable plaque.

Features of Vulnerable Plaque on Ultrasound

So what are the features of vulnerable plaque
that you can see with ultrasound?
Well, hemorrhagic plaque typically is hypoechoic.
Now certainly this isn't a specific finding,
and occasionally fibrous fatty plaque can be hypoechoic too,
but when you see hypoechoic plaque, you should be concerned
that it's possibly hemorrhagic,
particularly if more than 50% of the plaque is hypoechoic.
Another thing that you should look at is the surface
characteristics of the plaque, because if you see fissures
or little divots within the plaque,
as you see in these examples, these represent areas
where the blood flow is predictably gonna be relatively
stagnant and platelets can aggregate
and thrombus can form again, creating thrombus on top
of the plaque that can be knocked off
by the high velocity jet as it courses over the plaque.
And of course, the plaque is frankly ulcerated.
It's got a double whammy.
It's got a divot with the stagnant flow,
but also the fibrous cap is denuded
and the necrotic core is exposed to the surrounding blood.
And so you have two reasons why you might see thrombus
in the situation where you have ulcerated plaque.
And very often these surface characteristics are best
evaluated with either color or power Doppler.

Intravenous Ultrasound Contrast for Plaque Evaluation

Now, recent research has demonstrated that actually
with intravenous ultrasound contrast, you might be able
to identify both increased vascularity as well
as inflammation with plaque.
And one of the first studies
to show this was reported by Dr.
Feinstein's group, and they reported
that early phase intravenous contrast enhancement on
ultrasound would identify not just the surface
characteristics of the plaque, namely the ulceration
and the fissure within it, but also plaque neovascularity
and other groups have corroborated these findings
and have demonstrated that early contrast enhancement
of plaque does in fact correlate
with increased histological density of neovascular as well
as plaque that is hypoechoic on gray scale imaging
and plaque that is correlated with acute neurologic events.
And this is an example from
that first study demonstrating very high,
well signal, very bright appearance
of the contrast within the lumen of the vessel
demonstrating the ulceration within the plaque,
but also these little bright echoes
within the plaque itself.
Representative of neovascular within the plaque.
Evaluation
of plaque inflammation I think is also very interesting
and it's well known that microbubbles will adhere
to damaged epithelium
and will be taken up by inflammatory cells.
And this group of cardiologists published in radiology in 2010, a evaluation of a series
of patients with late phase contrast enhancement.
And they felt that if they saw late phase enhancement
with the plaque, that this correlated both with symptoms
as well as areas of plaque
that were hypoechoic on gray scale imaging.
And they believe that they're identifying actually
inflammatory plaque.
And here are some images from their paper.
And this is a pre contrast image.
You can see the lumen here with the white triangle
and the green triangle pointing to an area that is of plaque
that is hypoechoic as opposed
to this echogenic plaque more posteriorly.
Now 20 minutes after infusing sono view in this particular patient,
you can see really very few echoes within the lumen
because again, this is a delayed contrast enhanced image,
so 20 minutes post infusion of the contrast.
But that area of plaque
that was hypoechoic anteriorly is now very, very echogenic.
And again, they believe that this is due to retention
of the microbubbles within the inflammatory cells,
and they believe that they're identifying
inflammatory plaque.

Other Methods to Identify Vulnerable Plaque

Current research is looking for other ways
of identifying this vulnerable plaque,
and there are some high-end algorithms available suggesting
that you can perhaps actually depict thinning
of the fibrous cap with high resolution ultrasound.
People look for progression over time of the plaque
and plaque that is becoming more
and more prominent resulting in tighter stenosis is
more likely to be vulnerable.
You can use transcranial Doppler
to look in the intracerebral circulation for microemboli.
And of course, you sometimes can use MR though there is some controversy about this as
to whether MR really actually is any better than ultrasound
in terms of its ability
to identify intraplaque hemorrhage.

Grading Carotid Stenosis

Well, since plaque is the primary bad actor, the question
could be legitimately posed as to why you bother
to grade a carotid stenosis at all.
And the reason that we do this is that many,
many studies have shown,
I've listed the most important ones here,
that in both asymptomatic as well as symptomatic patients,
measurement of carotid stenosis is actually an extremely
good surrogate for assessing risk of stroke.
And these studies have all shown that patients
with carotid stenosis greater than 60 to 70%, again,
whether symptomatic or asymptomatic, derive a clear benefit,
namely a decrease in their incidence
of stroke if they undergo carotid endarterectomy.
And more recent studies have confirmed the same decrease in risk of stroke following
carotid stent placement.
And again, to do this, you're going to need a chart.
And this is the example or a rendition of one
of the very best consensus conferences sponsored
by the SRU that was headed by ED Grant.
And they generated in this great study the chart
that actually most people use on the wall in their vascular lab.
Many charts are used,
and you should use the chart of course
that works best in your particular lab
with your particular group of patients.
But a study was done by the IAC Society Accreditation Society.
And they in fact indicated as they did a survey
that the most popular chart,
the chart used most commonly is indeed this SRU chart.
And they are looking in this chart
for a stenosis greater than 70 percent.
And the primary Doppler feature
that they use is a peak systolic velocity greater than 230
centimeters per second with a
additional parameters of a ratio greater than four
or an end diastolic velocity greater than a hundred.
And this is what we use in our lab in the basis of
how we grade a carotid stenosis.
But one of the things that's very important to recognize
that they did point out in this wonderful paper is
that in addition to looking at these Doppler criteria,
you need to confirm
that there is plaque present on the gray scale
and color Doppler images.
And this correlation between your Doppler findings
and the gray scale and the color Doppler images is really
crucial in order to use this chart effectively.
And sometimes you will find that there is discordance,
and when you do, you have to recognize
that those spectral Doppler criteria will not be reliable.

Situations Where Charts Don't Work

So let's review some of these situations.

Elevated Velocity Without Plaque: Tortuous Vessels or Contralateral Occlusion

What if you have a situation
where the peak systolic velocity is elevated
but you actually do not see any plaque?
Well, the two things that you should think about is a
tortuous vessel or a contralateral occlusion or a stenosis.
So here is an example of a very tortuous vessel.
The peak systolic velocity is 163 according
to the SRU chart, that would be consistent with a 50
to 69% stenosis.
But if you look at the color
and the gray scale images,
other than this very curvaceous internal carotid artery,
there is absolutely no evidence of plaque
or stenosis at all.
And I'm gonna read this out as no stenosis
elevated velocity due to tortuosity of the vessel.
Here's another example
where you can see a peak systolic velocity
of 260 centimeters per second.
But if you look on the gray scale
and the power Doppler images, there's a little bit
of plaque, but it certainly doesn't decrease the lumen of
that diameter significantly.
And although by the velocity alone, according
to the SRU chart, this would correspond
to a greater than 70% stenosis really on the gray scale.
And the color there would be less than a 50% stenosis.
And this is due to the fact
that there is a contralateral occlusion
of the internal carotid artery.
And in the setting of a contralateral high grade stenosis
or occlusion, you're going to get compensatory flow.
On the opposite side, increased velocity in both the common
and the internal carotid artery
and peak systolic velocity
as a criteria alone will not be accurate
for grading the stenosis and using the ratio
and looking at the gray scale
and the power Doppler
or color Doppler images is going to be much more important.

Low Velocity Despite Significant Plaque: Tandem Lesions, Long Segment, or Near Occlusive

Well, what about the opposite scenario when you have lots
of plaque, but the velocity is not
as elevated as you would expect?
And the three things that you should think about,
there are the possibility of tandem lesions,
a long segment stenosis or a greater than a 95% stenosis.
And this is an example of a patient
who has a nearly 70% stenosis in the common carotid artery,
and a very tight stenosis at the origin in the internal
carotid artery and velocities are only 200
centimeters per second.
Now this is clearly not a 50 to 69% stenosis,
it's a near occlusive lesion, and it may be
because the lesion is so tight, but also
because of this proximal lesion that the velocity is lower than you would expect.
Here's another example
where you can see on the color Doppler image
that there's a lot of plaque.
There is a long segment stenosis.
This is clearly greater visually than a 70% stenosis,
but the highest velocity we could get was only about 110
centimeters per second.
By the SRU chart, this would be a less than a 50% stenosis.
And that is clearly wrong.
And the reason the velocity is so low is due to inflow
resistance in patients
that have very long segment stenosis.
And here is another very important case looking on the
transverse gray scale image.
You can see in fact that there is a very tight stenosis,
probably actually almost a nearly occlusive lesion,
but the highest velocity we could get was 189
centimeters per second.
And this would correspond to in fact, only
by the SRU chart, a 50 to 69% stenosis.
But obviously that's not correct at all.
This is a much tighter stenosis.
And if you go back to the Spencer
and Reid diagram, which very elegantly demonstrates
that as the diameter lumen decreases,
the peak systolic velocity increases exponentially
to a very tight stenosis, maybe about 95 or 96%.
But at that point, velocities actually plummet very,
very quickly till the vessel occludes.
And so if you pick any particular velocity here,
I've picked 110 centimeters per second.
You can see that this intersects the curve on the right side
where you have a relatively modest stenosis.
But it also, that line will intersect the curve on the left
side, where in fact you have a very tight stenosis.
And the only way that you can determine whether you're on
the right or the left hand side of that curve,
or whether you have a very modest stenosis
or a very tight stenosis, is by looking at the gray scale
and the color Doppler images as well as the waveform
and proximal to a very tight stenosis.
You're going to have a high resistance waveform pattern,
sometimes called the knocking or staccato waveform
and distal to a tight stenosis, you're going
to have a tardus parvus waveform.
And here, going back
to the case I just showed you in the proximal CCA,
you can see low velocity and no diastolic flow.
And in the distal ICA above the stenosis,
you can see the classic tardus parvus waveform.

Carotid Artery Waveforms

So let's talk a little bit about these waveforms
because not only will they help you identify these nearly
occlusive lesions, which you clearly do not want to miss,
but also they can help give you clues to disease
that might be outside of the field of view
of your carotid ultrasound study, either in the heart
or more distally within the head.

Tardus Parvus Waveform

So we'll start with the tardus parvus waveform, which
as you see here in this example, is characterized
by delayed systolic upstroke,
a decrease in peak systolic velocity, rounding
of the systolic peak.
And this occurs distal to a high grade stenosis.
And what's fun about this is that the pattern
of distribution can help you localize the stenosis.
So in this particular case,
you can see a delay in systolic acceleration.
So a more horizontal upstroke.
It involves the right common, the left common,
both vertebral arteries
and in fact is even more prominent in both
internal carotid arteries.
And notice also that the peak systolic velocity is
relatively decreased.
So you see this tardus parvus waveform in all
the vessels in the neck.
That means that the proximal stenosis has to be proximal
to every single one of these vessels.
And the most likely place, of course, is the aortic valve.
And this is what you see in patients
with severe aortic stenosis.
In this particular patient,
you can see the tardus parvus waveform in both the left
common as well as the left internal carotid artery.
But you have a very sharp upstroke in the right common
and right external internal carotid artery.
So the stenosis must be proximal to the left vessels,
but must not affect the right vessels.
And so the most likely place for
that stenosis is gonna be at the origin
of the left internal carotid artery.

High Resistance or Staccato Waveform

Well, what about the knocking or staccato waveform?
This is characterized also by a low peak systolic velocity
and decreased absent or reverse diastolic flow.
And this type of waveform occurs proximal
to either an occlusion or a high grade stenosis.
Here you can see an example
where the waveforms in both common carotid arteries are
quite asymmetric with substantially decreased flow in the
left common in comparison to the right.
And that should make you think
that there is some obstruction to flow up above.
And as you go up the vessel, you can see
that in the proximal ICA which is closer
to the obstruction, the velocities are even less
and absolutely no diastolic flow.
And this is due to occlusion of
that mid internal carotid artery.
In this particular case, it's a little more subtle,
but still if you look carefully,
you can see there's less diastolic flow in the right
common than in the left.
And as you go up the neck
and you compare the right internal
to the left internal carotid artery, you can see
that the peak systolic velocity much reduced on the right in
comparison to the left, 20 on the right
and 85 on the left.
And absolutely no end diastolic flow on the right,
though normal amount of forward diastolic flow on the left.
But what's different about this case in comparison
to the one that I previously showed you, is
that on color Doppler,
the internal carotid artery is widely patent.
So the obstruction to flow cannot be in the internal carotid
artery in the extracranial portion, it has
to be more distal to that.
And you should look in the head.
And here you can see on the CTA a dense MCA sign due
to an acute occlusion of the right middle cerebral artery.
Here's another example.
And in this case, you can see
that there are bilateral high resistance waveforms actually reversed early diastolic flow in the right
and substantially reduced diastolic flow in the left,
more diastolic flow in the left certainly than the right.
But this is absolutely not normal.
And in these particular patient, you can see
that both the right
and the left internal carotid artery are patent
on the color Doppler.
So again, the obstruction to flow must be above this point,
must be in the head.
And in this case, it needs to be bilateral
because both internal carotid arteries are basically gonna be obstructed.
It could be due to vasospasm, it could be due
to bilateral intracerebral occlusions.
But in this particular case, it was due
to increased intracranial pressure.
The patient had had a huge right-sided stroke.
You can see herniation across the midline as well
as uncal herniation.
And the reason that it was worse on the right than on the
left, of course, was 'cause the stroke was on the right,
but again, caused a diffuse increased intracranial pressure.

High Resistance in Aortic Regurgitation

Well, here's an example
where you have so-called high resistance waveform patterns bilaterally in both common carotid arteries.
You can see no end diastolic flow
and a little bit of early reverse diastolic flow.
But what's different about this case in the cases I've shown
you before is
that the peak systolic velocity is not decreased.
In fact, the peak systolic velocity is increased
and it's 160 on the right and 176 on the left.
And this is the kind of waveform pattern you actually see in
patients with severe aortic regurgitation.
And it's the Doppler ultrasound equivalent, if you will,
of the water hammer pulse
that they might note on physical exam.

High and Low Output States

Another time when these charts will not work,
is in either high or low output states.
And so when the peak systolic velocity in the common carotid
artery is either less than 60
or greater than a hundred centimeters per second, these the SRU chart will not be applicable.
Low output states more common in my practice.
These are usually due
to decreased ejection fraction from cardiomyopathy,
left ventricular dysfunction,
perhaps left ventricular aneurysms,
sometimes aortic stenosis.
You can see this also in the setting of a systemic hypotension or even thoracic aortic aneurysms.
And here is an example
where you have a peak systolic velocity
and the common carotid artery
of only 35 centimeters per second.
And if you were to wait
until the peak systolic velocity in the internal carotid
artery reached 230 centimeters per second,
before you said this patient had a greater than 70%
stenosis, the peak systolic velocity ratio would be 6.5.
Well over that four cutoff.
And relying on peak systolic velocity in this case would
result in significant underestimation and of ICA stenosis in this patient
who had an ejection fraction of only 15% due
to an ischemic cardiomyopathy.
The same thing is true in high output states.
In my practice, this is less common,
but you can see it in patients who have hyperthyroidism,
hyperdynamic state, sometimes aortic regurgitation,
as I've mentioned, an even thyroid toxicosis.
And in this particular patient
who was actually a young athletic guy,
he was actually on the varsity ice hockey team,
but had syncope, had a carotid ultrasound,
and the peak systolic velocity in his ICA was 176
centimeters per second.
And this would correspond by the SRU chart to a 50
to 69% stenosis,
which would be pretty peculiar in a very
healthy 19-year-old guy.
And looking on the gray scale
and the color, there's absolutely no plaque at all.
And if you look in his common carotid artery,
you see his systolic velocity is 126 centimeters per second.
And so the reason that this patient has high velocities is
just due to the high output state, a very hyperdynamic
probably just due to the fact that he had a
enormous cardiac output because he was so athletic
and he has no stenosis in his ICA at all.

Post-Intervention Patients

Another time when these charts typically will not work is the patient who's
undergone intervention, because doing endarterectomy
or performing a placing a stent changes the vessel hemodynamics,
and it becomes very difficult to then grade a stenosis
in a patient who's undergone endarterectomy.
The surgery changes the hemodynamics, they get a patch
that increases diameter,
it causes the peak systolic velocity to change,
and it decreases the compliance of the vessel wall.
So here's a patient post endarterectomy
velocity about 197 centimeters per second.
According to the SRU chart, that would be a 50
to 69% stenosis.
But looking at it on the gray scale, clearly
that is a much tighter stenosis.
So following endarterectomy, you can't use the same criteria
as you do for the native vessel.
The peak systolic velocity is likely lower.
Nobody knows exactly what number to use.
So pay attention to the ratio, the gray scale,
and the color Doppler findings.
Following stent placement, again, hemodynamics are changed,
but actually in a completely opposite direction.
And peak systolic velocity is generally elevated.
Here you can see a stent.
It's clearly wide open, no intraluminal echoes.
Velocity is 300 centimeters per second,
but there's no stenosis there.
But the stent decreases the compliance
of the vessel wall results in partial occlusion of the ECA,
usually that causes shunting of blood into the ICA
and residual wasting
or narrowing, as you see here, is very, very common.
And that probably results in increased velocity as well.
So all studies agree that the peak systolic velocity
and ratio threshold numbers are gonna be higher in patients
following stent placement for a given percent stenosis than
for the native vessel, but there's
no agreement on the numbers.
These may be lab and stent type specific. So what do you do?
You look for change in peak systolic velocity over time,
and again, correlate carefully with the gray scale
and color Doppler imaging.

Outcome Analysis and Evolution of the SRU Chart

Well, I want to finish up by talking about some stuff
that's in the about the SRU chart
that's in the fine print of that very wonderful article
that I've referenced already.
And ultimately, one has to pick a number that's going
to work for the vast majority of patients.
I've gone over exceptions to the rule, which are important,
but again, when you think about the majority, you need
to come up with a number or some Doppler criteria
that are going to work within your lab.
And I think it's important to recognize how the SRU came up
with the numbers that ED Grant
and colleagues chose
because a lot of thought went into this.
And one of the things that you should recognize is that
for any given stenosis as you can see in this chart from some work
that ED Grant did before the carotid consensus conference, that there is a wide range
of velocities for any given percent stenosis.
Another way to look at it is that there is in fact
of very good accuracy over a wide range
of peak systolic velocities for greater than 70% stenosis.
What's different, of course, between using a cutoff
of 175 versus a cutoff of 300
is not the accuracy,
but of course is the sensitivity and specificity.
So if you use a lower number,
you're gonna be more sensitive.
If you use a higher number, you're going to be more specific
and you won't be able to achieve both.
So one of the things that you always need
to be thinking about is outcome analysis in addition
to accuracy.
And this is a concept that was initially brought to my attention anyways by a really
fabulous, very thoughtful paper from the Netherlands.
And what they basically acknowledge is
that the consequences of missing a stenosis, in other words,
having a false negative may be more
or less favorable than the consequences
of performing an unnecessary intervention
because of a false positive.
And this is very, very important
as you evaluate your charts in current clinical practice.
So if you go back to the SRU chart,
they could have chosen a peak systolic velocity of 300.
In fact, if you look at Dr. Grant's data,
300 would be at the point where you see the typical mean peak systolic velocity
for a greater than 70% stenosis.
And had they chosen a number like 300,
you can see here they would've had very few false positives,
but they would've had a lot of false negatives.
Instead, they chose back in 2003,
a peak systolic velocity of 230, which is a much more
sensitive criterion
for diagnosing a greater than 70% stenosis.
And as you would
therefore expect, they had more false positives
and many fewer false negatives.
Now, that was a very reasonable choice to make at
that point in time because there was a lot of data
that demonstrated that there was still benefit
for intervention in patients
with more moderate stenosis in the 50 to 69% range,
just not as much benefit as there was with patients
with stenosis greater than 70%.
So the decision was made that it was actually better
to have false positives that was less risky than
to have false negatives
where you would be denying a patient the potential benefit
of performing an intervention.
However, in 2017 times are changing
and the incidence of stroke in the last two decades has
decreased by close
to 40% in patients over the age of 65.
No one knows exactly why that is,
and it's hard to definitely attribute cause.
But this is paralleled by changes in medical management,
namely increased use of statins,
anti-hypertensive medication,
and more aggressive anti-platelet therapy, as well
as a overall decrease in the incidence
of smoking in the general population in the United States.
In addition, there is recognition now
that the reported risks of intervention, both
with carotid endarterectomy
and stents in clinical trials,
does not necessarily translate into
routine clinical practice.
In other words, the surgeons
and interventionalists
that were involved in these trials were experts
with a lot of experience.
And in general practice,
these interventions may be performed by people
who don't have as much expertise or experience.
And so the complication rate in general practice is probably
much higher than it was in the clinical trials.
And when you combine that with the fact
that in today's world with optimal medical management,
the risk of stroke in patients with carotid stenosis
who are receiving optimal medical management is only perhaps
maybe 0.5 to 1% per year, you're reaching the point where
researchers are recognizing that actually the risk of stroke
with patients on medical management is less than the risk
of stroke to patients that go under surgery.
And so now increasingly, people think that patients
with more moderate stenosis actually do better
with medical management, particularly asymptomatic patients.
And so as we think about our charts in the future,
we may want more specificity in the greater than 70%
stenosis range, and we may want to move on
to higher threshold numbers.

Summary

So in summary, don't forget to look at the plaque.
Start with that. That's the primary bad actor.
The stenosis is actually a secondary phenomenon.
Remember that the standard charts will not work
for the high low output state tortuous vessels,
contralateral stenosis or occlusions, tandem long segment
or near occlusive lesions,
and they won't work in patients post intervention.
And always, always,
always correlate your velocity measurements
with a gray scale
and color images as well as waveform analysis.
And remember that whatever criteria you choose,
the closer you are to the your cutoff value,
the more likely you are to be wrong.
And the farther away you are from your cutoff value,
the more likely you are to be right.
And whether or not you end up with more false positives
or false negatives will be dependent upon the sensitivity
and the specificity of the cutoff value that you use.
And so, as management algorithms change,
so must your chart change.
And so in this time, as we're waiting to see how management algorithms developed,
there are two ongoing trials.
Now, the CREST two trial
and in Europe, the ECST trial
that are actually now comparing revascularization with new,
more aggressive medical management.
These trials are due to close in 2020.
And at that point, we may have answers to these questions,
but in the meantime, when life is uncertain
and patient management is a little bit in flux,
consider correlative imaging if you are close
to the discriminatory levels and take your statins.
I want to, in particular, thank Mark Cleaver,
who really was the person that really began
and has authored the seminal research on carotid artery waveforms.
But I wanna thank many other members of the society
who have inspired me
and who have very patiently answered all of my questions.
Thank you very much.