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Hello, and welcome to Noon Conference hosted by Modality.

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Noon Conference connects the global radiology community through free live

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educational webinars that are accessible for all and is an opportunity to learn

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alongside top radiologists from around the world.

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Today, we're honored to welcome Dr.

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Malik for a lecture entitled Vessel Wall Imaging. Dr.

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Malik completed his radiology residency at Boston Medical Center

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and neuroradiology fellowship at New York University.

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He's now staff neuroradiologist at Case

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Western University Hospitals in Cleveland, where he is director of

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epilepsy and neurovascular imaging.

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At the end of the lecture, please join Dr.

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Malik in a Q&A session where he will address questions you may have on today's

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topic. Please remember to use the Q&A feature to submit your questions so we can

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get to as many as we can before our time is up.

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With that, we are ready to begin today's lecture. Dr.

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Malik, please take it from here.

1:00

Good afternoon, everyone. My name is Waseem.

1:02

I'm one of the neuroradiologists at Case Western Reserve in Cleveland,

1:06

Ohio. And today I wanted to talk about vessel wall imaging.

1:10

And I'm sure this is a topic many of you have heard about, but maybe not all of

1:14

you are performing at your institutions.

1:17

Or if you are, maybe you don't have much experience interpreting them.

1:22

So the goal of today's talk is just to do a lot of the basics about

1:26

vessel wall imaging, get you familiar with a lot of

1:29

the most common diseases that we

1:33

assess using vessel wall imaging, and then demonstrate some pitfalls,

1:37

and then obviously answer any questions you may have.

1:39

I have the Q&A open on my phone here, so if you guys do ask questions, I'll

1:43

try to keep an eye out on it. If I miss it, I apologize.

1:46

We'll try to get to it at the end of the talk. Okay.

1:50

So,

1:52

let's talk. So here's our outline.

1:54

So first, we're just going to do very basics about what vessel wall imaging is.

1:59

Then we're going to talk about the protocol for vessel wall

2:02

imaging, indications for vessel wall imaging, and the majority of the

2:06

talk is going to be just cases showing how vessel wall imaging

2:10

changed patient management for patients here at our institution.

2:14

So these are all cases from our institution here at Case.

2:18

Again, we're going to talk a little bit about the potential pitfalls and then where

2:21

I see vessel wall imaging in the future.

2:24

Okay, so what is vessel wall imaging?

2:26

At its core, it's just high-resolution black blood imaging of the vasculature,

2:30

and all of the talk today is going to be only based on the intracranial

2:34

vasculature, but you can do black blood imaging with vasculature

2:38

anywhere in the body. So, this is what it looks like.

2:42

So we have a sagittal T1

2:44

of the MCA. So we have an MRA here just showing where we are along that

2:48

right M1 segment. And we'll take a zoom in on what the normal vessel looks

2:52

like. And here as you can see, black blood imaging, so all of the flow

2:56

within the vessel is completely nulled out.

2:58

We do our best to null all the CSF around it out.

3:01

As you can see, we can do a little bit better here, but we null out the CSF around

3:04

it, and then the only thing that should be left is the vessel wall.

3:08

And you can see that it's nice and smooth surrounding the whole M1 segment.

3:11

So this is a normal appearance of the MCA.

3:16

And then we do vessel imaging both pre- and post-contrast.

3:19

And so we have both the pre- and post-contrast shown here, and we'll zoom in on

3:22

both. As you can see, they look pretty much identical.

3:26

And this is what a normal vessel imaging will look like.

3:29

So no abnormal enhancements, no intrinsic signal

3:33

abnormality.

3:34

So normal pre- and post-vessel imaging in a patient.

3:40

So why do we do vessel imaging? So the most common indication

3:44

is differentiating vessel stenosis.

3:46

So a patient comes in, whatever symptoms they might have, CTA

3:49

shows an area of stenosis. And so then the question is: what's causing

3:53

stenosis? Is it atherosclerotic disease? Is it vasculitis?

3:57

Is it moyamoya? So all of

4:00

those pathologies can look the same on CTA.

4:03

And so we use vessel imaging to try to differentiate those.

4:07

We can also look for sites of positive remodeling.

4:09

We'll talk a little bit more about what positive remodeling is.

4:12

But essentially, it's a disease process that will be occult on conventional

4:15

angiography and can only really be picked up on vessel wall imaging.

4:19

So those are the two most established indications.

4:22

Some other indications that we're seeing coming out in the literature more and that

4:25

we also do here at our institution as well, assessing

4:29

an atherosclerotic plaque, as well as assessing an area of vasculitis.

4:32

And based on the degree of enhancement, you can kind of

4:36

guess on how active that disease process is.

4:40

It's also used at looking at aneurysms.

4:42

So if a patient presents with subarachnoid hemorrhage, say they have multiple

4:45

aneurysms and you're not sure which aneurysm ruptured,

4:48

if you're able to identify enhancement in one of those aneurysms on vessel imaging,

4:52

you have a better idea of which aneurysm is the culprit.

4:56

You can also do it in a patient that has, say, an incidental aneurysm that was

5:00

found, and they're not sure if they want to intervene upon that aneurysm now, or

5:04

maybe they want to intervene upon it later.

5:06

If there's no enhancement, it suggests that the aneurysm might be stable,

5:10

rather than if there's enhancement, it would be unstable and would require

5:15

someone to intervene more quickly.

5:17

So those are the less

5:20

acted upon indications, but things that I think we will be seeing much

5:24

more in the future. So our protocol for vessel

5:28

imaging, we always have a brain MRI with and without when we

5:31

obtain vessel imaging, and we'll talk about why that is in the pitfalls section.

5:36

We obviously want to have an MRA associated with it, so we can see the area of

5:40

stenosis and correlate it to the area of vessel wall abnormality.

5:44

And then we get the vessel wall imaging, which is just a high-resolution

5:47

T1 weighted image. Here we do a SPACE sequence

5:51

that has a very low sensitivity to chemical shift and susceptibility.

5:55

But whatever sequence you do, you want to make sure that the voxels are isotropic

5:59

because you want to be able to

6:01

reformat the vessels in any way possible to get the best

6:07

picture of the vessel. We always try to get it in a short axis, so we can

6:11

look at the pattern enhancement best.

6:13

So you want to make sure that you have those volumetric voxels

6:17

for reformatting. And then obviously blood and CSF suppression, so

6:21

that way we isolate just the vessel wall.

6:23

Here at our institution, we do quantitative MRA in a few

6:27

cases, and we'll show an example of that.

6:29

And then sometimes you can see profusions performed alongside,

6:33

especially in patients who are undergoing bypass and they want to assess

6:37

how those bypasses are faring.

6:40

Okay, so this is going to be the majority of the talk.

6:42

We'll just go over some cases. And so here's the first case.

6:46

So, this first case, a 66-year-old female, history of recurrent

6:50

infarcts presents with left homonymous hemianopsia.

6:52

And so her past medical history is hyperlipidemia, type two diabetes, and

6:56

hypertension.

6:57

So this is her MRI from June 2023, and we can see that she has this

7:01

small infarct in her right occipital lobe. Small amount of edema.

7:04

Okay, nothing special. So we go to CTA, and we can see that

7:08

the right PCA is diffusely diminutive.

7:11

But in addition, we also have this area of high-grade stenosis of the proximal

7:15

right M1. And we can see that again here.

7:17

And then on the CTA neck, she really doesn't have any atherosclerotic disease

7:21

in the cervical vasculature. So,

7:24

this patient, at this point, there were presumed atherosclerosis and

7:28

managed vascular risk factors. So this was the note from the neurologist.

7:32

And so the patient was started on dual antiplatelet therapy.

7:35

However, the patient comes back four months later, represents with a left

7:39

homonymous hemianopsia. And so her CTA shows pretty much

7:42

the same things. But now we can see on the MRI she has a much larger right

7:46

occipital infarct. And so this was a bit of a conundrum for the clinicians.

7:50

And so their note reads as follows, "Progression of stenosis over several

7:54

months is very atypical for intracranial atherosclerosis.

7:57

Concerned about an inflammatory cause." However, her LP and labs were

8:01

completely negative for anything inflammatory.

8:04

But because of how odd the presentation was, the patient was started

8:08

on empiric valcyclovir, which is not a benign medication.

8:12

It has some side effects, I think some GI side effects.

8:15

I'm not a pharmacist. I'm not 100% sure.

8:18

But then she was also started on dual antiplatelet therapy.

8:22

Now she comes back another month later, represents with left-sided

8:25

numbness.

8:27

MRA shows the exact same findings, but now she has these new right

8:30

MCA territory infarcts. So her story was just very confusing.

8:34

And you can see from their note, right MCA stroke in setting of

8:38

vasculitis versus athero.

8:40

Now they wanted to start steroids, continuing antiplatelet therapy,

8:44

consider vessel imaging or biopsy.

8:46

And so obviously we want to do the least invasive thing possible, so

8:50

we underwent vessel imaging. And so here we have two

8:53

axial vessel imaging protocols. So a pre and post, and there

8:57

is the area of stenosis at that right M1.

9:00

And then on the post, you can see some eccentric enhancement.

9:03

So at that same level, now we have sagittal imaging,

9:07

and we're showing here in the yellow, the normal vessel, and then some signal on

9:10

the inferior aspect of the vessel. And then let's zoom it up on the post.

9:16

Stenotic vessel on the top, and then some crescentic

9:19

abnormal enhancement along its inferior aspect.

9:22

And so this eccentric, irregular enhancement along the

9:26

vessel is very classic for atherosclerotic

9:30

disease. And we'll talk a little bit about that in a second.

9:33

And just to show that right PCA also has

9:37

some eccentric enhancement associated.

9:38

So it looks like she has multiple atherosclerotic plaques of the intracranial

9:42

vasculature. And so why was this helpful?

9:45

Well, because we made the diagnosis of intracranial atherosclerotic disease, now

9:49

the patient is a candidate for angioplasty where they're not a candidate for

9:52

angioplasty in vasculitis. They know to continue dual

9:56

antiplatelet therapy, and most importantly, we were able to avoid any steroids

10:00

or immunosuppressants that would be given in the setting of vasculitis.

10:04

And so this is a patient that underwent angioplasty.

10:08

Here is the area of stenosis and then the vessel after angioplasty.

10:11

And just so you know,

10:13

if this were a case of vasculitis, the vessel wouldn't respond this way with

10:17

angioplasty, and that's why angioplasty is not indicated in vasculitis.

10:21

So this is confirmed intracranial atherosclerotic disease.

10:25

So, with intracranial atherosclerotic disease, it is thought to be

10:28

about 10% of infarcts are caused by intracranial atherosclerotic

10:32

disease. Though it's thought to be underestimated.

10:34

And on vessel wall imaging, you can have intrinsic T1 hyperintensity

10:38

if there's hemorrhage within the plaque.

10:40

And then the most important finding is this eccentric enhancement.

10:43

And so you'll see this abnormal eccentric enhancement that is shown in this

10:46

schematic here.

10:49

Vessel imaging is also used to assess for high-risk features

10:52

of plaque,

10:54

like assessing for plaque instability.

10:56

And so degree of enhancements of the plaque has a high

11:00

risk for

11:02

rupture. So the more avid the enhancement, the higher risk for rupture.

11:06

Surface irregularity, intraplaque hemorrhage, which we'll see on the T1.

11:10

There's also a ratio of plaque thickness to

11:14

patent lumen. And so, the higher that ratio, the more

11:18

likely it is for rupture. And then, also remodeling

11:22

patterns. So we briefly discussed a positive remodeling in the

11:26

indications section. But essentially, when you have positive remodeling, you have

11:29

atherosclerotic plaque that grows outside

11:32

of the vessel lumen rather than inside.

11:34

And so if it's growing outside, it's not going to cause vessel stenosis, and so

11:38

it'll be occult on conventional imaging.

11:42

But it actually has a higher risk for infarct than

11:46

someone that has negative remodeling.

11:48

And so you're only able to pick that up on vessel imaging.

11:51

And so here's an example of that from the literature.

11:54

So a patient has this right MCA territory infarct.

11:57

All their conventional imaging is completely normal.

11:59

However, they have this area of eccentric positive remodeling in the

12:03

right ICA terminus, and that was presumed to be the cause for their infarct.

12:07

And here's an example from our institution as well So there's this punctate

12:11

infarct in the right cerebellar hemisphere.

12:14

When we look in the vessel wall imaging, you can see that the right vertebral

12:18

artery is patent, but there is this eccentric soft tissue that

12:21

demonstrates avid enhancement, and it's not showing up on

12:25

MRA. So this was an infarct secondary to positive remodeling

12:29

in the setting of intracranial atherosclerotic disease that was occult on the

12:33

MRA.

12:35

Okay. So that was a case of intracranial atherosclerotic disease where vessel wall

12:38

imaging was able to differentiate that from vasculitis.

12:42

So the next case is a 77-year-old male who presents with left-sided weakness,

12:46

past medical history of hypertension, hyperlipidemia, hyperparathyroidism, and

12:49

dementia.

12:51

And so here's their head CT and brain MR.

12:54

And head CT was normal, but you can see on this brain MR, multifocal

12:57

infarcts,

12:59

bilateral internal watershed territory, right periatrial white matter,

13:03

weird vascular distribution, and you can see why.

13:06

So here's their CTA. Bilateral ICA terminus,

13:10

high-grade stenosis, completely occluded, possibly.

13:13

And then all of this

13:14

lenticulostriate collaterals.

13:19

And so patient went on to diagnostic angiogram.

13:22

You could see again that high-grade stenosis at the ICA terminus and

13:26

these massive lenticulostriate collaterals that give you that puff of smoke

13:30

appearance.

13:32

So, the impression at this time of the

13:36

DSA reads bilateral occlusive disease of the ICAs with

13:40

extensive moyamoya-like neovascular changes and leptomeningeal

13:44

collateralization. This is consistent with progressive steno-occlusive disease

13:48

due to chronic atherosclerosis. And you can imagine why they presumed chronic

13:52

atherosclerosis, because this patient is a 77-year-old male.

13:55

You don't expect

13:56

moyamoya disease in someone of that demographic.

13:59

So, it was presumed secondary to atherosclerosis, and patient

14:03

underwent

14:05

bypass. This was one month before we had vessel wall imaging,

14:09

and so patient was brought back the next month for vessel wall imaging.

14:13

And as we can see here, here is the high-grade stenosis on the

14:17

pre, and then on the post, there really isn't much enhancement at all.

14:20

And differentiate it from the degree of enhancement that we saw on the

14:24

atherosclerotic case just prior to this.

14:27

And so this is a classic appearance for moyamoya disease.

14:30

And just a little bit background about moyamoya disease.

14:33

Remember that there's moyamoya disease and moyamoya syndrome.

14:36

And so disease refers to the idiopathic process, and

14:40

it's non-inflammatory, non-atherosclerotic.

14:42

While moyamoya syndrome is going to be due to some underlying etiology,

14:46

most commonly it's either going to be due to atherosclerosis, or it can be due to

14:49

vasculitis or other inflammatory cause.

14:52

And so classically, moyamoya is going to be younger patients.

14:55

It has a bimodal distribution around four and then also within the

14:59

fourth decade.

15:01

And then demographics classically have an Asian population and

15:05

slightly higher female predilection.

15:07

Most common risk factors for moyamoya syndrome, however, are going to be NF1,

15:11

sickle cell disease, and previous cranial radiation therapy.

15:16

So

15:18

again, in moyamoya, whether it's disease or syndrome, you'll have complete or near

15:21

complete vessel stenosis, classically at the ICA terminus.

15:25

You have extensive lenticulostriate collaterals giving that puff of smoke

15:28

appearance like we saw on the DSA. And then on MRI, we can see the two signs of

15:32

Ivy sign and brush sign, which we'll show in a second.

15:35

And so with vessel wall imaging, it's always going to be negative remodeling, so

15:39

you won't have the positive remodeling like you see in ICAD.

15:41

And then the enhancement is going to be based on, again, if it's disease or

15:44

syndrome. So with moyamoya disease, you have no or minimal enhancement,

15:48

while with moyamoya syndrome, it's going to be secondary to whatever the underlying

15:52

pathology is. So if it was due to intracranial atherosclerotic disease, you would

15:55

expect some eccentric enhancement like we saw in the previous

15:58

case. So just

16:02

showing here for people who might be taking boards soon, I know we just

16:06

finished the boards, but if you are taking boards this year, this classic puff of

16:08

smoke appearance is essentially pathognomonic for moyamoya disease.

16:13

And then here is an example of the Ivy sign.

16:14

So this is our patient that we are presenting right now.

16:18

So this is their brain MRI before they got a bypass.

16:21

And you can see FLAIR hyperintense signal throughout the

16:25

circle vasculature. And then on their

16:29

post-op, you can see again, since they got a right-sided bypass, you have still the

16:33

Ivy sign on the left, but you have resolution of the Ivy sign on the right.

16:37

Okay.

16:40

Remodeling on VWI. So the question, can you explain why

16:44

you

16:45

may, by remodeling on VWI.

16:48

I'm not sure if you mean by

16:52

positive remodeling, or maybe if you can try to clarify

16:56

that, and then I'll get back to it. Maybe we'll leave it for the end.

17:00

Okay, so this is an example of Ivy sign.

17:03

And then this is obviously not our patient.

17:05

This is a pediatric patient, but you can see they have diffuse anoxic injury.

17:09

And

17:10

you have prominence of the deep medullary veins

17:13

on SWI imaging or GRE. And this is an

17:17

example of the brush sign. You have high concentration of deoxyhemoglobin within

17:21

the veins, giving it a more pronounced appearance on

17:25

SWI. So this is the brush sign, can be seen in any

17:30

deoxygenated

17:32

setting or anytime you have higher oxygen extraction fraction in the brain.

17:37

Okay. So that was moyamoya disease.

17:40

And so why was it beneficial to diagnose moyamoya

17:44

disease rather than moyamoya syndrome in this patient?

17:47

So

17:48

one of the most common complications for moyamoya disease is they have a high

17:52

risk of intracranial hemorrhage.

17:54

And so because we were able to say this is moyamoya disease and not moyamoya

17:58

syndrome secondary to intracranial atherosclerotic disease, they were

18:01

discontinued from dual antiplatelet therapy, and they were only continued on

18:05

aspirin at 325 milligrams daily. So

18:09

even though the surgery may not have changed, they might have bypassed the patient

18:12

anyway, but they did change their medical management.

18:16

Okay, next case. So 44-year-old female presents with headaches, dizziness, and

18:20

vision changes, and has a history of marijuana use.

18:22

So 44 years old. So here's her brain MRI showing multifocal

18:26

infarcts and

18:28

several different vascular distributions.

18:30

And then there's also this subcortical edema in the right parietal lobe that

18:34

doesn't have any associated edema with it or any associated

18:38

restriction.

18:40

And here's her CTA, and

18:44

remember she's 44 years old, but all these vessels look very thin and

18:48

irregular.

18:50

I'll show you the post-treatment images if you guys are skeptical.

18:53

But

18:54

you can see both her MCAs are diffusely narrowed.

18:57

Her basilar artery is also diffusely narrowed.

18:59

She has all these areas of stenosis and bilateral ACAs.

19:04

So very weird appearance. So they were also unsure what was happening, concerned

19:08

for vasculitis or vasculopathy, hypercoagulability in the setting of

19:11

dehydration, concerned for cardiogenic versus hypercoagulability etiology.

19:15

So obviously, they're not really sure what's going on.

19:18

And so at this point, we recommended vessel imaging to see if it could be of

19:21

help. And so we'll show you a couple of different areas of stenosis

19:25

and how it looked on vessel imaging.

19:27

So here is the left ICA terminus, or sorry, I guess superclinoid left

19:31

ICA. And on the vessel imaging, it really doesn't have much enhancement.

19:36

Basilar artery as well, diffusely narrowed, irregular, doesn't have much

19:40

enhancement. And then we're looking at the CTA.

19:44

All those areas of stenosis also don't have any appreciable enhancement

19:48

or intrinsic T1 hyperintensity. And so this is a classic appearance of

19:52

RCVS, reversible cerebral vasospasm constriction

19:56

syndrome. And for this patient, it was presumed secondary to marijuana.

20:00

She was discharged in December 2024 on calcium channel blockers and

20:03

ASA, and I checked on her chart as of yesterday, she has not

20:07

returned to our institution. So it seems like this is

20:11

the true diagnosis, and what's beneficial about this is

20:15

because they were concerned about vasculitis,

20:18

and we were able to rule out vasculitis with vessel imaging, we were able to avoid

20:21

steroids and immunosuppressants.

20:23

And so just to show if anyone was skeptical about the initial CTA,

20:27

you can see abnormal basilar on the left, and then this is what

20:31

she looks like a few months, two months later,

20:35

on calcium channel blockers. And then same thing here.

20:39

All her MCAs are abnormal. And here they look

20:43

much more normal for her age. And same here, all those areas

20:47

of stenosis and bilateral ACAs are improved.

20:51

Okay, so classically the RCVS patients will present with

20:55

thunderclap headaches, and CTAs will show

20:59

reversible multifocal cerebral vasoconstriction.

21:01

Most common risk factors are peripartum drugs and migraines, and most common

21:05

complications are strokes, subarachnoid hemorrhage, and PRESS.

21:08

And so the most important treatment is to withdraw exogenous trigger.

21:13

After that, you can administer calcium channel blockers and

21:16

also control blood pressure and

21:20

provide seizure prophylaxis.

21:23

So this is what RCVS will look like on vessel

21:27

imaging. Again, we'll have negative remodeling, meaning that

21:30

the disease is causing vessel stenosis.

21:33

We'll have concentric wall thickening to differentiate from ICAD, where it'll be

21:37

eccentric,

21:39

and no or mild enhancement similar to Moyamoya,

21:42

differentiating from vasculitis, which will have

21:45

avid enhancement.

21:47

And one other thing to differentiate it from Moyamoya, since both can have the

21:50

negative remodeling, concentric wall thickening.

21:52

With Moyamoya, classically, it's focal and proximal, while with

21:56

RCVS, it's more distal and more diffuse.

22:01

Okay. So again, just some more relevant case

22:05

imaging. What you'll see with RCVS, you can have these sulcal effusions, as we see

22:09

in our patient here. You have subcortical edema.

22:12

You can have multifocal stenoses on the CTA.

22:15

In addition, because of stenoses, you can have infarcts like we saw in our patient.

22:19

And don't be tricked if you see leptomeningeal enhancement.

22:22

That's also a finding that can be seen with RCVS.

22:26

Okay, so next case is a 45-year-old female, presents with the worst headache of her

22:29

life.

22:30

See how we're doing on time. Okay, 23. So worst headache of life.

22:34

That's a buzzword for looking for a subarachnoid hemorrhage.

22:37

And you can see that they have multiple areas of hemorrhage in the interpeduncular

22:41

cistern and bilateral occipital horns.

22:43

You can see it within the prepontine cistern.

22:46

And then GRE also shows those areas of hemorrhage.

22:49

So this is where it was tricky. She went on to DSA, and you can see both

22:53

vertebral arteries have aneurysms.

22:55

One of them is smaller but more regular on the right, and then the left

22:59

aneurysm is more regular, but it is also much larger.

23:02

And you can see that same appearance on the 3D imaging as well.

23:07

So at this point, it's a conundrum.

23:09

Which aneurysm do we think is ruptured?

23:12

And we obviously

23:15

don't want to sacrifice the wrong vert because when they do coil this

23:19

aneurysm, they're going to sacrifice the whole vert.

23:21

And you can imagine that can be an issue if we sacrifice the

23:25

wrong vert. So vessel imaging was employed to help us figure out which

23:29

aneurysm is the one that ruptured.

23:31

So here's our MRA, and you can see that the right vert aneurysm is

23:35

smaller but is much more irregular.

23:37

And then when we look on the pre and post,

23:40

there's avid enhancement along that irregular tip of the aneurysm.

23:44

So this was concerning. And then we look in the left vert, and this

23:48

defect here was thought to be due to tortuous or turbulent

23:52

flow.

23:54

And then there was some signal in that same area, but because

23:58

it looks like turbulent flow on the MRA, we presumed that this was going to be

24:02

turbulent flow and not enhancement

24:05

suggesting instability. And so we'll discuss a little bit about turbulent flow in

24:09

the pitfalls section. But this patient went on to

24:15

coil the right vertebral artery aneurysm.

24:17

And you can see here

24:20

aneurysm is successfully coiled and that right verte is no longer

24:24

supplying the basilar artery, so everything supplying the posterior circulation is

24:28

coming from the left verte now.

24:30

And this was her head CT two days later.

24:33

The

24:34

subarachnoid hemorrhage is completely resolved, and she doesn't have any posterior

24:38

infarcts.

24:40

So this was a case of vessel imaging to help us to

24:44

identify the culprit cerebral aneurysm that

24:47

ruptured.

24:49

And

24:50

just some background about cerebral aneurysms.

24:53

Incidence is thought to be about 4%, though

24:56

since we've gotten AI

24:59

algorithms to identify aneurysms, it's coming closer to around 10% it is thought.

25:03

Saccular subtype is the most common, with ACOM being the most distal, most

25:08

common location. Several risk factors including first-degree relative,

25:12

underlying connective tissue disease, NF1, and autosomal dominant polycystic kidney

25:16

disease, and is the most common cause of non-traumatic subarachnoid hemorrhage, and

25:20

is obviously something that's really important to diagnose because a third

25:24

can expire and a third can be left with severe disability.

25:29

So with conventional imaging, we're looking for central subarachnoid hemorrhage

25:33

differentiating from trauma where you would have peripheral subarachnoid

25:36

hemorrhage. We can see infarcts secondary to vasospasm.

25:40

MRI will show flare suppression or failure of flare suppression of

25:44

CSF in the sulci. And then for CT or MRA,

25:49

the high-risk features for

25:52

unstable aneurysms would be something large, greater than seven millimeters,

25:55

irregular shape, as we saw in our case, or a length to neck

25:59

ratio more than 1.6.

26:02

So vessel wall imaging is helpful with cerebral aneurysms to identify,

26:06

again, ruptured aneurysm or to identify a high risk of

26:10

rupture and try to figure out patient management.

26:13

And when we talk about degree of enhancement, it's usually relative to the

26:17

pituitary. So we use the pituitary as an internal control, and it's

26:21

thought that degree of enhancement can be associated with future

26:24

vasospasm. And so that's another thing that we comment upon when

26:28

reading vessel imaging for aneurysms.

26:32

Again, just some board-relevant cases.

26:35

We just had a case yesterday with our maintenance of certification asking

26:39

about location of aneurysm based on

26:43

pattern of subarachnoid hemorrhage.

26:44

And so, just memorize these most common

26:48

locations and associate them with those areas of aneurysm.

26:54

This is a

26:55

companion case, also an aneurysm.

26:59

So 55-year-old female presents with headache and nuchal rigidity.

27:02

And CT

27:04

was normal, but then the CTA shows this

27:07

abnormal aneurysm arising from the

27:11

M1, M2 junction on the left. And so they weren't really sure what to do with it

27:15

because her symptoms were

27:17

typical for subarachnoid hemorrhage, and she actually had an LP, and the LP

27:21

was indeterminate for subarachnoid hemorrhage, so they weren't sure what to do with

27:25

this aneurysm. In addition, there was some concern about

27:29

this left verte looking kind of funny.

27:30

They thought there could be some type of dissection or intramural

27:34

hematoma.

27:36

So they went on to DSA to look at that left verte. The left verte looked normal.

27:40

But then they can also see that bilobed aneurysm at the

27:43

M1, distal M1 here. And so

27:48

went on to vessel wall imaging, and so vessel imaging was able to answer both

27:51

questions. So there was no abnormal signal within that left verte, so we

27:55

were able to exclude any pathology involving that left verte.

27:58

And then we look at that left M1 aneurysm, and there is

28:02

no enhancement associated with the aneurysm.

28:06

So vessel imaging here was able to tell us that this is likely

28:10

stable, and it's not something that needs to be intervened

28:14

upon emergently, even though her symptoms were concerning and

28:18

this has this bilobed weird appearance of an aneurysm.

28:22

And so this was diagnosed as a stable

28:25

aneurysm and also no evidence of verte dissection.

28:28

And she had a repeat MRA in May of 2026, which is about a year and a

28:32

half after the images that we just showed, and that

28:36

aneurysm was stable.

28:38

Okay. So I'm not sure if this might be the last case, but this is

28:43

35-year-old female, presents with fluctuating left facial and

28:47

arm sensory symptoms and has headaches as well.

28:50

So here's her MRI showing multipocal infarcts in the right MCA

28:53

territory. Then there's a high-grade stenosis of the M1,

28:57

M2 on the right.

29:00

And so here's the vessel wall imaging, and we have a sagittal pre and a sagittal

29:03

post. There's some mural thickening, concentric mural thickening of the

29:07

vessel, and there's avid enhancement that even extends beyond the vessel

29:11

wall into the surrounding parenchyma.

29:15

And we weren't able to include the M2 portions within the

29:19

vessel wall imaging protocol, but we can see even on the

29:22

post-gad, the vessels are diffusely enhancing both

29:26

M2 superior and inferior divisions, as well as some parenchymal

29:30

edema next to it. And so this is a classic appearance of

29:34

vasculitis. Her CSF was positive, and

29:38

follow-up imaging showed resolution of parenchymal edema after

29:42

she got treatment.

29:44

And there was still some mural enhancement, but it's known that the imaging will

29:48

lag a bit behind patient management or

29:52

patient presentation.

29:54

Okay, give it a second while it loads.

29:58

Okay, so CNS vasculitis is a heterogeneous group of inflammatory

30:02

disorders involving any vessel wall in the brain, spine, and NGes.

30:05

And so we usually classify it as primary or secondary, primary being limited to the

30:09

CNS and no involvement of other systems, while

30:12

secondary will be due to some systemic or infectious process.

30:16

And so vasculitis on vessel wall imaging will have negative

30:20

remodeling, meaning that the vessel will decrease in size, will become

30:24

stenotic, and there's avid concentric enhancement.

30:26

And differentiate it from ICAD, will have avid eccentric enhancement.

30:32

Okay. And so this is just a summary of all the different patterns

30:36

that we looked at. So for normal vessels, we have a normal lumen with

30:40

thin wall without any enhancement.

30:43

With ICAD, you'll have positive or negative remodeling, maybe both,

30:48

eccentric avid enhancement. Vasculitis will have only negative remodeling,

30:52

meaning vessel is stenotic and it'll have concentric avid enhancement.

30:56

And then RCVS and Moyamoya will have negative remodeling, but it'll have minimal

31:00

to no enhancement.

31:03

Okay. And so we'll briefly talk about the pitfalls.

31:06

So this was a 23-year-old female that presented with right paresthesia and

31:09

weakness. And so her DWI was normal, and vessel

31:13

imaging showed areas of IV signs. So we're concerned that there's some

31:16

proximal stenosis. And so here's her MRA,

31:20

and both ICAs are diffusely diminutive and irregular.

31:24

And then when we go to the MRA head, her ICA terminus

31:28

is reconstituted bilaterally when it's thought to be

31:30

secondary to supply from the right posterior communicating.

31:35

And here's the quantitative MRA, which I briefly mentioned before.

31:38

But with this quantitative MRA, we can see that the flow in the right posterior

31:42

communicating is very elevated. So normal is around 10

31:46

cc per minute. Here it's about 196 cc per minute.

31:49

And it's going from posterior to anterior, confirming that her entire

31:53

anterior circulation is being supplied by the posterior circulation.

31:56

And this was just a DSA confirming that this is a vert run.

32:00

And you can see the entire anterior circulation is being supplied by the vert run

32:04

being that posterior communicating artery.

32:10

And so they went to DSA. And you can see again,

32:14

high-grade stenosis, a bilateral terminus, but we really don't see that

32:18

huge

32:19

leptomeningeal collateral puff of smoke that we saw in our

32:23

previous case. So this is the case from earlier today,

32:26

the Moyamoya case from earlier today.

32:29

And so this is what we expect to see with that puff of smoke, but here we

32:33

don't really have that puff of smoke appearance.

32:36

They went on to vessel imaging, and you can see, like we just saw in our previous

32:40

case, avid concentric mural enhancements

32:44

involving that area of stenosis. So we're like, "Okay, this is done.

32:48

This is classic vasculitis." However,

32:52

CSF markers did not show anything.

32:54

No elevated protein, no inflammatory markers.

32:58

There was no parenchymal changes on the MRI,

33:01

and there was no distal vessel involvement. Everything was just proximal.

33:05

And so actually, this patient was diagnosed with Moyamoya and not

33:09

vasculitis.

33:11

And so patient then underwent

33:13

STA-MCA bypass and did not have any steroids

33:17

administered. So I think probably the biggest pitfall

33:21

is there's some overlap of patterns of enhancement.

33:25

So with RCVS and Moyamoya, even though we like to say that there's no or minimal

33:29

enhancement, some of them can enhance and look very similar to

33:33

vasculitis.

33:34

And you can also have a vessel enhancement that has nothing to do with

33:38

primary vasculopathy, like if a patient had a recent thrombus or

33:42

if they were a

33:45

recent thrombectomy. So whenever we read these cases, we

33:48

always try to have as much clinical context as possible

33:52

because of this overlap of imaging

33:56

patterns.

33:58

Here's another pitfall. So

34:01

this is the proximal cavernous segments of bilateral ICAs, and it

34:05

looks like there's some vessel stenosis there, maybe some ICAD, some

34:09

eccentric enhancement. However, when you look on the MRA, there really isn't

34:13

any

34:14

area of stenosis of that proximal left ICA.

34:17

So this is an example of turbulent flow or slow

34:21

flow causing lack of

34:24

black blood. So we weren't able to suppress the blood as much as we would

34:28

like, and that can show up as this artifact.

34:30

So that's why whenever we get vessel imaging, we always get the MRA

34:34

associated with it to make sure we're not getting tricked by

34:38

turbulent flow or slow flow.

34:41

And here's another

34:43

pitfall. So this was a patient that had,

34:48

I think they may have had some

34:51

vague symptoms like dizziness. I forget what, to be honest.

34:54

But this was their vessel imaging.

34:57

We have a sagittal of bilateral PCAs, and we have this area of

35:01

enhancement along the posterior aspect of the PCA.

35:03

So initially, I was thinking this could be positive remodeling.

35:06

Do they have some ICAD? Should we put them on antiplatelet therapy?

35:11

However, we look on the post gad

35:13

brain, and we can see a vein coursing very close to that right

35:17

PCA. So this is a

35:21

vein that travels very close to the PCA and mimics

35:24

positive remodeling. And so that's why all of these

35:29

vessel imaging cases will be performed with a post gad brain as well

35:33

to avoid this pitfall.

35:37

Okay. So the pitfalls again, nonspecific enhancement,

35:40

turbulent flow. We briefly saw in that previous case, lots of motion

35:44

artifacts, and then also adjacent venous enhancement.

35:49

So those are all the cases they had and the pitfalls.

35:52

Some future directions where I think we should see for vessel imaging,

35:57

everything we've talked about is very qualitative.

35:59

We say

36:00

minor enhancement or avid enhancement or high-grade stenosis,

36:04

low-grade stenosis. I think if we start quantifying these findings, it may be

36:08

able to help us

36:11

differentiate some of the ambiguity when it comes to differentiating

36:15

Moyamoya and

36:17

vasculitis, for instance. I think we will start seeing it more as a screening

36:21

tool, especially in the settings of cryptogenic stroke because of cases

36:25

of positive remodeling, as we saw.

36:27

And then we might also start seeing it involving

36:31

vasculature outside of the CNS as well.

36:34

Okay. So in summary, we talked about what vessel wall imaging is, how we

36:38

obtain it. We talked about its most common indications

36:42

being differentiating vessel stenosis, and then potential indications mostly being

36:46

associated with aneurysms.

36:49

Majority of the

36:51

talk has been cases demonstrating the most common differentials and how it's

36:55

changed patient management. We talked about the pitfalls, and then finally,

36:59

we briefly discussed the future directions. Okay.

37:03

Thank you, guys. Just acknowledging some of our team from

37:06

neurosurgery, neuro IR, and our techs who's really helped make this

37:11

possible. And then,

37:13

happy to take any questions now.

37:23

Okay. Should I just start reading off some of these questions from the Q&A?

37:27

Yeah, if that's what you'd like to do.

37:28

I was just about to hand it back over to you.

37:31

Okay. Yeah. So first one, "What do you mean by positive and negative remodeling?

37:35

Thank you." So, when we say positive

37:38

remodeling, it means that there's some vessel disease

37:42

that is growing outward from the vessel lumen.

37:46

And so, when you do a normal CTA or MRA, we're only

37:50

looking at the flow within the lumen.

37:52

And so if something is growing and going

37:56

away from the lumen, we won't be able to see that on the CT or MRA, but we will

38:00

be able to see it on the vessel imaging.

38:02

And so that's why we use vessel imaging to assess for positive remodeling.

38:06

Negative remodeling means whatever the disease is in the vessel wall, it's

38:10

growing into the lumen, and it's causing stenosis.

38:13

And so because it's causing stenosis, we will be able to see it on the CTA or

38:17

MRA.

38:18

So that's the difference between positive and negative remodeling.

38:23

"In the RCVS case, could the

38:27

posterior lesions represent PRESS?" Yes, absolutely it can represent PRESS.

38:30

And so there is overlap between RCVS findings and PRESS as well.

38:34

"Couldn't atherosclerosis cause endophytic plaques

38:38

and negative remodeling?" Yes, absolutely it can.

38:41

And so that's why

38:43

we said that atherosclerosis can have both positive and negative

38:46

remodeling. The problem is with the positive remodeling, because we won't be able

38:50

to see that on the conventional imaging.

38:52

And so that's why we utilize vessel imaging in cases of

38:56

atherosclerosis.

38:58

"In the setting of vasospasm in aneurysmal subarachnoid hemorrhage, what are the

39:02

features of enhancement and how long can it last?" In the setting of vasospasm

39:06

in subarachnoid, what are the features of the enhancements?

39:11

So in my

39:13

experience,

39:15

for

39:17

a patient that's had subarachnoid hemorrhage and has had vasospasm, I don't see

39:21

enhancement of the vessel wall in that vasospasm.

39:25

It is somewhat

39:29

limited also because in the cases where there is vasospasm, there's

39:33

usually a lot of subarachnoid hemorrhage around it, and that can prevent

39:37

appropriate CSF suppression.

39:40

But from what I've seen, I have not seen enhancement of the

39:44

vasospasm walls.

39:48

Okay. Let me see. Sorry, something jumped.

39:53

"When should one be worried about false negatives, particularly thinking of the

39:56

stable aneurysm case?"

40:00

It's hard for me to really say.

40:03

I think that's why we always have to take the entire

40:07

clinical context into account.

40:13

We've been doing this for maybe about two or three years.

40:16

I have not had a case yet where

40:19

an un-enhancing aneurysm

40:23

eventually ruptured,

40:26

soon after the

40:28

vessel imaging case. So,

40:32

yeah, it's really hard to say. I think we should always be worried about false

40:35

positives, but I think the best way to avoid that is by taking the

40:38

entire clinical context into account.

40:41

Okay.

40:43

"What grading do you use for circumferential

40:46

enhancement, and do you want to see 360-degree

40:50

enhancements?"

40:53

So we don't really have a grading system.

40:56

Again, that's why I was saying it's very qualitative.

41:02

We showed you that case of eccentric enhancement for ICAD, and we showed you

41:06

the case for concentric enhancements for

41:09

vasculitis, and so it's very much just

41:14

trying to differentiate between those two patterns, and it's usually pretty clear

41:18

one way or the other. And do you want to see--

41:21

Yeah, obviously we'd want to see 360-degree enhancement in cases of

41:25

vasculitis, and we want to see less than 360 degrees in cases of

41:28

atherosclerosis. Again, it's not always that clear, but

41:32

that's preferably what we'd like to see.

41:35

"How long does a vessel imaging protocol take?" So

41:38

the

41:40

vessel imaging sequence itself is about five and a half minutes.

41:45

Since we do pre and post contrast, that's going to be 11

41:49

minutes. And then we have to get the whole brain MRI with and

41:52

without, and that's usually another,

41:56

I think around 15 minutes or so.

42:00

And then the MRA is

42:03

around another three minutes.

42:05

So I don't know. You guys can calculate all of those together.

42:09

So it's not a short sequence, unfortunately.

42:14

Okay.

42:15

"Is the best imaging for vessel wall disease MRA or

42:18

MRA with dark blood

42:21

or

42:23

T1 fat sat MRI?"

42:33

I think it's going to depend on what the clinical question

42:36

is.

42:39

If it's a run-of-the-mill stroke,

42:42

I think it's not necessary to do all the vessel

42:46

imaging stuff, and I think an MRA by itself will be

42:49

fine. If there is some type of clinical

42:52

conundrum where we need to assess the stenosis more, then

42:56

obviously we want to do the whole vessel imaging protocol, a brain MRI with or

42:59

without MRA and

43:02

vessel imaging.

43:05

I'm not sure if you mean for the T1 fat sat, if this is like the

43:08

dissection protocol that we do sometimes

43:12

here, if that's what you're referring to.

43:17

But we usually do that for the neck, we're not doing that for the intracranial

43:21

vessels.

43:23

Okay.

43:24

What has been your experience with granulomatous vasculitis?

43:26

That's a great question.

43:28

We had one case

43:30

where

43:33

they were concerned for something of that sort, but it was an extracranial

43:37

vessel and

43:40

it appeared negative on the vessel imaging, but appeared abnormal on the

43:44

ultrasound, and

43:47

that was only just one case. So don't have much experience with it.

43:52

But it's definitely something that it would be interesting to see

43:57

higher numbers of cases and see what the patterns are in vessel

44:00

imaging. Can you demonstrate how you correlate time of flight

44:04

with vessel wall to rule out slow flow?

44:07

Do you expect the caliber to be smaller in the time of flight as well if the

44:10

enhancement were real? Exactly, yeah.

44:12

And

44:14

so

44:16

if there is slow flow on the vessel imaging,

44:20

that will prevent us from saturating out the blood as best we can.

44:24

But you should still see that

44:27

normal vessel lumen on time of flight.

44:30

So if it looks stenotic on the vessel imaging, but then looks normal on the

44:34

time of flight, then we're thinking that this is going to be just slow

44:38

flow, especially if it's in areas of common

44:42

artifact, wherever there's tortuous vessels, like in the carotid

44:46

siphons.

44:47

Do you expect the caliber to be smaller on time of flight as well if the

44:51

enhancement were real? Yes. Yes, we would.

44:57

In the pitfalls cases, the case that showed concentric

45:00

enhancement proved Moyamoya at the end, despite presence of

45:04

enhancement. Yes. Yeah, and that's why it was in the pitfalls section,

45:08

because there's some overlap between Moyamoya and

45:11

vasculitis. Because classically,

45:15

the teaching is Moyamoya shouldn't have enhancement, or if it does, it's minimal.

45:20

But in that case, there was very avid enhancement.

45:24

But

45:25

I would have avoided that pitfall if I looked more into the clinical history

45:30

and seen all the labs were completely negative.

45:34

If I looked more into the structural imaging, they didn't show

45:37

any

45:39

parenchymal edema or distal vessel involvement.

45:42

And so that's why we always tried to read it within a clinical context as

45:46

much as possible and know that vessel imaging isn't perfect, that there's going to

45:49

be a lot of overlap.

45:52

Is intracranial vessel imaging feasible on 1.5? Do you have experience with it?

45:56

Yes, we do. We have done it on 1.5

46:00

in patients who were, for some reason, unable to get a 3 Tesla,

46:06

and it turned out fine. There was really no issues with it.

46:10

Sequence used for vessel imaging. Okay, also 1.5 Tesla.

46:13

Yeah, so we ran the same exact sequence as we did on our

46:17

1.5T, and the imaging was fine. I think what's

46:21

more important, actually, is the coil.

46:24

And so having a 32 or 64 channel head coil

46:28

can be more important than having a 3 Tesla magnet.

46:32

In atherosclerosis, can enhancement also be absent?

46:39

I think it can.

46:41

But usually if it's the culprit aneurysm, there's going to be

46:45

enhancement associated with it.

46:48

And most of these times when we're getting vessel imaging, it's in patients who are

46:51

symptomatic.

46:53

So I'm sure it can, but in my experience, most of

46:57

our plaques have been enhancing.

47:00

Is the quantitative a commercial product? Yes, it is.

47:03

It's called NOVA, and we're using it

47:07

here because we're part of a multi-center trial, and we just

47:10

started using it on some clinical patients as well.

47:13

Could it be done on 1.5 Tesla? Yes, it can.

47:16

What do you use the quantitative MRA for?

47:18

Does it help you explain a slender vessel when the supply is coming from the

47:22

contralateral side, eg small right ICA, because AC is supplied

47:26

by left, is there any other applications?

47:28

So for us, we're using it for two main things.

47:33

Patients who are about to undergo a bypass, and then also patients who have

47:37

arteriovenous malformations, and they're looking for

47:42

pre and post-treatment planning.

47:43

So for patients who undergo bypass,

47:47

they want to see the velocity of flow,

47:51

especially within their right superficial temporal artery,

47:54

because that's what they're using for the bypass.

47:57

And

47:59

they also use that as a follow-up to make sure

48:03

that the velocity of flow is still preserved within whichever vessel is being

48:07

worked on. So if the right superficial temporal artery velocity is

48:10

decreased on the follow-up exam, then they're concerned that the graft might

48:14

be

48:15

pathologic. So that's the number one case, and the other

48:19

one for AVMs. If a patient has an AVM and they want to look at

48:23

velocity of flow within a specific vessel that's going to be treated, and then

48:27

they also do it again as follow-up to look at that specific vessel to see

48:31

if velocity is persistently low. Because sometimes you can't

48:35

tell

48:37

exactly how that vessel is faring with just conventional imaging.

48:42

Pre- and post-contrast 3D T1 with fat and blood suppression plus

48:46

MRA and T1 with contrast, is this enough?

48:48

Pre- and post-contrast

48:51

3D T1 with fat blood suppression plus MRA and T1 brain with

48:55

contrast.

48:57

Let me see.

49:03

I'm sure

49:07

that could be enough. I like to have the full brain MRI

49:11

because

49:13

I always like to,

49:14

if there's some troubleshooting, I would like to have all the other sequences in

49:17

place to avoid the major pitfalls of the adjacent venous

49:21

enhancement. I think, yes, that will be

49:24

enough.

49:27

But if they're in there, like getting a flare

49:31

in T1 pre, it doesn't really add that much extra time, and it

49:35

might really help you troubleshoot in the future.

49:40

What protocol for dissection in neck and what

49:43

protocol

49:46

for--

49:48

Sorry, I'm having a hard time reading this one.

49:50

What's the protocol for dissection in neck, and what's the protocol for vessel

49:54

imaging?

49:59

So, if I'm reading this correctly, you're asking what the dissection protocol is in

50:03

our neck

50:05

and what the protocol is for the vessel imaging.

50:07

So we talked about the vessel imaging protocol already in the head.

50:11

For the neck, we use a 2D T1

50:14

fat-saturated axial,

50:17

essentially to look at

50:19

vertebral dissections.

50:22

That's something we've been doing for quite a bit now.

50:27

And yeah, that's pretty much the only thing.

50:28

It's a T1 fat sat 2D axial.

50:33

The vessels have vasospasm. Can this appears enhancement only within the wall?

50:35

Yes, it absolutely can. And it especially occurs in the proximal verts.

50:40

But yes, vasospasm is definitely another

50:44

pitfall we can see.

50:46

Will in vertebral artery

50:48

dissection, only the string

50:51

sign is present?

50:56

I'm not sure what they mean.

50:59

So I haven't heard of the string sign, but I'm assuming string sign means that it's

51:01

a very thin avert.

51:03

But if it's dissected, then you should expect to see some T1 enhancements

51:07

in there as well, which you can see both with the

51:11

neck dissection protocol and the vessel imaging protocol.

51:15

Is to obtain blood suppression, is this additional

51:19

software or just parameters? No, just parameters.

51:23

This is not an additional software needed.

51:26

Okay. I think that's all the Q&A questions.

51:29

I don't know if there's anything in the chat that

51:34

I should see.

51:40

Just quickly reading through the chat.

51:44

How to differentiate focal wall enhancement and vessel wall imaging due to unstable

51:48

versus ruptured aneurysm versus dissection?

51:53

Well,

51:54

I think we would use the CTA or MRA to help differentiate

51:58

that,

52:00

because an aneurysm and a dissection will appear very different on

52:04

CTA or MRA.

52:06

Do we need to compare with superior temporal vein artery to determine the quality

52:10

of vessel imaging?

52:14

I'm not sure why we would use that to determine the quality.

52:18

I think what I use to make sure that the quality of vessel imaging is good is

52:22

we have appropriate

52:24

blood suppression and appropriate CSF suppression.

52:27

We don't have

52:29

much motion artifact and

52:33

making sure that the areas that should be enhancing are enhancing, like in

52:37

the pituitary or like normal mucosa,

52:42

to make sure that the patient enough contrasts to look for enhancements.

52:45

That's how I would compare or how I would

52:49

determine quality of vessel imaging.

52:52

Are there areas where you expect normal vessel wall

52:55

enhancements? Yes. So vasospasm, as we briefly

52:59

mentioned, especially in the proximal verts.

53:04

I'll say

53:08

that's pretty much it. The areas where it looks like there is enhancement, like in

53:12

torturous areas like the carotid siphons, but that's not actually true vessel

53:16

enhancement. But you shouldn't see true mural

53:19

enhancement. All the things that look like they're enhancing the vessel wall

53:23

won't be the vessel wall itself.

53:26

Okay, I think that's all the questions.

53:31

All right. Yeah, looks like you got them all.

53:33

Okay.

53:34

Thank you so much for sharing that lecture with us today, Dr.

53:37

Malik, and answering all those questions.

53:40

No problem.

53:41

Thanks to everyone who joined us, participated, and asked such great

53:45

questions.

53:46

You can access the recordings of today's conference and all our

53:50

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53:53

We'll also email out a link to the replay later today.

53:56

Be sure to join us next week on Thursday, July 9th at 12:00

54:00

PM Eastern, where Dr. Alka Singhal will deliver a

54:04

lecture entitled Ultrasound Spleen.

54:07

You can register for that at medality.com and follow us on social media

54:11

for updates on future noon conferences. Thanks again, and have a great day.