0:00

Hi everyone.

0:01

Thank you for returning, um, today

0:04

for our week two Office Hours case review with Dr.

0:07

Lorenz. Um, just a reminder, if you have any questions,

0:11

you can enter them in the chat

0:12

or use the hand rate, uh, raising emoji.

0:15

We'll call on you or you can ask Dr. Lorenz directly.

0:18

So, Dr. Lorenz, whenever you're ready.

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Cool. Alright, so you are week two

0:24

into this amazing course.

0:26

Um, you have one week underneath your belt, which is just

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as any first week we should be.

0:32

It's just how much did I understand through this, you know,

0:35

uh, wall of information and so forth.

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And then now week two is, okay,

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let's start putting some into practice, right?

0:42

So one of the things that is practical is how do I do the,

0:46

uh, evaluation in use of a, um,

0:50

software device such as TE Recon?

0:52

So I've got my te recon up here,

0:54

and we're gonna do a case one evaluation here,

0:58

and let's go ahead and,

0:59

and again, the way that they,

1:01

this particular vendor has utilized it as a anatomic, uh,

1:04

way of distributing these little micro apps

1:08

or mini apps, which is, um, neurologic and the neck,

1:11

and then cardiovascular, um, and chest and the den, pelvis

1:15

and orthopedic and so forth.

1:17

And then some quantitative component here.

1:19

So you can choose any of the cardiacs listed here.

1:23

What these mean then,

1:24

is when you move from the patient query to then the viewer,

1:27

it just reorganizes the,

1:29

the micro apps into different areas.

1:30

So any one of these will be fine.

1:33

So we'll just use that one there.

1:35

And as you can see, it just moved us

1:37

from patient list to viewer.

1:38

Okay, so we've got a viewer that is split up into three,

1:43

um, multiplanar Reformats, that's the NPR

1:46

as you can see there, and axial choroidal and sagal.

1:49

And then this volume rendered here.

1:51

So we're gonna click this button here

1:53

to remove the extra chest wall here.

1:56

So one thing that was asked is

1:57

how can we automate then the evaluation, um, you know,

2:01

to provide us in with certain views?

2:03

Well, one is, is that this has what's called an engine,

2:07

an a PS, that you can have, um, tear recon tune at your

2:13

CT scanner or on your, on your workstation,

2:16

where it will then acquire the image,

2:18

but then it will create then, um,

2:20

curve plan reform lines in here,

2:23

and then do an auto evaluation.

2:25

So, and then send those items to the packs.

2:28

Super easy, not hard to do.

2:30

It's, it's called an A PS and they can do that.

2:33

But in terms of doing it for yourself at the workstation,

2:37

um, the volume renderings, um,

2:39

in this first row here will affect this 3D volume rendering.

2:43

And so you can hold down the left and right and then remove

2:46

or add on, um, pixels as needed

2:50

to evaluate what you need to do.

2:52

The second row here is the, um, curve planar reforms.

2:56

And so what that will do is, um, give you some information

3:01

in terms of the reform.

3:03

So we're gonna pick LED, this is the LED vessel, obviously.

3:06

I'm gonna hold down the shift button.

3:08

And I got this target as you can see here,

3:11

and I can do it anywhere on any of them,

3:13

but I'll just do the LED here.

3:17

And what it will do is find the,

3:18

what's called the full width half maximum, which is the, um,

3:22

image analysis basis of hounds field unit density, um,

3:27

in a pixel, and then draw 50% a line that's 50%

3:32

between those two maximums.

3:35

So, um, that's what it's done here.

3:37

We're just gonna bring it here.

3:38

And so it's curved up to the beginning of the vessel

3:41

and it's curved down all the way to the end.

3:43

So this is what's called a curved planar reform.

3:46

You can see that CPR right there.

3:48

We can do an SMPR, which means a straightened, um,

3:53

multiplanar reform.

3:55

Now, with all these different additives to it,

3:58

what you're doing is you're taking the axial acquisition

4:02

and you're taking that information

4:04

and spreading it among more pixels.

4:07

So this is just an x and a Y pixel distribution.

4:11

This, of course is an X, Y, and z, uh, pixel distribution.

4:16

And, uh, and so the spatial resolution is going

4:20

to be less in this view comparatively to this view,

4:25

and obviously less than this view.

4:27

So your highest spatial resolution is the evaluation

4:29

of it in axial.

4:31

That's why I personally, I try to teach it for you

4:34

to be evaluated on axial,

4:35

but then you can do then, um, a curve plan

4:38

or a formatted evaluation here if in case you need to.

4:41

Now, the other ways of evaluating this if needed, um,

4:45

is again, and that's the volume rendering one here.

4:47

So we have all three of our, here is

4:50

where we do this double oblique technique.

4:52

So we will take then an evaluation of the vessel

4:59

and then follow the vessel across and double oblique.

5:03

So we're always looking, as you can see right here,

5:06

down the short axis here.

5:08

And that then would be done across the entirety

5:12

of the vessel in every stop in, in movement.

5:17

Now, you can tell that this is not the, uh, fastest,

5:20

most efficient way, um, of evaluation.

5:24

There are other ways, of course, one way here is,

5:26

is this way and this will, um, essentially do

5:30

what we just did, which is to evaluate the vessel,

5:33

but display that information, that x, y,

5:36

Z information in three dimensions.

5:38

And that's why, as you can tell, it's got some pixeling

5:41

because it, um, obviously is taking the information on axial

5:45

and trying to distribute it on there.

5:46

So it's not highest resolution.

5:51

So I don't personally consider like that.

5:54

So there's the NPR evaluation,

5:57

the double oblique evaluation, the curve planar evaluation.

6:01

There's the short access evaluation,

6:03

and then there's the axial evaluation.

6:06

And that's, I think what I tried to allude to

6:07

before is where you are evaluating this vessel

6:14

in terms of what you are assuming to be the, um,

6:19

amount of, um,

6:23

luminal stenosis that is involved here.

6:26

So let's just take this

6:28

and we're gonna use this as our guide, right?

6:30

Okay, so this is our amount of plaque here,

6:33

luminal stenosis, this is the double oblique

6:35

to confirm it right in here.

6:37

Now, if we were to go to the top of the vessel,

6:40

and you can see we are at the top of the vessel here.

6:41

That's what this red line is showing here.

6:43

And we're gonna go to the bottom of the vessel.

6:44

We get the entirety of the vessel, right?

6:47

So now let's think about it.

6:49

This is the 50% area of the vessel, right?

6:52

So we're at 50% of the vessel.

6:56

If you always go, um, in terms of evaluating on your axial

7:01

to the 50% of the vessel,

7:03

you can then make an assumption if the amount

7:06

of plaque is at 50% of eva, um, involvement or not.

7:11

So if we're at 50%, does this amount of plaque cover 50%

7:16

of this green line to that green line there?

7:19

That is, is it meeting that amount

7:23

and is it meeting it on the lateral aspect,

7:25

or is it meeting it on the superior or the inferior?

7:29

And we can see that obviously it's not,

7:32

we can confirm it on the short axis

7:35

and see obviously it's not, so this is less than 24%

7:39

and we can then calculate, uh, up to 24, uh, hyen,

7:43

49% based on that similar sort of thing, right?

7:46

So we can take this amount of plaque here

7:49

and see that it's not 50% of involved at the, at the middle

7:53

of the vessel, and it's probably not 25 to 49% involved

7:58

because it's not beyond the 20.

8:00

What I would do is take half of this and divide it in half

8:03

and see that's not why,

8:04

because this is blooming the cardiac, um, calcification.

8:08

Coronary blooming adds like an additional,

8:12

I gotta be less scientific here,

8:14

but it's probably depending on your machine, somewhere

8:16

between 20 and 30 extra percent of luminal stenosis

8:21

depending on your machine.

8:22

Now, the newer machines, it's a lot less blooming, um,

8:25

and there are algorithms to make it even less so,

8:27

it becomes more accurate.

8:29

So you can't quite use it,

8:30

but we obviously know it's not 50%.

8:33

We obviously know it's not 25 5 and 49%, it's less than 24%.

8:37

And we can see that confirmed right along here.

8:39

So did we have to spend the extra

8:40

30 seconds to do it that way?

8:42

No, we don't. Okay.

8:45

That is probably one of the more difficult concepts to eva,

8:48

uh, to use, is that there are multiple ways of evaluation.

8:52

The gold standard way is to take the long

8:55

and the long, the double oblique, so the long

8:58

and the long to arrive then at the short axis

9:00

and the double oblique to do this evaluation.

9:04

But the problem is, is that you're doing

9:06

that spatial evaluation on frontal and sagittal, which ALS

9:10

and sagittals, as you know, are less resolution

9:12

because they are reconstructions of the a axial data.

9:17

So that's not the great thing.

9:18

What you wanna be attuned to is be able then to

9:21

evaluate on the axial data

9:22

and be able then to make that, um, case as to the amount

9:26

of luminal stenosis.

9:29

Um, so yeah, work with that and see how you do with it.

9:33

You can confirm then your, um, supposition of

9:37

how much plaque is involved in here

9:39

by doing this, uh, quick eval.

9:42

So as we kind of look here, we can see

9:44

that there are more areas of, um, of plaque

9:47

that is low attenuating along this tree.

9:49

So let's go back to this case here.

9:51

Um, this is our 41-year-old male family history

9:54

of early coronary artery disease,

9:56

myocardial infection in his mother at age 55.

9:59

So, uh, family history, um,

10:03

but nothing particularly to him here.

10:05

And if we look at this, again, this is not fake data,

10:08

this is real data based on attenuation.

10:10

So what are we using this for?

10:12

Is there enough attenuation here, here, here at the ends

10:16

of it that show us

10:17

that profusion is occurring, uh, really well?

10:20

What is the, uh, degree of coronary reserve that is

10:24

how plump are the vessels

10:26

or how much, uh, vasoconstriction is occurring here?

10:29

How much plaque we see potentially a little bit here

10:31

and maybe a little bit there,

10:33

but no significant amounts of plaque

10:35

as you can see in other, um, um, biologic types.

10:39

Okay? So as we kind of make our way along in here,

10:42

we can see then at the, um, at the LM

10:46

that there is no plaque, right?

10:48

And then we get do about right over here,

10:50

where then the LCX should be coming across.

10:53

Uh, yeah, so there's the LCX right there.

10:56

So it's a very early, um, uh, bifurcation short segment,

11:01

lm, uh, very early bifurcation,

11:03

or if you wanted to say that there's no lm,

11:05

that's totally fine too.

11:06

Uh, there probably it appears

11:08

to beak an N and coming off here.

11:10

So I would say at least a short segment, lm.

11:13

Okay, so if we follow the LAD, then here, approximate LAD,

11:17

um, as it kind of makes its way across here, um, you know,

11:21

there's that less than 24% plaque there.

11:23

The D one obviously has some, uh, plaque

11:27

that's less than 24% there,

11:29

and there's some low attenuation going along in there.

11:31

And then here we have then these areas of frat bite.

11:34

As we're moving superiorly inferiorly through the vessel,

11:36

we can see then low attenuating load attenuating.

11:39

Um, and so though there are multiple lesions within the LAD,

11:43

but none of them have been an obstructive stenosis

11:46

percentage as well as a low attenuating plaque

11:50

or high risk features component to it.

11:52

As we travel the LCX, we can see that this very nice thick,

11:55

uh, very enlarged LCX.

11:57

So it's got a high degree of profusion

12:00

to the left ventricle,

12:01

and we can see a very early OM coming across here.

12:04

There is some disease within that om, as you can see,

12:07

um, along there.

12:08

And so if we were to evaluate that, we would see them

12:11

that low attenuating disease right there,

12:12

typically there's no concavities into vessels.

12:15

Sometimes vessels will come off superiorly

12:17

or at an angle, uh, like that.

12:20

And then, so you could potentially then

12:22

be worrisome about plaque.

12:23

But in this case here, that's low attenuations,

12:26

um, that's going along in there.

12:28

And then there's another, um, obtuse marginal off there.

12:31

So this is the LCX, as you can tell,

12:34

it's staying within the atrial ventricular groove comes

12:36

across very nice clean vessel, okay?

12:39

Otherwise, alright.

12:40

And then, uh, the very tiny bit of disease here, if we go

12:43

to the, you can see that little lip right there.

12:46

So less than 24% there, but it's just that rat bite, right?

12:49

The little bite bite, bite bites going on in there.

12:53

And then if we, um, follow, we can see conus

12:56

that's gonna come across and head laterally.

12:58

And then the RCA is gonna follow along here

13:02

and just maybe a little bit of rat bite some disease there.

13:04

So let's go ahead and, and take a quick look

13:06

at the curve planer.

13:13

So here's the curve planer for the RCA

13:15

and you can twirl this around.

13:17

Um, and, uh, if you wanted to, depending on, you know,

13:21

how things are kind of looking for you, um, be able then

13:24

to determine that there's just very little disease, um,

13:27

at all here, you can turn this around

13:28

and just see if there's any areas that are getting

13:30

to that 50% range.

13:32

Again, 50% is sort of the, if you were gonna make it binary,

13:36

do we do further invention or not?

13:38

Less than 50%.

13:40

Most other further interventions in terms

13:43

of evaluating biomarkers

13:44

or functional assessments are not necessary.

13:48

Okay, so what do you guys think of the bone?

13:50

Pretty not too hard, right? Okay.

13:52

So in this case here, uh, in this particular one here,

13:55

the Keyon to remember is that CAD rads, um,

13:59

range is from zero to five,

14:01

and then we'd have a progression in

14:02

luminal stenosis percentage.

14:04

Um, the addition of P one to P four in terms

14:07

of increasing amount of plaque is designed

14:09

because that was an independent, uh, risk factor in terms

14:13

of major reverse cardiac events.

14:15

Um, there are lots of different ways.

14:16

There were additional biomarkers that we can use, uh,

14:20

aside from just the coronary origin course termination

14:23

and luminal disease, um,

14:26

and plaque to evaluate then the, the integrity

14:29

of the entire system, um, in there.

14:32

So, and then of course, ca rats does not apply to a vessel

14:36

that's less than 1.5 millimeter.

14:38

Now, 1.5 millimeter is really, really difficult, um,

14:44

to ab to make an absolute mark, um, across scanners.

14:48

So we get to about here, let's see, it looks like, uh,

14:52

how far are we here?

14:54

Two, supposedly.

14:56

Okay, so we're about right over here

14:58

where it's about two millimeter.

15:00

Yeah, I'd say about the distal LED is when we get into some

15:02

difficulty, uh, or the distal RCA is

15:04

where we get into difficulty where it's one

15:06

and, and a little bit less.

15:08

So, um, I would, I,

15:10

I would caution looking at anything deeper there, the,

15:13

the PDA is is, is pretty good most of the time.

15:17

Um, but once you get into that, that area there, just kind

15:21

of take a moment, take a deep breath,

15:23

don't call everything a cad rat's, five low, you know,

15:26

blockage and stuff because your resolution is,

15:29

is gonna suffer anything less than 1.5 millimeter.

15:33

But I would say two, you know, just to keep it safe. Okay?

15:37

Uh, let's see what else.

15:40

That's really about it in terms of what to keep in mind, um,

15:44

about what we can do.

15:45

Um, and then, yeah, so I, I think that was kind

15:50

of an easy kind of just an early, you know,

15:53

show you the case and get an idea then on case one, um,

15:56

so this was, um, you know, 25, 40 9% in

15:59

that mid LAD section there.

16:01

Cataracts tube, no big deal, right? Super easy.

16:05

Okay, any questions on that?

16:11

Let's go then to case two for case two.

16:15

This is a 56-year-old female probable, uh,

16:19

cardiac chest pain.

16:22

It's always interesting, probable, um, uh,

16:25

detectable high sensitivities, uh, troponins request

16:28

for cardiac ct.

16:30

So based on the age,

16:31

there's a couple different things to think about.

16:33

Um, but what we wanna do is based on data is ensure then,

16:38

um, that a coronary, um, you know,

16:41

disease is not, not the issue here.

16:42

So as we can see then coronary blood flow

16:45

across looks pretty good.

16:47

We've got good coverage everywhere and

16:49

although we are seeing epic corners

16:51

or obviously it's micro vasculature, you know, throughout,

16:54

um, you know, that space there.

16:55

So everything looks pretty good.

16:57

Nothing too difficult right now in terms

17:00

of the acquisition and the qa.

17:03

Um, this is obviously an artificial cone.

17:06

Um, uh, but the, the technique looks good.

17:09

Um, the heart rate optimization is fantastic.

17:12

The opacification looks good, um,

17:14

and not no, uh, additional contrast

17:18

that's seeping within the SVC.

17:20

So we had a very tight, um, bolus

17:23

and everything looks really good.

17:24

Obviously Lima RMAs look fine too.

17:26

So the acquisition's great. Absolutely perfect.

17:29

This is what you'd like to see every day of the week, right?

17:31

Alright, so let's just kind of dive into here

17:33

and then start from the, um, sinus of al Salva, LCC, then

17:38

to the quick early bifurcation here,

17:40

show a short segment lm, that looks pretty good.

17:42

We'll get into the LAD right here

17:44

and then was, we have an early D one.

17:47

And then, uh, we can see then that rat bite, um,

17:49

occurring here on the axis

17:51

and see that there's, um, some disease.

17:54

There is a, a tiny bridge, um,

17:56

but nothing really too worrisome here.

17:59

Got a good, uh, diagonal that comes across.

18:01

And then the, um, LAD stays within the

18:03

anterior in ventricular wound.

18:06

Okay, so let's go over

18:07

to LCX here, follow along.

18:11

There's a little bit of disease right there that's, uh,

18:14

mixed, uh, calcified

18:16

and low attenuating plaque with the,

18:17

with an obtuse marginal coming across.

18:21

And so, as you can tell, then it didn't even get close if,

18:24

if we're looking at the vessel superior,

18:30

this is obviously less than 50%, um, give

18:34

or take if it's 25, um, percent or greater or less.

18:38

And we can do that on the NPR

18:39

or if you're, you got a good nose for it,

18:41

you can already tell that it's less than 24%.

18:43

Okay, so here we've got, um, uh, at a, an acute, um, takeoff

18:48

of the RCA,

18:49

but you know, no intramural course here,

18:52

dies right into the atrial ventricular groove.

18:54

And then there's some disease right there.

18:55

We're getting a pretty good short axis view

18:57

so we can then just take this as our view.

19:00

Um, this is 25, 40 9% right there.

19:02

Um, and then as this makes a way, we can see then the rest

19:06

of the vessel looks pretty good.

19:07

So P-D-A-P-L-A.

19:09

Um, so what's our take on this one here?

19:14

Well, uh, in, in particularly on this one here,

19:17

that we've got an individual who's got, um, you know,

19:20

some early disease, but, um, nothing too crazy, right?

19:24

25 high from 49%. So what are the take homes?

19:27

Uh, let's see, basically again, just another reinforcement

19:31

that 25, 40 9% is gonna be your probables

19:35

and your areas of, um, concern.

19:37

The high risk plaque features are really the ones

19:39

that are gonna be what we want to hammer in here.

19:41

So let's take a quick look at those

19:43

and see if we can do, uh, find some of them.

19:45

'cause they are, uh, um, on here we had positive remodeling.

19:49

We had low attenuating plaque.

19:50

Quite a few really fun things here.

19:52

So let's just take this RCA, see if it finds it.

19:56

No, Matt? Yeah. Oh, okay.

20:03

Okay. So we, um, created our tree

20:07

and we could see that the disease

20:08

is obviously right in here.

20:10

So we're gonna straighten that out.

20:12

Um, there is a little bit of contour abnormalities.

20:15

We're not gonna use this for the, um,

20:16

percentage of stenosis.

20:18

This is actually for just the evaluation of, um,

20:21

what the plaque looks like and the plaque morphology.

20:24

And we can see that there is

20:26

really great looking disease here.

20:29

Um, so we can just pull this around

20:32

and we can see then that we have low attenuated plaque, um,

20:34

calcified plaque and um,

20:39

and cart this guy around here.

20:41

And see then that there are areas where, um,

20:44

that those speak, um, positive remodeling here,

20:46

and then some spit, uh, stipple calcification right there.

20:50

So we have lots of features

20:52

that are already a source of with this.

20:53

Now what's interesting is where is this depositing?

20:55

It's in the proximal aspect of the vessel.

20:58

This is right before, as you can see,

20:59

before it dives, um, inferiorly downward.

21:03

So there is a flow velocity difference

21:08

right here compared to as it makes its way down

21:11

and along in here, usually in the curve

21:13

we can have some disease, but it's

21:15

as the curve makes its way and slows down

21:18

because of, um, vessel size

21:19

or it's making its way from superior to inferior

21:21

and it's gonna curve downward.

21:23

So right here and right here is

21:25

where we're gonna typically see a lot of the plaque issues.

21:27

And that's because of resistance.

21:29

If we were to do, um, the elastography

21:31

or the resistance evaluation, the stiffness,

21:33

sheer wall stress, as I talked about earlier in the lecture,

21:36

uh, you'll see a lot more sheer wall stress

21:38

and resistance in this area right here

21:41

and then right over here as opposed to right over here.

21:44

So, um, yeah, that's not surprising

21:47

where we're gonna see then, um, a significant amount

21:49

of plaque, um, deposited.

21:51

And you can see that then that change right along there.

21:53

If you wanted to, you can do a plaque analysis.

21:56

Again, the system should be,

21:58

and how you do it should be designed to tell people

22:02

what it is exactly you're

22:03

measuring and how you're measuring it.

22:04

And if it is the same, different, um, across patients, um,

22:09

or, or in policy.

22:12

But we can see here that there's a low attenuating plaque,

22:15

um, degree here.

22:17

And some of this could be epic coronary plaque

22:19

or epic coronary fat.

22:20

So I don't try to use this too often

22:23

because this particular feature has to then be tailored

22:26

and narrowed and,

22:28

and so it just becomes much more difficult.

22:30

That's why I like the qualitative assessment.

22:32

It's fast, it's super informative,

22:34

but at the same time, you know, you it's reproducible.

22:37

So here we got our low atte winning plaques along in here,

22:40

which corresponds then to

22:42

what we were chatting about earlier where, um, the plaque

22:46

that's being, um, deposited in this vessel right up here can

22:50

potentially crosstalk with the fat.

22:52

Um, the, the, the FAI, um,

22:56

that's a biomarker that's along in here.

22:58

It will then see changes, um, in that,

23:00

what's low attenuation then becoming then higher

23:03

attenuation with edema.

23:06

Alright, so there's the calcium along the group.

23:08

So, um, that's kind of fun.

23:10

Let's take a quick look at the, the LID real quick.

23:15

I don't remember if there was too much in there.

23:16

Yeah, there's a little bit along in here.

23:19

Um, so as we're kind of looking along in here,

23:21

you can see then the, the rabbi, rabbi, rabbi, right?

23:24

Where's it all current? It's all current. Approximately.

23:29

If you were designing a system, um, does the system

23:33

of plaque occur in other vessel, uh, other tubes,

23:38

proximally or distally?

23:39

Um, I guess is, uh, if you were to take your water pipe, uh,

23:43

your hose, where is most of the plaque occurring?

23:47

Where is things? Is it at the, the tiniest uh, lumen?

23:51

Is it at the osteum? Is it at that area of resistance?

23:55

And so it is typically the area of resistance.

23:58

So it's not just the size of the, of the thing

24:01

because the con constrain of lumen size will then relate

24:06

to then velocity inversely, right?

24:08

And, um, you know, physics laws behind that with rnli.

24:12

But what's interesting is, is that it's the resistance.

24:15

What is the resistance to flow that allows then, uh,

24:18

for accumulation or disruption of the layers

24:21

and then accumulation of material.

24:24

And so this is why I think actually this is a really

24:26

interesting thing, but we're kind of missing the boat,

24:28

if you see what I'm saying.

24:30

What causes an increased resistance in the system,

24:33

nitrous oxide, pathophysiology, and systemic hypertension.

24:37

If we can then modulate

24:39

and evaluate the hypertension in the system

24:43

as a surrogate marker,

24:44

and then as well as a nitro oxide,

24:46

we'd actually have a better, I think, a corollary

24:48

to why we're getting then the plaque deposition here

24:50

as opposed to blood lip levels, for instance.

24:54

But anyway, um, plaque is, um,

24:56

depositing in this proximal segment.

24:58

We don't really see too much going on here.

25:01

Now this could also be bias that is

25:03

that my spatial resolution's not so great down here

25:05

and I might be seeing a, a distribution

25:08

of plaque along here too,

25:09

that's completely relevant as well.

25:11

Um, so just earn that out there.

25:14

But as you can see here, um, you know, one 24%

25:18

or less, okay, so how are we gonna call this one?

25:22

Um, take home on this one is is that there was

25:29

25 49, the L-I-D-L-C-X, nothing really great,

25:33

and then 24%, um, or less than the r ca.

25:35

And so here, this is our, we'll focus right on here,

25:39

the 50% line.

25:41

So this is, uh, more than 24%.

25:44

So it's in that 25 49

25:45

because it's, it's about halfway, uh, from here.

25:48

So take that, that edge of the vessel, there's right there

25:51

that's, um, the 50% mark

25:54

and if we were cut that in half, is this amount

25:56

of plaque, uh, beyond that?

25:58

Yeah. So then it's greater than 25%. Does that make sense?

26:03

And we can also do plaque analysis on here too.

26:10

I find this stuff pretty easy.

26:13

Um, but the bigger questions is

26:15

how do you make this efficient?

26:17

How do you do a hundred of these in a day

26:20

with your cardiac MR plus

26:22

the other things that you'd have to do.

26:24

So that's where the report generation, that's where having,

26:28

um, uh, clarity in the word choices.

26:33

So you're not making creatively

26:34

making up new words every time.

26:35

It's just pick listed where you just say, mom, moderate,

26:38

severe, mild, moderate, severe,

26:40

da da, and all on and on and on.

26:41

Those are the efficiencies that we as, as, um,

26:46

experienced cardiac imagers will bring to the table.

26:49

And that's what you want to do.

26:50

You do not wanna be bespoke

26:52

and tailor, uh, exams, uh, that,

26:57

that just means then well one

26:59

that potentially it's a very complex exam,

27:01

but it also could mean then that you just don't have the

27:03

efficiency systems in place yet.

27:06

And so, uh, while we're going through the less sexy

27:10

non-obstructive cases, these are the cases actually

27:13

that are bread and butter.

27:14

These are the ones that you should be considering.

27:17

How am I gonna develop the verbiage utilizing the cataracts

27:21

templating so that I can do a hundred of these

27:24

because essentially 50% or uh,

27:27

or more of your, if you were to do a hundred

27:30

of these should be falling into that cataracts one, two, um,

27:34

maybe even three level

27:35

and then maybe 25% will be in the higher levels, right?

27:40

So let's get into, uh, case number three here.

27:44

Case number three is a, uh,

27:47

53-year-old case.

27:51

Three, right?

27:57

Uh, 53-year-old male with history of tobacco use

28:00

and recurrent chest pain.

28:02

The graded, uh, exercise treadmill was equivocal

28:05

with limited, um, chest pain,

28:08

but no ischemic ECG changes request

28:11

for CTA and further risk.

28:12

So he's got personal risk, he's got, uh, familial risk

28:15

and he's got risk calculation that puts him into, uh,

28:18

you know, potentially moderate areas.

28:20

No previously declared disease of CAD.

28:24

But, um, so chest pain with no known CAD

28:27

puts in a pretest probability that it's gonna have at least,

28:30

um, uh, with those risk factors,

28:32

he's gonna have at least cataracts two

28:34

or somewhere cataracts one, cataracts two sort of area.

28:37

So shouldn't be surprising then

28:38

that we'll find some disease.

28:40

So let's take a look at the profusion quote unquote

28:42

perfusion map and see then how things turned out.

28:45

Good. Uh, declarative evaluation of the anatomy

28:47

with our, um, contrast.

28:49

You can see then a good diagonal here

28:51

and we can see some lumpy bumpies going on over here, here.

28:55

Um, and, um,

28:56

this nice diagonal here is got

28:57

a pretty good strong one here.

28:59

LCX looks pretty good. Let's just rotate this guy here.

29:02

And beautiful RCA, no big issues here.

29:05

So it shouldn't be surprising

29:06

that it's gonna be maybe a little bit of disease.

29:09

Um, um, but nothing too crazy.

29:11

So superiorly inferiorly on that lm.

29:14

And where do we find the, if we go

29:16

to the center, where is the disease?

29:17

Yeah, it's less than 24%.

29:19

So very little a disease within there.

29:29

So you guys following, we're at the midway

29:32

through the vessel and there's obviously not

29:34

occlusive disease, you know, to that point there.

29:37

So it's not meaning that,

29:38

nor is there a significant amount here.

29:40

So this is, is less than 24% superiorly.

29:43

We've got disease, right?

29:44

And, but eight clears up

29:46

before here, so it's gotta be less than, you know,

29:48

obviously not 50%, but, and then less than that.

29:51

And then we've got no real disease down there, um, except

29:54

for along here, along the edges.

29:56

All right, we've gotta trifurcation, um, kind

30:00

of looks like a ation,

30:01

but this could be a septal branch here.

30:03

Let's just see if, how far that one goes.

30:06

Nah, it dies out and here.

30:09

Bridge, bridge, bridge or, yeah, that's just a septal here.

30:12

So let's call this guy. So a very bifurcation

30:16

with a very prominent, um, septal branch

30:21

and a very prominent obtuse moderator, uh,

30:23

obtuse marginal branch along here.

30:25

So along here we can see them

30:26

and there's a little bit of low attenuating plaque,

30:29

but nothing too serious.

30:31

How did I know that This is the LID

30:32

and this is not a tri, um, you know, uh, a ramus, well,

30:37

again, the anatomy, and I'm gonna foot stomp this, is

30:40

because if you remember the anatomic convention of

30:43

what the LAD is, what the LCX is

30:45

and the RCA, you'll never miss a total occlusion.

30:48

So the LAD anatomically by convention is the large vessel

30:52

that stays within the anterior in ventricular groove.

30:56

And so, although there are bridges associated with it, um,

31:00

you know, it's, it stays within.

31:02

Um, you can see that little tiny bridge right there.

31:05

It stays within the anterior interventricular groove. Okay?

31:09

So, uh, kind of knew that

31:11

that was gonna be the vessel there.

31:12

Um, and there's a few areas

31:14

of low tending plaque right along there and there,

31:17

but less than 24%, right?

31:18

And the along in here in the second diagonal,

31:22

'cause this is the first diagonal and those are septals.

31:24

So a little less than 24% disease, okay? LCX.

31:29

So lm LAD,

31:30

less than 24% low atating weighting plaque, go to the LCX.

31:34

Again, LCX convention Y stays within the atrial ventricular

31:38

groove following that bad boy along there.

31:42

And, you know, looks okay, no big deal. No big deal.

31:46

Now let's just say the 72% wasn't there was motion

31:49

you could potentially move, um, it forward

31:52

or backward in terms of the, um, uh,

31:56

if you did a retrospective move it, uh, cardiac cycle

31:59

that way or this way.

32:00

Um, so it would be 69%, 68%, or you know, 82%

32:05

or whatever, and get more information.

32:06

That's totally fine. Here at the ostia of the RCA,

32:10

we could see then this low attenuating plaque here,

32:12

obviously less than 50% stenosis.

32:14

Um, there's just a tiny bit, uh, along in there, uh,

32:18

less than 24%, um, bifurcation,

32:23

there code's going off.

32:24

Um, that was the essay node that went off there

32:27

and it looks like a pretty good vessel, right?

32:29

A little bit of motion there. Not too difficult

32:32

to adjudicate 'cause there wasn't any plaque, long air.

32:35

And then just a little bit down here.

32:37

So some areas that there was, was, um, some motion.

32:40

Now what's my take on motion?

32:42

If it involves an entire segment,

32:44

then you technically can call that an n

32:47

where you're not unable to evaluate.

32:50

Um, so it's a non-diagnostic segment

32:52

and you should declare that at down there

32:54

and say what segment it is.

32:55

Um, but I, I think we can make assessments on it even on the

32:59

motion if there is plaque or not,

33:02

and, um, be able to say then you know,

33:05

that there's no real plaque.

33:07

Could there be a greater than 50% obstructive, uh,

33:12

amount of stenosis right in this area here

33:15

that we're not seeing somewhere else?

33:18

I mean, there's always a realm of possibility,

33:20

but that's highly unlikely.

33:22

So I wouldn't really use an N in the case

33:25

and that's why we didn't in the, in terms of it.

33:28

Um, but there is some pretty good amount of plaque here.

33:31

I think that this case is kind of highlighting then

33:33

what is the, uh, amount of plaque, um,

33:37

across the entirety of this vessels.

33:39

And then why, um, we can have a higher degree of plaque,

33:43

but maybe a small amount of,

33:46

um, um, stenosis.

33:49

And so that is actually a biomarker

33:54

that's really, really important one

33:57

because the Scott Hart trial showed

33:59

that low attenuating plaque

34:01

or plaque with high risk features actually leads

34:04

to more major adverse cardiac events

34:07

than just straight up, um, stenosis.

34:09

Yes, SNO disease is very important

34:13

and uh, has its own,

34:14

and we saw the plaque, um, capital Meier curves for that,

34:19

but plaque is really a big deal.

34:21

Super big deal. So a little bit of plaque along in here.

34:26

Uh, this is motion probably so not

34:29

I think too worrisome over there,

34:30

but let's just get into that LED

34:32

and we could see then all the plaque

34:33

that's gonna be right there.

34:35

Just follow this guy across here, pull this one up.

34:38

Let's just do the measurement from there from here.

34:45

Now obviously it's, that's not correct.

34:47

It's, and we could, we could shape this and,

34:51

and shape it across here, but no worries.

34:54

Um, but it's really more, this, this is

34:56

what we're looking at, like, so

34:59

that's not too bad here.

35:03

That's where we get some really good areas there.

35:06

And so this is a P two, this is

35:08

where there is more than mild amount of plaque,

35:11

and you can tell that the plaque is evolving, uh,

35:14

at least three segments proximal L-C-X-L-A-D and RCA.

35:17

So I mean that's a, that's a significant amount of it.

35:20

There is that myocardial bridge.

35:22

Um, but again, that's not a big concern.

35:23

Can you see the bridge here? Uh, yeah, you can.

35:26

So we can see then that there's, that's

35:28

where it's gonna be bridged right along in there.

35:30

Um, and it kind of dives in there.

35:33

Uh, you can also find it, uh, along here.

35:44

All this guy in there, yeah, you see

35:46

that just a tiny bit there.

35:48

No big deal, right? The rule on bridges is that rules

35:51

of twos, it's gotta be, uh,

35:53

deeper than two millimeters longer than two centimeters

35:56

and luminal stenosis, well, to finish out greater than 20%,

36:00

not 30%, but um, so that's important.

36:03

Okay, so this one here is a cadrad one less than 24%,

36:07

but a P two, um, indicating then multiple segments

36:10

of plaque here.

36:12

So it's kind of important there.

36:15

Um, any other, let's see, what else do we have on that one?

36:18

No superficial myocardial bridge in the mid LID.

36:21

No big deal. Alright, so any questions on case three?

36:27

No. Okay, so then let's get to case four.

36:37

Case four 61-year-old male with a recurrent chest pain

36:40

and abnormal resting ECG request for CTA.

36:45

So, um, what we're gonna do about this one here,

36:51

I, I think, um, this one was also a similarly

36:55

very approachable case.

36:56

There was no, you know, hidden things here.

36:59

We'll do the RCA, um, how do you guys wanna do it?

37:02

So on the volume rendering here, maybe some best, um,

37:05

plaque, plaque, plaque there,

37:06

but man, look at those, um, branches.

37:09

Really good penetration, right? And then RS a nice, right?

37:14

Let's come on over here. So, uh, we're, uh,

37:17

where are we in that cardiac cycle?

37:19

Anybody tell based on this here?

37:24

Well probably closer to, uh, late diastole,

37:29

uh, um, or early dias, um,

37:35

you know, early systole y

37:36

because there's a, uh, potentially, um, some narrowing of

37:40

that, uh, ventricular obstruction or left ventricle, LVOT.

37:46

But the other thing could potentially consider then is, um,

37:49

focal basal, uh, septal hypertrophy due to what?

37:53

Um, due to um, aortic valve stenosis due to, uh,

37:57

systemic hypertension in this case here

37:59

where we have valvular disease here

38:00

with this mitral annular calcification, my suspicion is, is

38:04

that there's gonna be a valve with there

38:05

dysfunction associated with this too.

38:07

So we can, um, determine then the amount of, um,

38:12

stenotic changes that are gonna occur at the vessel level,

38:15

um, by those additional components

38:18

or by also then how much resistance is in the system here.

38:22

So as we're kind of looking along here, we see

38:24

that there's a fair amount of black here.

38:27

Um, but if we use that 50% rule, um, so if we get to the 50%

38:31

of the vessel here, how much disease is occurring here in

38:34

this first, first segment here?

38:35

Well, I mean not that much, right?

38:39

Is this a significant amount of disease?

38:41

Well, let's just find out. And then how about here?

38:44

And a lot of disease here, here.

38:46

So now we got a little bit extra amount of space to go

38:50

and we're gonna definitely want to evaluate this.

38:53

So just on the axle we can tell

38:54

that there are gonna be some areas on the LAD

38:56

that we're gonna want to do.

38:58

A secondary eval right here is gonna be tight

39:01

and uh, by tight I mean 50% and above.

39:03

So we're gonna take a look at that. D one, D two looks okay

39:06

and yeah, right, definitely right along to there.

39:11

So proximal mid LAD, we're gonna take a look at that

39:14

and see what can cover out prox RCA less than 24%

39:19

we're going, um, you know, seeing the short axis of mid RCA,

39:23

not a lot right there, right?

39:24

Less than 24% right there.

39:26

And then distal RCA and PDA, not a lot there.

39:30

PLA, you know, not a lot going on there.

39:32

Let's go back to the LCX here, follow this guy there.

39:35

Little bit of disease right there. So less 24, um, oops.

39:41

And then a little bit of disease right there. Less than 24.

39:44

So our big things that we're gonna want

39:46

to take a secondary look in is gonna be the

39:48

prox in the mid LAD.

39:51

Let's go over to those guys.

39:54

Okay, so very nice, clear, um, evaluation.

39:57

We can then just take a quick, um, CPR view

40:02

and see how does it look?

40:04

Looks really tough. Um, awful, right?

40:06

So I want, uh, to get your guys', uh,

40:09

eyes focused on the morphologic distribution, uh,

40:13

or deposition of plaque.

40:16

If you notice, plaque oftentimes in a tube

40:20

does not lay it just straight across here if it's chronic,

40:24

what it tends to do is spiral

40:25

or helical plaque deposition along in here.

40:28

'cause there's a vortal flow within the blood vessel,

40:32

which then will, uh, create then areas, um, constantly

40:36

of, um, pressure.

40:38

And then those areas will then create then deposition.

40:41

So then you'll typically see as you kind

40:43

of rotate this thing along, plaque following that board

40:46

of seal, um, deposition.

40:48

And it'll look helical or spiral or so forth,

40:50

however you wanna describe it.

40:52

But what we're getting at here is that we're at 50 to 69%,

40:56

we're at 50 to 69% right there.

40:59

So there are definitely some areas here where the amount

41:01

of plaque is greater than that green line.

41:03

Now the green line is again, not what you should take

41:06

to the bank because it is based upon

41:08

assumptions and indirect.

41:10

But as we kind of move along here, we saw in the axial

41:13

and it didn't, it looked pretty tight right there.

41:16

And as we're kind of looking along in both

41:18

of these areas here, and let's just bring this over here.

41:20

Um, so we can take a look there.

41:22

Um, yeah, I mean that's significant in terms of how much,

41:26

you know, uh, ES is occurring at the short axis.

41:30

So if we don't believe in on the NPR, the CPR

41:33

and then the axial, let's just go to the long, uh, diagonal,

41:36

which, um, some people consider the, um, gold standard.

41:41

Just gonna do that

41:45

and go,

41:51

all right, so what does that look to you?

41:53

That looks like 50%, right?

41:55

Alright, so let's just take that.

41:57

So that's then you know, about 50%

42:01

and then we can see then kind of make our way across here

42:06

and that's some significant plaques.

42:08

Kind of follow this guy a little bit here.

42:13

Now we're getting to our spatial resolution

42:14

as we continually to zoom in a bit here.

42:16

So we gotta take some of this with a grain of salt here.

42:20

But there is that obviously

42:22

that high attenuating plaque calcium,

42:23

and then there's that low attenuation plaque here

42:25

and that seems to be greater than 50% of that vessel.

42:29

What is the length of that vessel?

42:32

Um, we're probably around the three.

42:34

Uh, so we're at four and a

42:35

half, four point a half millimeter.

42:36

So we're at our area where we should be diagnostically,

42:39

diagnostically able and accurate to measure that.

42:42

And so we're at the 50% right there.

42:45

And so that, uh, obviously has some areas

42:47

that are 50 to 69%.

42:50

So I think, uh, the main thing to take about here is

42:52

how do you evaluate that fairly quickly on the axial

42:55

to get rid of your, um, to make it binary your, um,

43:00

your don't worries and then your worries.

43:02

And then once you get to your worries,

43:04

how then are you able then

43:05

to be more concrete and specific about it?

43:07

So this is 50 to 69% of the mid LID um,

43:10

and that's a pretty good amount

43:11

of plaque right there, right?

43:13

Uh, 25, 49 in the distal LED and,

43:17

and very minimal on the other, um, vessels here.

43:19

So at this, uh, length of vessel, we should be able to be

43:23

that, um, specific and be able to, to see that.

43:27

So obstructive coronary artery disease

43:30

because it's 50 to 69%, you can offer, uh,

43:33

functional assessments in terms of FFR, ct, um,

43:37

CT profusion, uh, couple,

43:39

and then of course spec, um, pet,

43:42

um, or ICA.

43:44

So there's a lot of different ways of looking at that.

43:47

Any questions on that one i's kind of fun.

43:52

Okay, last a let's take a look.

43:56

So, but the last case here, we have a 53-year-old male

44:00

with a history of mixed HLP hyperlipidemia, um,

44:03

hypertension, recurrent chest pain, abnormal stress.

44:07

So his pretest probability based upon some of those factors

44:10

and um, and some functional assessments is he's in the, um,

44:15

you know, he's, he's got some corona artery disease we

44:17

expect in some disease to be there.

44:19

So what we would've done in conventionally

44:22

or in the past was we would've sent him straight to, um,

44:25

an invasive coronary angiogram for the evaluation

44:28

of the lumen.

44:29

That is the lumen gram there.

44:31

Now with, uh, with higher special resolution resolution,

44:34

the coronary CTA, we can do the evaluation

44:37

with the coronary CTA examination

44:39

and be able then to get a pretty good idea.

44:41

So what we're looking here is for obstructive plaque.

44:43

So obstructive plaque with those features should then go

44:46

towards, um, potential, uh, risk modification, um,

44:50

medical therapy optimization

44:53

and then make sure that things look well.

44:55

So we would know he's has a disease, pretest probability,

44:58

he's got disease with that stuff, right?

44:59

Okay, fine. Now is how much of that is obstructive or not?

45:03

And if it's not obstructive good

45:05

because what did we say in terms of the out, uh, outcome

45:09

of ischemia trial is that medical therapy is non-inferior

45:14

to intervention in terms of the outcome.

45:17

If you put, if you had somebody with, uh,

45:19

coronary artery disease and you were looking

45:20

at do they die from it or not?

45:22

So if we can get them on medicines

45:24

and do medications without going into the stent world, um,

45:27

then we've done our good job and, uh, should work out there.

45:31

So find a disease, see if it is greater than

45:34

or less than 50% stenosis get on medical therapy.

45:38

Should be pretty easy, right? So let's take a look.

45:41

So, uh, from a QA standpoint is more

45:44

of the contrast on the left and the right check.

45:47

Um, how's the motion? Very good motion control.

45:49

What do you think about the spatial resolution here?

45:52

Um, this is obviously a a a bigger individual, uh,

45:56

because in here we're not seeing the front

45:59

of the chest or the back of the chest.

46:00

So this individual is obviously 25 5 centimeters or greater.

46:03

What is, what is this, um, conned?

46:06

Um, so yeah, we're about 20 centimeters here.

46:10

Um, so what that means is that this individual is a,

46:13

a bit bulkier in the anterior posterior chest.

46:16

Why that's important is

46:17

because, um, then resolution starts to suffer as has to go

46:20

through a longer ap, um, to get to the detector.

46:24

So if the source is right here

46:25

and the detector is down here, you know it has to travel

46:28

through more tissue and so then

46:30

therefore more quantum scatter

46:32

and absorption is occurring with the new technologies such

46:35

as photon counting, that may not be the case.

46:38

Um, and we're able then to subtract out that um,

46:41

that amount of, um, noise.

46:43

So this is quote unquote noisier

46:45

because of the size of the patient, the thickness

46:47

of the patient and the length of the,

46:49

and the AP length of the patient.

46:53

Very important uh, to know

46:54

that if you get individual who's barrel chested or thick

46:57

or whatever, then you have to try to ramp up as much of

46:59

that MA as possible, um, or the kv

47:04

or both to try to get a good penetration exam

47:07

and then try to get as many photons through.

47:09

So we've got the LM right here, LMS got a,

47:12

a bit tortuosity here

47:13

and it comes curing little bit of disease right there.

47:17

Um, but at the bifurcation we've got this high attenuating

47:21

plaque and as you can see from this being superior, bit

47:24

of noise right there, um, from plaque.

47:26

But then, um, not too much going on in here.

47:28

So less than 24% diagonal's, got some dia um,

47:32

some disease there.

47:34

And then we get into then where the rest of the disease is.

47:36

So this is less than 24%.

47:38

'cause if we can get to the center of the vessel

47:40

and there's um, no evol uh, involvement,

47:44

then we're less than 50%, right?

47:47

And so then rat bite, rat bite with chronic,

47:50

um, calcification.

47:51

So this sort of, sort of corresponds to his disease

47:55

and then we can see then that it just trickles out.

47:57

So that looks pretty good. Alright,

47:59

so let's follow the uh, LCX here.

48:01

LCX, very nice plumpy vessel.

48:03

And then there's a couple obtuse marginal branches

48:06

and it moves along there.

48:07

Very little disease, a little bit

48:10

of disease down here in the distal RCA less than 24%

48:16

mid looked fine coming up, up, up.

48:19

And again, this is where

48:20

because of slow flow resistant flow,

48:22

we should see a bit more of the disease

48:23

and we do into the conus.

48:26

Um, and then along in here,

48:28

'cause this is a bit torturous, we have resistant flow, uh,

48:32

disc lanar flow

48:33

and we can see then there's a little bit

48:34

of disease right along in there.

48:36

So what do we have here?

48:37

Uh, particularly in this individual we have, um,

48:40

multifocal regions of calcified plaque, um, you know,

48:45

less than 24% stenosis.

48:47

Let's go ahead and just take a quick look at

48:49

the curved plan R.

48:52

We'll draw one quick one through the RCA, look

48:54

how torturous that is.

48:57

But really very few areas of of plaque.

49:00

We'll just spin this bad boy around

49:01

and you can see here then bites, bites,

49:04

but um, bigger bites.

49:05

But then just a, a long segment

49:08

of just these low attenuating plaques here.

49:10

And that's just due to long-term disease.

49:13

Take a quick look at the LCX here, LCX, similar sort of,

49:17

uh, you can see the rat bytes all throughout the entirety

49:20

here, but the nitrous oxide was able

49:23

to distend this vessels.

49:24

So there's good endothelial production of NO,

49:29

but we do have long-term disease here

49:31

and this is probably related to um, just, uh, you know, some

49:35

of the things that we were chatted about.

49:38

Graham, let's just take a quick look at the, um,

49:41

oops, LAD.

50:00

So let's go back here, clean that off here

50:04

and just grab the,

50:10

grab the LAD that way.

50:12

Sorry that took a little bit of time.

50:13

All right, so we've got the LAD grabbed up right there.

50:16

We could see LM to LAD

50:18

and we could see some, um, areas where there's um,

50:21

you could see the spiral of plaque there.

50:24

Um, but again, you know, less than 21%.

50:27

Um, nothing, nothing getting there to that 50% mark there.

50:31

So, uh, a little bit of disease, but nothing too crazy.

50:33

25, 49.

50:35

Um, but you know, yeah, pretty, pretty easy, pretty, uh,

50:39

no difficulty along there.

50:40

Let's see all my notes.

50:42

Anything else I should keep an eye on?

50:44

Um, I think usually in the 60-year-old crowd,

50:48

70-year-old crowd is that the dilation of the, um,

50:51

aorta becomes more than pretest probability positive.

50:55

So, um, there are a couple different, um, let's see,

50:58

let's do assisted dispair oh D, right,

51:07

so 42, uh, 40.

51:09

So that one's a little bit dilated there.

51:11

You mentioned that, you know, it's well below the 45, um,

51:15

millimeter, um, aneurysmal dilation

51:17

where we want a six to 12 month.

51:19

Um, the rate of change as is occurring is probably instilled

51:23

that quote unquote senescent where it's just age related.

51:27

Um, but if this was a 50-year-old with that,

51:29

absolutely let's keep an eye on him.

51:31

Uh, we can also of course do a um, uh,

51:35

double oblique for the, for the sinus of al Salva

51:39

and just see where we're at there.

51:41

Um, so let's just do a quick one there since we're here.

51:45

Um, this guy, he's a little torturous, right?

51:49

And it's kind of sitting a little, little wonky.

51:52

Typically you line up then on the sinus, the sinus here

51:55

and we can see then that's, uh, that's a little,

51:59

a little bit off, not too much

52:01

and that's probably dilation

52:05

of one cusp versus another.

52:07

But let's then do a quick,

52:12

so about 41 37.

52:13

So, um, a little bit dilated there.

52:16

So violation of the sinus of Valsalva

52:18

and the ascending thoracic aorta if you want

52:20

to do a 12 month, uh, follow up per the new thoracic aorta.

52:24

2020, what is it? 22, I can't remember.

52:28

2022 guidelines related to 40 millimeter

52:31

and above evaluation, that's totally fine.

52:33

Um, and add that on there.

52:35

I think we mentioned that in the, in the standard.

52:37

Alright, so five cases in week two describing then the

52:41

evolution from cataracts, one to cadrad two

52:44

with inverting then RADS one.

52:47

Um, but introducing more low attenuating plaque

52:49

and how you should be able then to evaluate that.

52:52

Um, we had one case here that it was a CADRAD three

52:55

where there was 50 to 69% stenosis.

52:58

Um, that's kind of the decision matrix

53:00

where most cardiac images are gonna be in that cadrad two

53:03

to RADS three utilization of, um, alternative, um,

53:06

biomarkers such as FFR CT can be very useful at

53:10

that cadrad three area, uh, CT perfusion as well as um,

53:15

uh, such things as such as plaque analysis.

53:17

So, um, does anybody have any questions that I can answer

53:21

for you all, um, on this particular case here?

53:24

These are here should be hopefully pretty easy.

53:26

Um, you know, slam down cases.

53:38

No, no,

53:41

I don't see any questions coming in

53:43

through the chat Dr. Lorenz.

53:45

Cool. Great. Well, uh,

53:47

email us if you have any questions related to, um,

53:50

your interpretation of the exams.

53:53

I'd like to see you guys consider then now,

53:56

not just interpretation of being accurate

53:58

or not in terms of your CAD rath,

54:00

'cause that part is, that's not the whole point of this.

54:03

The point is how do you become effectively efficient

54:07

but then also add more to this.

54:08

And that's by thinking about the system in terms

54:11

of blood flow movement through a tube.

54:14

And then also what is the pretest probabilities.

54:16

So we knew that some of these individuals,

54:18

because of their age, because of some

54:20

of the clinical factors, was

54:22

that there was gonna be a pretest probability disease.

54:24

So those are the big takeaways from week two, week three,

54:27

we will get an obviously into the obstructives

54:29

and then what, you know, how we would do an interpretation

54:32

of those obstructive disease cases.

54:35

Okay, thank you again, Dr. Loren.

54:36

And just a reminder, um, this is being recorded

54:39

and the raw footage will be made available within the next

54:42

two hours and email to you, um, to your personal email.

54:46

Thanks again, Dr.

54:47

Loren, and we will see you next week for week, uh,

54:50

office hours, week three.

54:52

Take care.