0:01

Hi everyone, and thank you for joining us today

0:03

for week five Office Hours

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for the cardiac CTA online training course.

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Dr. Lorenz will be reviewing week five cases,

0:10

so if you do have a question, feel free to ask him directly,

0:14

or you can put your question in the chat

0:15

or just use the hand raising emoji and we'll call on you.

0:18

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

0:21

Awesome. And, um, you guys are doing fantastic.

0:26

The way that we structured week five was,

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if you notice from week four is we were really trying

0:34

to push you guys into stenosis

0:36

and accuracy of stenosis while, um, ensuring

0:39

that you remember, um, definitional, um, segments.

0:44

That is where

0:45

and why do we call the last circumflex, the last circumflex,

0:49

and then LAD and so forth.

0:51

Um, throughout, we've also been working on some

0:53

of the major, um, biomarkers that coronary CTA offers, uh,

0:58

comparatively to other modalities that is, um, uh,

1:02

better spatial resolution in terms of anatomic determination

1:07

of stenosis, non-invasively,

1:10

but more importantly, the plaque here.

1:12

Now we're gonna transition into cab rat five.

1:15

Yes, some cabbage and graft related anatomic evaluation,

1:20

but we're gonna come back to that, um, plaque component.

1:23

Why? Well, it turns out that plaque

1:26

and plaque, um, um, aggregate

1:30

is actually an extremely important biomarker.

1:33

There are a couple studies that are evaluating plaque versus

1:36

stenosis, plaque, um, and early plaque detection

1:40

and event rate and major adverse cardiac events.

1:43

So can't get too deep or, um, into that yet.

1:46

But my takeaway is typically that, um,

1:49

and there has been great studies, uh, such as, uh,

1:52

promise in Scott Hart that did show that, um, uh,

1:56

high-risk plaque features absolutely do have, uh,

1:59

an asymmetrical involvement in major adverse cardiac events.

2:03

So we should always be on the lookout on the amount

2:06

of plaque, black burden,

2:08

but also then that that is really gonna be

2:10

a big deal breaker.

2:12

So, week five kinda sucked, right?

2:15

There were a lot of different things.

2:17

Many of you, um,

2:18

thankfully weren't complaining about the image quality.

2:23

You will not get a, um, a Mona Lisa, you know,

2:27

or a high spatial resolution, uh, graft exam.

2:31

Why? Well, um, flow hemodynamics are off, right?

2:35

Um, we are, uh, dealing with, uh, a system that has been

2:41

managed and because of that management,

2:44

and that then relates to flow dynamics

2:47

that are gonna be obviously off compared to somebody

2:50

who has not had that.

2:51

Additionally, these are typically done on individuals

2:53

who have poor cardiac output, who have other comorbidities.

2:58

So regardless of your high spatial resolution, regardless

3:02

of your timing, regardless of your contrast rate,

3:07

they're very oftentimes is a, a,

3:11

I wouldn't say a sub quality exam,

3:13

but it's just a di more difficult exam.

3:16

And so that's a conundrum, right?

3:18

Because the concern is how do you determine the best

3:22

that you can in terms of stenosis, in terms of, um,

3:26

plaque involvement,

3:28

but then per CAD RADS 2.0, how then do you

3:33

move from the major epic coronaries

3:35

to then the distal post cabage

3:38

or the post Anas stern, uh, segment that is going

3:41

to determine your CAD rads

3:43

or the unaffected, um, minor vessel components such

3:47

as the diagonals and the obtuse marginals and and so forth.

3:50

So we have a bit of a challenge,

3:52

and I'm glad that many of you took it very well.

3:54

Some of you might have been off on a percentage, you know,

3:58

calling it a four A versus, um, a, a cadra five

4:01

where there was a complete occlusion.

4:02

That's totally fine, don't worry about that part.

4:05

Um, it's mainly in terms of how do you deal

4:08

with the information and then

4:10

how do you make an unimportant thing.

4:12

The last thing I'll suggest on here is,

4:14

I don't know if you're keeping up with the news and stuff,

4:16

but there are very, very large training clusters of, um,

4:22

of, uh, that in training models that are

4:26

acquiring data, particularly cardiac imaging at an extremely

4:31

high, um, iterative rates.

4:34

And because of that, then their capability of doing

4:38

what we are currently doing conventionally in 2024, that is

4:42

identification of percentage, identification of black in a,

4:46

not just binary, it's there, not there,

4:48

but then also semi-quantitative, um,

4:52

they're able to do that.

4:53

So speaking to you in terms of, um,

4:58

in terms of the, the potential risks that are gonna, uh,

5:03

occur is really important, uh,

5:06

because in 2027, some of these AI algorithms will then be

5:10

considered something

5:11

that you don't need to look into as well.

5:14

Okay, so let's go into a quick diag, uh,

5:19

diagnostic evaluation with case number one 49-year-old male

5:23

with a history of tobacco use, hypertension

5:25

and mixed hyperlipidemia, onset of chest pain.

5:30

Alright, and let's get this case going here.

5:33

So we have a pre, uh, pretest probability

5:36

of a certain amount of disease.

5:39

Uh, you know, we've got a couple things

5:41

that we're gonna be looking at, right?

5:44

Um, so from a quality assurance standpoint,

5:48

we do have, um, a degree of slow flow

5:51

where we have contrast still within the right side

5:54

of the system, but the majority is on the left.

5:56

Um, heart rate, uh, control looks pretty good.

6:00

So we're gonna take our LCC

6:02

and LM off of LCC and the bifurcation.

6:05

We can take one vessel at a time here.

6:07

And just on the axial, again,

6:09

axial acquisition is the highest spatial resolution.

6:12

We can determine them. We have some disease here in

6:14

the proximal segment.

6:16

We have a couple, uh, vessels that are coming off here,

6:20

so D 1D two, and then we can get into the mid portion here.

6:23

We're gonna cut to the chase here.

6:24

Obviously, as you can see here

6:25

that the mid LAD has an occlusion

6:28

of low attenuating plaque here from the superior aspect

6:32

of it all the way to the bottom.

6:33

We're gonna take this segment right here just to confirm

6:36

what we are seeing, and we can do a couple different, uh,

6:39

ways of evaluating this.

6:47

And, uh, this is of course a double, um,

6:51

oblique technique.

6:54

So we take two of the three axises

6:58

and we try to go in parallel to them so

7:03

that we have a,

7:12

So that we have an, an opportunity

7:14

to see the short axis of it.

7:15

Now again, the orthogonals, um, in this case, the coronal

7:20

and sagittal do have a little less data information in it

7:23

because this is a 2D acquisition as opposed

7:25

to a 3D acquisition at the time.

7:27

But, um, you can see clearly, uh, as well as I can here

7:31

that on the short axis, this is a complete occlusion here.

7:35

So mid LED with a 100% occlusion.

7:38

Let's, uh, dive a little bit deeper into the other vessel

7:41

that was the concern, which is the RCA.

7:47

And so again, um, there are several different ways

7:50

of doing the investigative analysis.

7:53

Uh, this double oblique technique, the CPR, um,

7:58

I think axial in the way that I'm doing it

8:00

and showing it is, is very good as well.

8:03

And, um, so let's just take another look there.

8:06

And so then we have what we call that wink sign there.

8:08

So, uh, very common, uh, to see that,

8:11

that there's a significant amount of stenosis,

8:14

uh, right there.

8:18

So let's just take a quick look at that.

8:20

And there are a couple different ways we can do that.

8:22

One on the axial, we can say that

8:24

that's obviously more than 70%.

8:26

So that would fit in line.

8:27

We can do the, again, the double oblique technique, uh,

8:30

for variation.

8:33

I'm gonna show you the CPR.

8:35

Now, the CPR clearly has identified, um, the RCC

8:39

and the OSM and then so forth.

8:41

We're just gonna straighten this particular one here.

8:43

And you can clearly see as well as I have

8:45

that this particular channel, let's get rid of that.

8:49

Got it there. That particular channel looks greater than 70%

8:53

stenosis with this,

8:55

this flow attenuation on both ends of it.

8:57

So you can see that in more detail along here.

9:00

There's a little bit of positive remodeling

9:01

and some stippling of

9:02

calcification along there too.

9:08

So I degrees of plaque, um, both in the mid LAD

9:12

as well as in the RCA.

9:15

Now, a lot of the, um, findings at this point

9:19

shouldn't be that difficult.

9:20

Um, we should be able to be making that, um,

9:23

those assumptions very well.

9:26

I think what the usefulness, um,

9:27

behind the anatomic approach is, is being able

9:29

to assess then not only the degree of stenosis,

9:33

but like I mentioned earlier, the amount

9:35

of plaque in the plaque stenosis.

9:38

So the number of segments, uh,

9:40

we had previously talked about this in week one, uh, uh,

9:44

week one, uh, was that there are approximately 17 segments

9:49

that, uh, can be, uh,

9:51

take these coronary art and be divided into.

9:53

And so it's extremely important to consider then how, then

9:56

how many segments are involved,

9:58

not only from a plaque standpoint,

10:00

but also from a, uh,

10:02

obviously atheros chronic disease and stenosis.

10:05

So in this case here we have several different, um,

10:08

and significant amounts of, uh, segments that are involved.

10:11

Um, there's a, a quick

10:16

graph I just want to show you here,

10:18

and if you can see this here, um,

10:20

all calls major cardiovascular events,

10:23

but essentially when we get it to the over here, CBD death

10:26

or the, the orange is

10:29

what we're gonna be taking away from this here.

10:31

The number of, um, segments in terms

10:34

of the plaque involvement actually has the same risk

10:38

of myocardial infarct as those

10:40

with single vessel obstructive disease.

10:42

So you don't actually have to have obstructive disease

10:45

that is greater than 50%.

10:47

You just have to have more than four segments involved

10:50

of plaque to have the same risk.

10:54

So we're dealing with several different things.

10:56

One in the CAD rads, a percentage of stenosis

11:00

with the greatest, uh, percentage assigning than, um,

11:04

the CAD RADS organization.

11:05

But we have another biomarker that is equally important,

11:08

and that's the plaque involvement.

11:11

And the amount of plaque

11:12

and the morphologic characteristics

11:14

of the plaque are very important, so important

11:17

that it actually has its own characterization behind it.

11:20

Additionally, it's so important that it also has its own

11:22

reimbursement component behind it, that

11:24

as we are quantifying plaque, either auto semi autonomously

11:28

or not, and then we are able then

11:31

to derive then a reimbursement from that.

11:34

So it's extremely important that we, um,

11:36

that we consider plaque.

11:39

Okay, let's go back into,

11:43

and if there's no questions on case one,

11:45

we're gonna keep clipping along here

11:48

'cause I think we might have some more, um,

11:50

questions related to some of the additional cases.

11:53

So case number, um, two is a, uh,

11:58

62-year-old female with a pre-diabetes, hypertension,

12:01

new onset of chest pain on exertion.

12:04

And so with this particular one, um, we brought in this

12:10

case

12:17

to highlight again, some more ca RADS four

12:21

or five, in this case five,

12:24

but, um, let's move

12:28

this here.

12:31

Okay, so let's just take a quick look at

12:32

the volume rendering here.

12:35

What do you see with the volume rendering?

12:38

We can see opacification of the LAD

12:40

and then the diagonal branch,

12:44

L-C-X-R-C-A looks a little atretic.

12:49

So we've got a couple things that we're going

12:50

to be working out, right?

12:52

And so one of the, um, interesting things

12:55

behind this particular case, um, is that this individual

12:59

had, uh, gone through, um, SPECT imaging

13:03

or functional imaging first

13:04

and was found not to have any issues.

13:06

So always fun to, um, do the anatomics

13:10

after SPECT

13:11

and functional imaging

13:13

to arrive then at some, um, considerations.

13:17

Okay, so let's go then through the actual evaluation

13:20

of this case here.

13:21

So qualitatively there is, um,

13:25

more contrast in the left side than the right

13:30

motion control looks pretty good.

13:37

So not a lot going on in the

13:40

L-C-C-L-M-L-A-D-L-C-X pathway, right?

13:43

I mean, there's a calcified disease less than 24% here

13:48

at the L-M-L-A-D, okay, fine.

13:50

Uh, a little bit of disease maybe right there.

13:54

Small bridge, obviously no super, uh, very superficial,

13:57

no dis no issues.

13:59

But just like we saw in the volume rendering, not a lot

14:01

of disease, um, that is significant.

14:04

And so I always wonder then somebody's complaining

14:08

SPECT was normal, but then the L-E-D-L-C-X,

14:12

which contains the majority of blood flow is also negative.

14:16

Then what is the concern then?

14:17

Well, depending on the age

14:19

and risk factors, you know, there are a lot

14:20

of different ways to take this to include

14:22

then deconditioning.

14:24

But, um, mainly, uh, I think

14:27

what we do next here is we consider then

14:29

where alternative blood flows.

14:31

And this includes the RCA, not that we would ever not

14:35

evaluate the RCA, but it's always important to, you know,

14:37

consider then, um, when you start looking in,

14:42

basically checking off that the LAD and LCX are fine.

14:45

What is next? So we're gonna spend a bit more time on this

14:48

RCA and you can already see that there's a cuff

14:51

of low attenuation, right at the ostia of the RCA.

14:54

There's a little bit of what we call a post

14:56

stenotic dilation.

15:00

And then boom, we get into this area of low attenuation.

15:04

It almost has what we call a, a ring, right, where there's

15:08

nearly a lumen ring still visible with that clot,

15:13

or I'm sorry, that, uh,

15:14

that plaque that's in the center there.

15:17

Depending on how this individual came into the, um, uh, the,

15:22

uh, the system, you know, this could be immediate thrombus,

15:26

uh, so in an acute coronary syndrome,

15:28

or this could be just plaque

15:29

that has finally just and then included.

15:31

So one of the question is, when do we call a vessel atretic?

15:35

Um, so atresia

15:37

or a, uh, a narrowing of the vessel, um, due to nutrient

15:42

or growth is typically done when there is, uh,

15:45

usually in my case for the epic coronaries when I see it

15:48

around one to two millimeters.

15:50

So typically there are five, then four, then three at,

15:53

at the distal aspect.

15:54

You can get to about maybe resolution of two millimeter,

15:58

pretty, pretty standard wise, two millimeter.

16:01

So if you see then a five millimeter vessel starting

16:03

to become, um, one millimeter, two millimeter,

16:07

that's an atretic vessel.

16:09

Now that typically applies to grafts.

16:12

We don't usually call the, the vessels that are native,

16:17

um, atretic.

16:18

There are some cases where it can be, um,

16:21

where there's a chronic toal occlusion, for instance.

16:24

Um, and that was one of our examples,

16:26

but here, let's just go ahead and take a look.

16:28

Now, how do you guys want to, um, evaluate this?

16:30

Well, I mean, on the axial, I think this is pretty clear.

16:32

This is 100%,

16:34

but you know, we've got a couple different, uh, ways

16:36

of valve, so let's just go to it.

16:40

This is the, um, curve plan R,

16:43

and then we can then see this.

16:45

And I love it that there's always a stripe,

16:48

and we can see that regardless of how we tors

16:51

and turn this vessel here, that that, um, uh,

16:55

low attenuating plaque is still very much present.

16:59

We can take a look at it from, um, from this,

17:01

whoops, oh my gosh.

17:06

Uh, take a look at it over here.

17:07

And then we can see then that, um, that regardless of

17:11

how we turn and twerk this, that it still has then, um,

17:14

that low attenuation still present.

17:17

Um, if that were not enough, uh, we can do the vessel track.

17:20

Now, vessel track, as I mentioned

17:22

before, does have a limitations related to, um, uh,

17:27

spatial resolution, uh,

17:29

because we're trying to reform, um,

17:31

the data into three dimensions,

17:33

but here we can see then that there's a, a significant, um,

17:37

low attenuation and an issue here.

17:43

Okay, great. So 100% occlusion of the proximal RCA, um,

17:48

and then some mild disease and the remainders of it.

17:50

But let's get back to then that, um, the functional,

17:52

the functional, uh, was normal, right?

17:55

So why is the function normal

17:57

and yet the, um, you know, our,

18:00

our anatomic was showing then disease.

18:02

Well, we get to, uh, thinking about this a little bit more.

18:05

Um, and it has a lot to do with coronary blood flow.

18:10

We have a lot of opportunity

18:12

and you can see then that there's obviously coronary blood

18:14

flow in the mid and distal segment of the RCA.

18:17

So there's a, a lot of opportunity for collateral flow.

18:21

I had said this several times before,

18:23

but we are barely imaging

18:28

the coronary vascular tree.

18:31

The epic coronaries are probably 10 to 20% of that tree.

18:35

The 80% of the tree is the micro vasculature

18:38

that we're not seeing that provides them

18:39

that collateralization in the capability to move blood

18:43

where it's needed when needed.

18:46

So although there is a total occlusion here,

18:48

we're just not seeing that amount of flow.

18:51

Um, and that's, um, that's always a very important thing

18:55

to kind of remember is that that collateral flow, um,

18:59

is oftentimes the saving grace here.

19:01

So if we had a spec that showed no focal ischemia,

19:06

that doesn't mean that there is no occlusion, it just means

19:08

that there's a good collateral network.

19:11

And so I think that's always something to try to remember

19:13

and that that's what this case was designed to do is to try

19:16

to get you into thinking about that.

19:18

Alright, um, I guess I can show you the invasive, um,

19:22

the ICA that we had with this individual.

19:25

Um, and then essentially it shows the,

19:27

what we were seeing here.

19:28

And you can see then, uh, the RCA, the proximal,

19:32

and then we can see them right here, right at the, um,

19:34

the vessel coming off here.

19:36

Um, the acute marginal is where we have a total occlusion

19:39

and cutoff sign here.

19:41

So, um, yep, it's real. It's, it's there.

19:44

It's definitely a concern.

19:46

And so it doesn't mean that we're out of the the woods

19:48

yet just because the functional says that it's,

19:50

um, it's normal.

19:54

Okay, any questions particularly related to that case?

20:01

Alright, well then let's start then

20:04

diving into our graphs.

20:08

Graph cases are, um, difficult.

20:10

There is no getting around that. They absolutely are.

20:12

And I think I mentioned a few reasons why earlier.

20:15

Um, I think what we should try to recall is, is

20:18

that the field of view is gonna be different.

20:20

We need to ensure, um, evaluation of the ostia

20:24

and the origination of the lima, um,

20:27

and the subclavian artery as well as, um, its entirety.

20:31

And, um, oftentimes if you don't have a good protocol in

20:35

place, which is where if you see clips

20:38

or history of, uh, cabbage on the scout

20:40

or something that you increase your, your field of view,

20:44

then you're gonna clip it

20:45

and you're gonna have to put an N in terms

20:48

of the non evaluation of that proximal segment.

20:51

So that's always a, a very important one there.

20:54

So let's get into this case here.

20:56

Um, this is case 360 5-year-old female with a history

20:59

of diabetes, hypertension,

21:00

and prior graft cabbage nuance at chest pain with exertion.

21:05

So very rarely do, uh, in the past

21:09

would we even bother with, uh, anatomic evaluation, mainly

21:12

because we couldn't have, we didn't have the benefits

21:15

of the higher spatial resolution,

21:17

nor did we have the opportunity to ensure good ification.

21:20

So we're not ruling out the, uh, the presence

21:24

or absence of disease.

21:25

We obviously have a, um, a history

21:27

of coronary artery disease and definitive treatment.

21:30

What we're looking for here is definition of anatomy,

21:33

so a pre-procedural mapping,

21:35

but also we're looking for is

21:37

what other vessels can be in play, not only in the, the, um,

21:40

therapeutic vessels that is our grafts, um,

21:44

but also then our native vessels, the minor ones, diagonals,

21:48

obtuse and acute marginals that, um, are still in play here

21:52

that have a human dynamic response.

21:55

So let's go into case three and review that.

22:01

All right, so, um, capture a little bit

22:05

of the lima right along there.

22:06

Obviously we do not get the entirety of it.

22:10

And you can see then that is clipped right there.

22:12

So an n for, um, that first segment.

22:15

Um, but so in terms of nomenclature, we

22:20

expect there to be extensive disease

22:22

or some reason for, uh, a significant occlusive disease

22:27

prior to the anastomosis.

22:29

So my shorthand statements is extensive disease in the lm if

22:33

it's there, extensive disease in the proximal mid

22:36

LED, if it's present.

22:37

Um, and I write off those components in the native vessels.

22:41

However, we do have

22:43

to do our diligence on the minor vessels.

22:45

That includes the diagonal branches.

22:47

And so this is, this case is the perfect example of that.

22:50

So, um, let's go ahead

22:52

and first of all, identify the branches.

22:55

And so we do have, um, disease here in the proximal,

22:58

and then we finally get into our diagonals along in here.

23:02

So one, two, and there's the third. So one, two, and three.

23:07

Now what is going on right there,

23:09

unfortunately at the superior

23:12

and inferior aspect, there's that low attenuation right

23:14

through there, but then

23:16

as we see there's a re opacification, um, of that one.

23:20

Um, whereas we can see in comparison

23:23

an ostia of D two.

23:26

So we put this casing here to demonstrate that

23:31

there is a way of determining an ostia in an origin

23:36

of diagonal branches.

23:38

And then there is an absence of disease

23:41

in one, in another branch.

23:43

So you had an internal control to evaluate this.

23:46

And so that low attenuation plaque is still present

23:49

and is 70 to 99%, um, occlusive.

23:55

So that is always, um, that's a problem.

23:57

Um, and uh, so, uh, I challenge everybody to try

24:02

to look at the diagonal branches mainly

24:04

because they feed a significant portion of the septum.

24:07

Um, uh, additionally we wanna do our diligence

24:11

for the remainder of the vessel here,

24:12

but so at some point here, um,

24:14

as it makes its way the DLAD will have an anastomosis

24:18

to the Lima, and so there's Lima right there.

24:21

And so, uh, we'll get into that in just a second,

24:24

but we're gonna clear the remainder

24:25

of the native coronary arteries.

24:27

So here we have an obtuse marginal,

24:29

and we can see a good osteo branch there,

24:33

LCX fully once, but not twice, right?

24:35

So it stays within the atrial ventricular groove.

24:38

And we had a little bit of motion right there,

24:42

but it looks like it, uh, stabilizes

24:45

and stays within and that looks good.

24:48

So Optus marginal for where we care about

24:51

and then proximal in distal LCX look rate.

24:53

Let's jump on over to native RCA.

24:57

So we have a branch here,

25:01

goes along here, and

25:06

there's a little bit of disease

25:11

you can see flowing with it here,

25:13

but nothing too crazy, right?

25:16

Yep, 50 to 69 right along in there

25:22

and poop maybe something right there as well.

25:25

50 to 69.

25:28

Um, but not too bad in terms of the D distal RCA

25:32

and then PDA and then PLA having then, uh, an appearance.

25:37

Okay? So nothing too crazy on the remainder of the native.

25:40

So now, uh, nomenclature for the graphs, we talk about,

25:45

um, two different types of material for graft.

25:48

We talk about venous graft and arterial graft.

25:51

Venous grafts are from the saphenous vein and they're SVG

25:55

or saphenous vein graft.

25:56

And they're typically called aorta coronary, mainly

25:59

because they are anastomosis from the aorta to a portion

26:02

of the coronary artery.

26:04

Um, obviously distal to the occlusion.

26:07

So in this case here we have a nubbin sign, which is

26:10

where there is a, an A right aortic coronary graft, A SVG,

26:14

um, SVG graft that is completely occluded.

26:20

And then if we track, um, more anteriorly, we

26:25

c potentially another, this is a port for a graft

26:30

and there is, um, nothing there.

26:33

So in this case here, we have then very likely another, um,

26:37

occlusion of a, of a graft.

26:39

Uh, this is very likely a, um, you know, an occlusion,

26:44

uh, to a graft in the distal aspect

26:49

and don't really see anything else along with those.

26:54

So occlusion at the origin of, um, right

26:57

and, uh, potentially left aortic coronary grafts.

27:02

And then let's go into then the lima.

27:05

The lima, again, we don't see the origin of it from this,

27:07

uh, subclavian artery, but we can see then it's mid

27:10

and distal portions and it has, these are little,

27:13

little clips here where you just see 'em, pop 'em

27:16

and pop out, and it just essentially clips that keep it in,

27:20

in this space here and doesn't travel too far.

27:23

And so then we can see that it's gonna go

27:25

to the distal LED right about there.

27:30

And then following that there is good a ification

27:33

of the distal LED.

27:35

So the graft portion of it has a normal course in

27:38

termination and new luminal disease.

27:40

What does new luminal disease look like?

27:43

Well, luminal disease will have like the other, um, uh,

27:47

vessels that'll have then, um, an intramural finding.

27:50

But what we can say is, um, we can remark on atresia.

27:56

Now, this is, um, essentially a, a, a simple concept,

28:00

which means what is the size

28:02

of this vessel versus this vessel?

28:05

If we did not remove the osteo

28:07

or the origin of that vessel,

28:08

it's still arising from the subclavian

28:10

as the right internal memory artery is.

28:13

They therefore should have the same size.

28:16

That is, we haven't removed its nutrient components.

28:18

It, it's, it's still, you know, obviously attached.

28:22

We just, we just removed it, um, you know, uh, taking the,

28:26

the distal aspect and attached it on there.

28:29

So if that's the case, but the vessel is smaller,

28:31

then that's called atresia.

28:32

And you can clearly see the, um, the comparison difference

28:35

between the LIMA to the RMA

28:37

and see that this vessel is smaller, more narrowed.

28:40

And this is called atresia.

28:43

Now you will find that commonly that's, that's okay.

28:45

That's not really the, the big thing to take away from this,

28:49

what to take away from it is, is

28:50

that there is an end on the proximal aspect,

28:52

there's an luminal disease on here

28:54

and that there are EC clips associated with its course

28:57

to its anastomosis here.

28:59

Additionally, the other thing to take away from this first

29:01

cabbage case is that this NUBBIN sign

29:05

is the typical origin of, um, of an SVG graft,

29:10

uh, that has been occluded.

29:11

And that's not uncommon typically that can occur.

29:15

Um, and so, uh, in this case here we have, um, we have two

29:20

that, um, have occlusions, but what are we seeing here?

29:25

We are still seeing, when we do our trifecta sign,

29:27

we're seeing good opacification of L-A-D-R-C-A

29:31

and LCX of similar opacification in the same space.

29:36

And, um, so essentially what we're indicating is, is that

29:40

although there is occlusion, there is good perfusion

29:43

and, um, I think

29:45

that's the main takeaway why we do an anatomic evaluation

29:48

as opposed to just a functional evaluation of

29:50

how things are looking like.

29:52

Okay, so the writeup on this one here is a hundred percent

29:55

occlusion of the first diagonal branch,

29:57

which is the still a native branch

29:59

that then determines the cadrad designation.

30:02

So cadrad five due to

30:03

that D one having a hundred percent occlusion.

30:06

There is also occlusion within the aorta, coronary grafts

30:10

or SVG grafts and then AIA atresia of the lema graft

30:14

and an n associated marker, um,

30:18

for the proximal aspect of the Lima whole, a whole lot

30:22

to dig in on that one.

30:23

Right now, if you wanted to be kind to your, uh,

30:28

your colleagues, you can do many different things, uh,

30:31

which includes then visualization of the, uh,

30:36

of the Lima graft in.

30:37

So there's lots of opportunity to do that.

30:40

Let's see if we can, um, we're gonna

30:46

see if we can pull that vessel out there.

30:48

Nope. Okay, well let's go over here, find it.

30:53

Okay, we're gonna pull that there.

30:56

Alright, so here, um, we're obviously missing some detail,

30:59

but we're getting a fair amount there

31:01

where you can see then it's an,

31:03

it's anastomosis right there.

31:05

And so then we can see then that that portion

31:07

of it looked pretty good.

31:09

Obviously if we wanted to, we can trace this up.

31:11

It's just missing here. It's obviously right here.

31:13

We can pull this, um, and grab the rest of it.

31:16

But if you wanted to trace it out, you don't have to.

31:20

I, I find it's a lot of work

31:22

unless they ask where is the OST osteo of the,

31:26

and then typically we do some sort of, um, comparison

31:30

to the, in terms of, uh, distance from the,

31:34

from the subclavian artery where the osteo begins

31:37

and then its course and, and so forth.

31:39

And then we can go and create the, the,

31:41

the volume renderings behind that.

31:44

Okay, any questions on that one?

31:49

No. Alright, so let's go into the next case.

31:53

This is case four.

32:04

All right, so case four.

32:06

Um, history given as a 68-year-old male history of cabbage,

32:11

um, which is, uh, he had, uh,

32:14

and thankfully they wrote out the history of it,

32:15

so we were expecting the Lima, um,

32:18

and SVG to the ramus intermedius, um,

32:23

and SVG to the PDA.

32:25

Um, so we have a left aortic coronary

32:28

and a right aortic coronary that should be there too.

32:30

And then obviously a Lima hypertension,

32:32

mixed hyperlipidemia, worsening chest pain.

32:34

So we're gonna still evaluate the minor, um,

32:37

native coronary vessels.

32:39

Uh, we're going to bypass metaphorically

32:43

and um, figuratively pre anastomotic native vessels.

32:48

So the proximal

32:50

and mid LAD,

32:51

we're not gonna care too much about OB obviously of that

32:53

because we have a lima and we're not gonna care too much

32:56

of the proximal mid and distal RCA

33:00

because we have a graft to the PDA.

33:02

And similarly we have a ramus intermedia.

33:04

So we're going to, um, take a look, um, at that vessel

33:09

and not care too much.

33:10

Obviously there's a, an occlusion going on there. Okay.

33:13

But, um, I always like, uh, again,

33:15

getting the information I can from, um,

33:17

from the volume renderings here.

33:19

Um, and uh, so what we're seeing is pretty good, right?

33:23

Very good delineation of the lima

33:25

and it's anastomosis obviously all of this stuff,

33:28

extensive coronary disease, don't need

33:30

to make too much fuss about that.

33:31

Similarly here, some, um, some disease here,

33:34

but a pretty good looking obtuse marginal,

33:36

we'll swing this bad boy around here

33:39

and we can see then, um, aortic coronary grafts here, right?

33:43

These are obviously not normal vessels.

33:45

Uh, we don't have any native vessels

33:46

that come off this high, um, on the thoracic aorta.

33:49

So these are a coronary grafts one going left for

33:51

as I mentioned, and one going the right word.

33:54

And then we have the RCA here, um,

33:56

that obviously had some sort of occlusive disease here,

33:58

so we can get a lot of information from, uh, from this.

34:02

And it does look like there's pretty good a ification.

34:04

So, um, this is always a really nice, nice setup, right? So

34:17

let's get into it.

34:21

So I always like, um, having my, my fellows

34:25

and my residents kind of game theory

34:27

or at least, you know, plan.

34:29

What do you think the CAD rads are gonna be?

34:31

So you saw the volume rendering, you heard the history,

34:34

you have obviously a symptom, which is chest pain.

34:36

What do you think it's gonna be that way?

34:38

Then we can, we can take the failure,

34:41

which is hopefully the wrong answer in the guessing,

34:44

and be able then to adjust accordingly.

34:45

If we're always doing the

34:47

after, you know, evaluation, which is the CAT rads is this

34:51

because we were told it was this,

34:53

'cause we looked at it, then we don't ever get to

34:55

change our sensitivity and our specificity

34:58

accordingly with every case.

35:01

So here we're gonna start with the um, LCC LM

35:05

and we can see extensive disease there.

35:07

Um, we obviously have, um, disease in the lm,

35:11

but it's non occlusive.

35:12

So we'd give that, you know, a 20, uh,

35:15

a less than 24% in the LM extensive and P and MLAD.

35:20

We're not gonna worry too much about that.

35:22

But basically we're gonna do like we did with the last case,

35:24

is we're gonna try to identify a pretty

35:26

good diagonal branch.

35:28

There is some disease associated with it,

35:29

but that doesn't look too bad.

35:32

And then D two looks okay, we're gonna be waiting for

35:36

that anastomosis right there.

35:37

So we're gonna evaluate and scrutinize that

35:39

and that looks pretty good.

35:41

A little bit of disease distally in that LAD,

35:43

but nothing that looks occlusive.

35:46

Okay? So LAD with its tributaries, the diagonals checks out.

35:50

Let's go into that ramus.

35:52

We noticed that, um, or indicated

35:53

that there was gonna be a bypass.

35:56

So that's the cuff

35:57

of low attenuation plaque that is occlusive.

36:00

And um, and then there's potentially

36:05

some disease along there too.

36:07

Okay? Now again, this is not where the, the um,

36:11

SVG graph is gonna come in.

36:12

It's gonna come in a little bit later over here.

36:13

So we are just looking again at the

36:15

proximal native component.

36:17

Here's proximal LCX.

36:19

Have a little bit of disease again here, less than 24.

36:22

There's an obs use, marginal coming across there,

36:24

some disease long here, nothing too crazy, right?

36:28

Okay. Alright,

36:30

and then now let's uh, take a quick look at that.

36:33

RCA, we had reminded ourselves

36:35

of an aortic coronary graft to the PDA.

36:37

So there's gonna be somewhere

36:39

where there's an extensive disease

36:40

and so that's necessary right in here.

36:42

We can go superiorly all the way to inferiorly and uh,

36:45

before we even get the cprs, we can see that

36:47

that's extensive and obstructive.

36:49

And then also similarly there too, so we have a lot

36:53

of disease throughout the force of the proximal and mid

36:56

and distal RCA, but that's okay

37:00

'cause we had a graft and there it pops in

37:03

almost like a little, uh,

37:05

superman coming in right here, right?

37:08

B ba bum. And then it goes right straight to the PDA

37:11

and then to the PLA at that point right there.

37:15

There's disease in the PLAP at PDA,

37:18

but um, obviously not significant disease.

37:21

Um, so those portions look fine.

37:23

Now let's take a quick look at the graphs.

37:26

So on here, we'll, at the anterior aspect,

37:28

we're gonna have those two graphs

37:29

that we saw in the volume render.

37:31

So here's the first right?

37:32

Aortic coronary graft

37:34

and the, um, origin looks fine, course looks fine.

37:39

Termination with anastomosis looks great, very.

37:43

And then no disease, right?

37:44

So right aortic coronary checks out.

37:46

Let's take a quick look at the left.

37:48

So some tortuosity is gonna be expected, particularly

37:52

as they make their way, um, in,

37:54

in what's called a subpulmonic, um, course, um,

37:59

inferiorly down towards, uh, the either uh, a diagonal

38:02

or ramus intermediates or an a nouse marginal.

38:06

So I don't worry too much about that.

38:09

I do worry about, um, intramural,

38:11

I do worry about high degree of stenosis, um, or,

38:15

or narrowing, um, there,

38:17

but in this case here, that looks pretty good.

38:19

Alright, so we have a little cuff

38:22

of low attenuation around that.

38:24

Um, that just probably means that this is, um, uh, you know,

38:28

a graph that's still undergoing, um, evolution

38:33

and I mean it looks great, right?

38:35

Uh, we're not seeing anything, uh, uh, anything wrong there.

38:39

And um, obviously the ramus is right along in here

38:42

and it just seems to just end right along there.

38:44

So, um, those parts look pretty good again, um,

38:48

this would ordinarily be like an OB juice marginal,

38:51

but looks fine coming, you know, being an a ramus obviously.

38:55

So the left AAL coronary looks fine too.

38:57

Alright, let's go to the, uh, lima

39:00

or left internal thoracic artery

39:03

and we can see that we get a good field of view off

39:06

of the proximal subclavian.

39:09

So normal origin, normal course, it's a little torturous,

39:14

but that's totally fine.

39:16

What is the vessel size comparatively we saw in atretic?

39:21

Is this atretic or not? Nope, no atresia there.

39:25

And we see a lot of clips along its way,

39:27

but then it meets up right there at the distal LED,

39:32

no stenosis or other changes and everything looks great.

39:35

Perfect. So what do we got here?

39:38

We got a CG with minimal disease, um,

39:41

or maybe even mild disease, 25 hyphen 49% stenosis

39:45

of the distal LED.

39:46

But uh, and that's just in,

39:48

in this area right on here, right?

39:50

I mean that, but otherwise not a big deal.

39:53

If you were to say cataracts one post cabbage,

39:57

that would sound a little ironic.

39:59

Uh, right, but that's actually what we have.

40:02

Um, we are discounting

40:03

or not concluding the extensive coronary disease in our

40:07

cataracts as degradation because

40:08

of definitive therapy has already been proven.

40:11

So it's the areas that are post the anastomosis,

40:14

so the distal LED, the diagonals, the obtuse marginals, um,

40:18

the acute marginals and so forth.

40:20

Obviously the, um, the grafts as well.

40:22

So this is a cataracts two.

40:24

Um, and the additional things you, um, talk about in here

40:29

is, um, that this is post graph.

40:33

Okay? Any questions on this one?

40:38

I think one of the nice things with this particular case is

40:41

that we have the opportunity to see the entirety of the,

40:45

the lima raft here.

40:47

So we're just gonna just take a quick look here and,

40:50

and you can see where it starts and where it ends

40:54

and be able to then to, uh, evaluate this entirety.

40:57

And so this is a very pretty evaluation.

41:00

This is what we strive for, um, as imagers,

41:04

and you can see then it goes all the way

41:06

to the distal la d there

41:10

and, um, no luminal disease along those lines.

41:13

So beautiful looking, uh, graft, um, that's intact.

41:16

We can obviously do the same thing, um, with, uh,

41:20

as we had seen on the volume rendering for each of these.

41:23

Um, then be able to follow 'em down if you wanted to.

41:25

Um, again, this is sort of redundant,

41:29

so I don't usually do this.

41:31

I I just do it on the axials unless there's any questions.

41:34

Um, and then we can evaluate it that way.

41:37

Similarly, we can go to the, the left aortic coronary graft

41:40

and just take a look at it in, its,

41:42

in its appearance, similar sort of thing.

41:45

Okay, so what have we learned so far?

41:48

Um, cabbage doesn't always mean a cad.

41:52

Rads four or five cabbage can, uh, is a definitive therapy

41:56

and we then designate the CAD rags according

41:59

to what's distal to the, to the graft

42:01

and the, uh, what's distal to the anastomosis.

42:04

Um, additionally the post-processing in the,

42:06

in the evaluation on orthogonal view can be done on axial

42:10

as well as volume rendered as we can see here.

42:14

Um, to get a good idea of the origin of course,

42:16

and the termination of both native and um, graft vessels.

42:21

So looks pretty good.

42:22

We also talked about with case one, um, plaque and, um,

42:25

and the amount of plaque

42:27

and plaque ve Alright, all right,

42:29

so let's talk about case five.

42:36

Case five is as a 72-year-old male with a history

42:38

of coronary order disease post cabage.

42:41

In this case we added a lima to lad, LED

42:44

and then an SVG to the obtuse marginal and SVG two PDA.

42:48

So three vessel cabage, um,

42:51

and SVGs to the LCX and the RCA.

42:53

Alright, um, family

42:56

or rather, uh, personal history of hypertension,

42:58

mixed hyperlipidemia

43:00

and worsening chest pain, improved on medical therapy.

43:02

Okay, so we're just gonna invest, uh, assess graft patency

43:06

and be able to then to look at that

43:07

and see if there's anything here.

43:10

Pretest probability, what do you think, uh,

43:12

we're gonna have with this individual?

43:14

Um, any thoughts on it?

43:18

I mean, I, I, I would, you know, pretest probability wise,

43:21

um, before looking at the volume renderings,

43:23

and I would say, you know, this is probably, um, yeah,

43:28

LED's really janky looking, right?

43:30

I mean, there's just not a lot going on in that space.

43:32

There's a one, a D one, a D two,

43:35

and a D potentially, uh, yeah, nothing else after that.

43:39

So this is limo obviously.

43:41

So in that case, when I,

43:43

I don't clearly see the native vessel very well,

43:45

what we were talking about

43:47

before is either there's an, there's an extensive amount

43:49

of plaque and plaque burden

43:51

or there's a loss of, uh, collateral flow or both.

43:56

So in this case here we have an aorta coronary

43:58

that's going leftward, we had already talked about that.

44:00

And we have then, uh, rightward aorta coronary,

44:02

which doesn't look as clean as the last one.

44:05

And then extensive disease in the RCA.

44:08

Okay, so I'm expecting a higher, um,

44:10

CAD rats than the prior case.

44:14

Um, from a quality assurance standpoint, again, regardless

44:17

of whatever you do, you're just gonna be dealing

44:19

with the harder cases here.

44:21

So do take a little bit more time, um, with the cabbages.

44:25

But um, here we have slow flow, um,

44:27

and disorganized flow, um, in the right

44:30

and the left, thankfully a little bit more

44:32

ification in the left than the right.

44:34

Um, optimization from heart rate standpoint looks great.

44:37

Okay, so LCC with an lm

44:40

and we have, um, significant disease, um,

44:43

in the distal aspect, um, of that LM there.

44:47

And there's that looks like that's the bifurcation

44:50

where the LCX is coming off.

44:52

Um, so in that case there, that's, I mean, it's pretty,

44:55

pretty bad here, but let's focus on the LED then here.

44:58

Extensive disease, you can take this in many different ways,

45:02

but axial wise, we go from superiorly to inferior.

45:07

We have been this just persistence

45:09

of calcified plaque disease, 70 hyphen 99% stenosis.

45:14

And that continues on to about right here,

45:17

where then just we lose, um, most of it.

45:21

We got this little n in the remains right there,

45:25

but that's a diagonal, it's this thing that we're looking at

45:28

because that's in the inner ventricular groove.

45:31

So where did we lose that?

45:34

We lost that somewhere right around here.

45:36

So extensive coronary artery disease,

45:38

pre anastomosis expected.

45:41

Now that we've know

45:42

and understand the extensive disease in the pre anastomotic

45:47

components and segments,

45:48

then let's take a look at the diagonals, right?

45:51

And diagonals. Oof, oof, oof. Oops. Pretty bad, right?

45:57

Lots of disease within, um, both, um, this diagonal,

46:08

not too bad right there, right

46:15

Now let's take a look at LCX.

46:21

So we're not gonna be fooled by the obtuse marginal.

46:25

There we go. There's LCX

46:28

and extensive disease, 70 99%, which again, we know

46:32

because we have, um, we have a, a vessel there.

46:34

So extensive disease bypass that.

46:36

Okay, so let's go then into the, um, RCA.

46:40

This is, that's obviously an SVG graft, dilated, um,

46:44

the native vessel, um, takes off right there.

46:47

We'll follow that really quick.

46:49

And it's just extensive disease.

46:50

Again, 79, you know, complete occlusion

46:52

or 79% I typically just say extensive disease.

46:56

And then again, occlusive right there.

47:01

Okay, so we know that those vessels are out

47:03

and you just give essentially just a very

47:05

quick statement about that.

47:07

What we're really caring about is

47:08

what do the grafts look like?

47:09

So let's just take the first or the right SVG graft, dilated

47:13

and obviously mention that and, uh, couple different ways,

47:17

but graft shouldn't dilate.

47:20

And in this case here we're getting about nine millimeters,

47:22

which is obviously, um, dilated.

47:25

And why is it dilating?

47:27

It's dilating because there's an occlusion, right?

47:29

Blood flow is unable to get through there.

47:31

It's coming through here passively

47:33

and it goes through there, but it's unable to get through.

47:35

So it dilates. So anytime you see a dilation

47:37

of an SVG graft, a venous graft, be really cognizant

47:42

that you're gonna be finding, um, an occlusion somewhere.

47:44

So complete occlusion along there, we can follow it along

47:49

ACLUs ACLUs and continues on.

47:52

So for the majority of its course from proximate

47:54

and distal aspect to the PDA,

47:57

the SVG graft is, graft is occluded.

47:59

There is flow in the PBA as you can see there.

48:02

And let's see if we can pick up the PLA

48:07

and there, right there and there is flow.

48:11

So how do you get flow where there is no flow?

48:13

Collateral flow.

48:15

So there is flow, collateral flow to the PDA and the PLA.

48:18

Alright, so let's find the rest of the other graft.

48:21

And that was our left aortic coronary graft pops off

48:26

good origin subpulmonic.

48:32

And we're gonna follow that to where,

48:34

to the obtuse marginal.

48:36

So there it's one obtuse marginal,

48:38

and here's the second obtuse marginal

48:42

and looks like that's the third.

48:45

So right around, um,

48:47

at the distal aspect there is where we're gonna have.

48:49

Then in this case it looks like it's actually

48:51

to the anastomosis, to the LCX right there.

48:56

Okay, so that one looks patent, eh,

48:59

there's actually some disease going on, right?

49:01

Oof, that one's top too,

49:03

but, um, not as bad as the, um, um, as the,

49:08

as the PDA graph.

49:10

Okay, Lima, let's not forget that one.

49:14

Let's come on back here. Oops, we didn't get the field

49:16

of view, so we're gonna have to give an end to that.

49:18

But let's take a quick look at, uh, vessel size.

49:22

They look, um, in agreement, follow it down.

49:25

Tortuosity is not a problem.

49:27

What is a problem is size of the vessel

49:30

and then luminal stenosis and don't really see anything.

49:34

Let's come to the last

49:35

staple, uh, right there.

49:43

Clip, clip, clip. So about right over here is

49:46

where we should expect in the last staple.

49:48

And um, things look okay, I would grant you, um,

49:53

if you did an end for that distal aspect of the,

49:56

of the Lima graph, totally understandable.

49:59

Why noe's index, you can't confirm

50:02

or definitively rule out that there's, um, luminal stenosis

50:06

or plaque within the distal aspect of, of the lead-up.

50:09

So, um, you can give an end on that,

50:12

that would be totally appropriate.

50:14

Noise index obviously is not, um,

50:16

is suboptimal at this point,

50:18

but that's, um, that's a, that's, uh,

50:20

that can be a big deal there.

50:22

Uh, let's see what it else. Yeah,

50:27

so I,

50:33

yeah, the, we, we talked about that misalignment artifact,

50:37

uh, uhhuh Uhhuh, yeah,

50:41

and that's, that's the concern is, is this, um, a,

50:45

an occlusion, a 70 99% occlusion right there?

50:51

Or is that artifact?

50:52

Uh, in our case, we did choose to call

50:57

that a 70 to 99% occlusion.

50:59

Um, much of that had to do with the fact that we, um,

51:03

had the ICA to prove it.

51:05

But, um, if you were to go with an N

51:07

that's totally understandable

51:08

and recommend, um, a definitive evaluation of the lumen,

51:12

a lumin gram, which is also called an

51:14

invasive coronary angiogram.

51:16

So, um, I think, um, at this case here we have, uh,

51:19

occlusion of several vessels to include RAFs

51:22

and then we have an n

51:24

or um, what we called a fife, um, uh,

51:29

complete occlusion of the distal lima graft.

51:33

So a lot going on in this one.

51:34

There are some, um, trap doors.

51:37

And so, um, this is always fun when we get to see those,

51:41

um, in play.

51:42

Let's see. Do, do, do, do, if we can, um,

51:47

take a quick look at the invasive coronary angiogram on

51:50

that one because that, I think that might be worth, um,

51:54

taking a quick look at

52:05

and, okay.

52:18

Okay. Yeah, so here we go.

52:20

And I'm gonna, alright,

52:25

so let's go ahead and change my screen here

52:27

so you guys can see this with me.

52:29

Alright, so, uh,

52:40

and, uh, these are videos.

52:42

Uh, they're available obviously in the, um,

52:44

in the notes section if you wanted to look at it here.

52:46

But, um, that SVG to om, there's a bit of stenosis there,

52:50

99%.

52:51

And so that was the big concern that we saw on, um, on

52:57

as it made its way.

52:59

Um, additionally here, that mid l led d stenosis,

53:02

distal LAD stenosis at the area of, um, anastomosis, that's,

53:06

that's the one that, uh,

53:08

we were looking at and concerned about.

53:10

Um, so those are always concerns.

53:13

It is hard, particularly with this noise index

53:15

to make these definitive.

53:17

Um, I personally am not a, a good fan of the,

53:21

I I just don't like using the,

53:23

and as a designator to say I don't like it, it,

53:25

I try to give 'em a best shot.

53:26

Um, but, uh, you know,

53:28

this resolution is obviously not, not always the greatest.

53:32

Uh, so if you need to use it, that's totally fine.

53:35

Um, and that's why we kind of left it open.

53:38

Um, in terms of the grading behind this, um,

53:41

so in this particular case here, uh, we did have, uh, um,

53:45

a cataracts five, which is

53:47

where there was a complete occlusion of the SVG

53:50

to PDA graft.

53:51

Um, and then 70 to 99% in that SVG om one, um,

53:57

and, you know, misalignment artifact

54:00

or an n uh, for that, uh, leanly graph there.

54:03

So that's, that's always concern.

54:05

Um, I, I like showing these not

54:09

because they're always universally gonna be

54:13

definitive and they should not be.

54:14

There should always be room for discussion on stuff.

54:17

Um, but if you're gonna put something on there,

54:19

it should then have a significant amount of reason why.

54:23

And so if you say, you know, an n on the distal lima portion

54:27

of it, totally understandable, I think that's great.

54:29

But in this particular case here, it's a severe stenosis,

54:32

um, in that particular, uh,

54:34

component of the, of the vessel there.

54:37

Okay, questions, concerns.

54:42

That is five

54:48

speed round cases.

54:52

Uh, for week five.

54:54

These are difficult and they are sometimes

54:57

difficult, uh, and not fun.

54:59

Sometimes they're difficult and fun,

55:01

but in this case these are difficult and not fun.

55:04

So, um, big picture to take away from, uh, from

55:07

what you guys are doing as I'm looking at the grading is

55:09

that you guys are nearly right on the money in terms

55:12

of the stenosis accuracy.

55:14

Your plaque looks great. Uh, I think that's fine.

55:18

The interpretation of graft look really good.

55:21

I was very happy to see that.

55:23

Again, cadrad, sation,

55:25

when you have graft is dependent upon the post anastomosis

55:29

or the native component of the vessel

55:30

that's unaffected by the graft.

55:32

Obviously diagonals, obvious marginals,

55:35

acute marginals and so forth.

55:37

So if you don't have any questions, um, I I think you guys

55:40

for your time and attention

55:41

and can't wait to see you next week.

55:43

Yes, thank you everyone for attending today.

55:46

Just a reminder, um, in the next couple hours I will be, uh,

55:49

emailing you all the raw footage from today.

55:52

Um, thanks again Dr.

55:53

Lorenz, and we'll see everybody next week.

55:56

Have a good.