0:00

Okay.

0:01

Hi everybody. Thank you for joining us today for week three

0:04

of Office Hours for the Cardiac CTA online training course.

0:08

I'm here with Dr. Lorenz,

0:09

who'll be reviewing all five cases.

0:12

Just a reminder, uh, if you have questions, um, just ask Dr.

0:16

Lorenz directly. You can also enter your question in the

0:19

chat or use the hand raising emoji, and we will call on you.

0:23

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

0:25

Awesome. So good to see you all.

0:29

Such an exciting time to be a cardiac imager.

0:32

I don't know if you're keeping up with all the craziness,

0:34

all the news, all the fun, exciting things.

0:37

Um, but I did want to share, um,

0:41

one thing that, uh, that did make the news here recently.

0:47

Let's see,

0:51

um, there we go.

0:54

So in our neck of the woods, the CMS

0:56

or Medicare, which is the Federal Reimbursement

0:59

and Payment System, uh, came out with a new, um, approval

1:04

for reimbursement of one of the biomarkers

1:06

that we've extensively been foot stomping, um, you

1:10

to, to evaluate.

1:12

And that is plaque analysis.

1:14

Uh, plaque analysis can be qualitative, mild, moderate,

1:18

severe amount of plaque in aggregate, um,

1:22

or in each individual vessel, or it could be quantitative.

1:25

And that's, um, per RADS two.

1:28

Um, as you're seeing here, is an extensive CMS, um,

1:32

evaluation, uh, indicating then the clinical utility, the,

1:36

uh, uh, studies that supported it,

1:38

but also then the value, um, based behind this.

1:41

And so not saying a, a significant portion of this came out

1:45

of Scott Hart, but one of the best trials that showed, um,

1:50

the capability of coronary CTA in terms of adjusting

1:55

and directly changing major adverse cardiac events.

1:59

In fact, it's so good.

2:00

Scott Hart two, which should be wrapping up in 2027.

2:04

Uh, a small subgroup of around 400 will come out, um,

2:08

I think next year or something.

2:10

But anyway, we're around 6,000 enrollees, uh,

2:13

into Scott Hart two,

2:14

and they're looking at the use

2:15

of coronary CTA as prevention.

2:18

So now it's for chest pain, chest pain evaluation.

2:21

One a evidence, Scott Hart two will be looking at prevention

2:25

that is, does coronary CTA prevent

2:28

major adverse cardiac events?

2:30

But taking that information, Scott Hart, what we were able

2:33

to find is that there was a really exciting thing in that,

2:36

um, plaque evaluation

2:39

and risk evaluation with plaque

2:42

and how low attenuating plaque or, uh, vulnerable plaque

2:45

or high risk plaque features actually have a huge thing.

2:48

And so I'm just gonna highlight, like here, um,

2:51

if you can see this, there was a linear correlation

2:54

between the quantification in absolute plaque volume

2:58

and major adverse cardiac events.

3:02

The only other time we've seen a linear correlation was in

3:07

terms of coronary artery calcium

3:10

in major adverse cardiac events, hence the use

3:13

of a CAC score to evaluate in risk predict, um,

3:19

events in the future.

3:21

Again, regardless of chest pain sentiment here,

3:24

now we have more evidence cited by the government

3:26

that there's plenty, at least my government,

3:28

that there's plenty of evidence that plaque prediction

3:32

as a model will, uh,

3:34

will change the outcome adverse events and the event rates.

3:39

So these are extremely exciting times, um, really,

3:43

really fun times to be a cardiac imager.

3:45

And so I just wanted to make sure, this just came

3:46

out by, I think last week.

3:47

And so it's a, it's a big thing.

3:49

This is essentially like FFR CT coming out,

3:52

another biomarker.

3:53

Um, this is, these are big, exciting times. Okay?

3:58

So if anybody doesn't have any specific questions on that,

4:01

uh, we'll just dive into the cases and review them.

4:05

So let's go ahead and share then that,

4:10

okay, so hopefully you're seeing my screen here

4:13

and, uh, Terry recon.

4:15

And so, um, we're gonna, in terms of the grading,

4:20

everybody did fantastic,

4:22

although I might've said CAD RADS three and you said four,

4:26

or I said, you know, CAD RADS three and you said two.

4:31

The, the difference in there is

4:32

nominal, and, and that's fine.

4:34

Yes, there is a decision tree difference in terms

4:38

of going from cataracts two.

4:40

So 25 to 49% stenosis to cataracts, three 50

4:43

to 69% stenosis, and what you can potentially do next,

4:47

but the idea behind it is that you're now in the ballpark.

4:49

Now, once you're in the ballpark, how are we going to

4:52

improve our specificity in correctly diagnosing

4:59

the cor uh, the right amount of luminal, uh, stenosis

5:03

and plaque, but also what does it mean if we,

5:08

if we're reading the case,

5:09

and what are the tools that we can use to kind of safeguard

5:12

that, is how can we get us into that higher a UC

5:14

by using, um, other items.

5:16

And so the weak cases that we had here, week three cases,

5:20

were all about trying to take some components of behind it.

5:23

So let's go through case one.

5:25

Uh, this is a 70-year-old male with a history of recurrent

5:29

probable cardiac chest pain.

5:30

Okay? So recurrent typically means that there is, um,

5:34

a perfusion, um, issue.

5:36

Typically, it means, um, that there is either plaque

5:41

but plaque invol, um, that is modeled and remodeling,

5:45

or that there is, um, a low, uh, coronary reserve volume

5:49

that is, there may be nothing in there, um,

5:52

to reduce the flow,

5:54

but the amount of flow available is lower

5:58

and slower than what is needed for the work.

6:02

Okay, request for CTA or anatomic evaluation.

6:05

So let's go into that one there.

6:07

And, uh, here again, we can choose any one of the, um,

6:11

um, apps.

6:12

All I did is move me from, uh, patient lists

6:14

or query to then viewer.

6:17

And if you notice the viewer, uh, lots of different,

6:19

um, items along here.

6:21

So we are going to

6:27

Get rid of the ribcage here.

6:29

Okay? So we're dealing with a 70-year-old male.

6:32

So there is obviously gonna be some changes you'd expect

6:36

with somebody who's had seven decades.

6:38

Um, but what we're looking for then qualitatively is

6:41

where are the areas of concern, right?

6:43

So we've got some areas right along here that we can see.

6:46

Um, but the tree looks pretty good,

6:48

not a significant amount of tortuosity.

6:51

Very nice and straight. Couple little areas there in D

6:54

And then, um, LCX looks a little wimpy,

6:57

but nothing too, too bad there.

6:59

Now we get to RCA,

7:01

if we remember from some previous lectures,

7:02

where's the majority of the blood flow gonna go

7:04

to the left side of the system.

7:06

The right side is sort of the carrier.

7:08

I believe it's reserved to be honest.

7:10

Um, and it's reserved

7:12

because it's supposed to have a ready supply.

7:15

So that nagging chronic chronicity of ischemia

7:19

or chest pains or stuff, typically it's associated with, um,

7:22

lesions along in here.

7:24

Now, I can't prove it, I haven't done a study,

7:26

but when I start looking at, um, morphologic cases

7:30

of coronary CTA

7:31

and chest pains, that's typically what I'm seeing here,

7:34

but it looks pretty good.

7:35

We've got a nice branch here in the PDA.

7:37

Okay, so let's dive in into this case here.

7:50

Now, as I mentioned, there's quite

7:51

a few different ways in doing this.

7:54

And it should be that what you take out of this course is

7:57

that you have more than one way of working through a case.

8:02

Um, if you're in an outpatient center with a, uh,

8:06

high volume, but low, um, uh, complexity

8:10

of individuals evaluation via the axial,

8:13

either in first pass

8:15

or in in final pass, is a fantastic way.

8:18

Why? Because this is the highest facial resolution, uh,

8:22

which models, uh, the acquisition.

8:25

So I tend to find this, uh, to be a very useful, uh, way

8:29

of doing the evaluation if I am not straddled with, uh,

8:33

significant complexity in my patient population.

8:37

If you are in a hospital setting,

8:39

typically you're gonna be dealing

8:41

with a higher complexity of patient.

8:43

And usually the, the needle in that haystack,

8:48

the haystack is on fire already.

8:50

So there's a quite of opportunity then

8:53

to over call, under call.

8:55

And then therefore we need to review.

8:57

And so as we're taking then the tree, the,

8:59

the main things again, is to try to take a quick look at

9:02

where the areas of concern.

9:04

Now, we do have obviously calcification

9:06

and lm, LAD, both prox and mid,

9:09

but as we're kind of just kind of moving along here,

9:12

and we are going from, again, the superior aspect

9:15

of the vessel of LAD down to the inferior aspect,

9:19

what we're seeing is a per, uh, consistency

9:22

and persistence of a certain amount of plaque here.

9:25

Okay? So we'll get to that one there,

9:26

but that's a little teaser

9:27

that we're gonna take a look at that area.

9:29

Let's just do an anatomic search pattern

9:32

starting from the lm from the LCC in evaluating that.

9:35

So again, if we scroll superiorly to inferiorly,

9:39

we are seeing then this focal area

9:41

of plaque par calcified less than 24% stenosis bifurcation

9:46

move into the prox, LAD, mid LAD.

9:49

So in this segment here, we are, um, going to, uh,

9:53

not marry our first girlfriend or boyfriend,

9:55

but we're gonna just take a quick look in here

9:57

and see this is an area of concern.

9:59

Now, as I'm looking at this,

10:01

and I'm at the 50% area of the, uh, of the vessel

10:05

where I can see both edges of the lumen.

10:07

And I'm sure that as I've turned this around,

10:10

that this is gonna be more than 50%.

10:12

If I looked at it in a short axis such as this,

10:15

I'm gonna see that it's constantly there.

10:16

It is still there. And up here, obviously superiorly,

10:20

it's more than 50% of that portion there.

10:22

And then here, it's still there.

10:24

So somewhere right in the middle here is

10:26

where I'm getting the long diameter of that vessel,

10:28

and I'm still seeing a significant amount of plaque,

10:30

at least 50% there.

10:32

So this is where I would be concerned that there's a 50,

10:34

69% stenosis, all the other calcium along here.

10:38

This is chronic, this is the stuff here

10:40

that is probably flow limiting,

10:42

but, um, in terms of day-to-day,

10:45

but not ischemia causing.

10:48

And so that's a very important thing to kind

10:50

of consider this vulnerable plaque, low attenuation

10:53

with focal vocality.

10:54

I mean, look at this stuff right along in here.

10:57

Um, this has not remodeled with time.

10:59

And so then therefore, this is probably the thing

11:01

that's causing then some issue.

11:03

We're gonna finish the rest of our, um, eval of the LAD

11:06

and we can see that there's some tortuosity,

11:08

some other additional areas of potential, um,

11:10

low attenuation, but then the LAD distal

11:13

LAD looks pretty good.

11:15

Okay? Uh, we've got a, a smaller D one,

11:18

and then we've got a more robust D two.

11:20

And again, as we're looking at this here,

11:23

superiorly inferiorly, find the middle of it, we can see

11:25

that there's maybe 25, 40 9%.

11:27

So now at this point, if you're a

11:32

confident reader, you can probably indicate then

11:34

that there's, there's disease, um, and,

11:37

and make that adjudication that's 50 to 69%.

11:40

Uh, and then move on, uh,

11:42

because again, your caseload is not gonna go away just

11:45

because, you know, you take an hour along here.

11:48

In terms of evaluation though,

11:50

we want to be the most accurate.

11:51

So we're going to move this line until it gets over here.

11:54

So let's move forward here,

11:56

and we're going to evaluate how much

11:59

of this plaque is covering.

12:01

And you can already see here, nah, you know,

12:03

we're at the 50% mark,

12:04

but let's just take a quick look here and see where we are.

12:07

And then we've got that little area

12:12

remaining here, and that is not good, right?

12:16

Okay, so 50, 69%, and then it comes right back up.

12:20

So this area right in here, that's the lumen,

12:22

that's the opacification, that's contrast, that is calcium.

12:26

And that black thing right there,

12:28

that's low attenuating plaque.

12:29

So nice big circle, you know,

12:32

maybe less than 24% right there.

12:34

And as we move along here, you can clearly see then

12:38

what we're seeing here,

12:39

and we can then, you know, just make sure we're 90, 90, 90

12:43

and everything is looking here.

12:44

And yeah, I mean badness, right?

12:48

So at least 50 to 69, it's probably somewhere

12:50

around the 70% range along in there.

12:54

Um, if we weren't so confident in that, uh,

12:57

read on using the diagonal approach,

12:59

we can then just use the CPR as well.

13:02

Reminder that utilization of, um, three dimensionality X,

13:07

y, and Z in something that wasn't acquired in that way,

13:10

you are taking then, of course, your spatial resolution and,

13:13

and, uh, resolving, uh, differently.

13:16

So we can swing these around

13:17

and we can see that that, um,

13:18

low attenuating lesion right there.

13:20

That's the one of concern,

13:21

and that's the one obviously that's causing Then, um, um,

13:25

the issue here, anatomic identification is a great place

13:29

to start and to be really good at.

13:32

So if you can just do the anatomic, um, evaluation,

13:36

you're on, you're right, starting where you need to be now,

13:39

then we gotta start thinking consequentially management

13:42

wise, what do we do with a 50 hyphen, 69% lesion,

13:46

a cataracts three functional assessment, right?

13:49

So the next thing is we have an anatomic reason

13:51

for pain in the coronary arteries.

13:53

Now let's see if it functionally is there.

13:55

So we're gonna stress or model, um, a stress,

13:59

and so we can do an FFR CT

14:01

and we can see if there's anything, um,

14:03

potentially associated with that.

14:10

So, um, let's go ahead and let me share my screen then

14:21

right here.

14:22

Sorry, that thing, just the little bar

14:24

keeps, uh, getting my way.

14:25

Sorry.

14:41

All right, so let's go ahead and share then this.

14:46

Okay, so this is the F-F-R-C-T that was associated

14:49

with that particular agent.

14:50

Again, 50 hy, 69% in the mid LAD.

14:53

And so, um, lm uh, bifurcation,

14:57

LCX, um, LAD.

14:59

And so in the mid LED, this is probably where the lesion is.

15:02

Now you'd say, well, why isn't the pen

15:04

associated directly to there?

15:05

Well, typically what you do is you associate the lesion,

15:09

and then what is consequential is the down

15:12

or the distal to the lesion flow.

15:15

So it's typically two centimeters

15:17

from the direction of the lesion.

15:18

So this pin is two centimeters from where

15:20

that lesion occurs, probably right there.

15:22

And that's what we're looking at is what is the consequence

15:25

of that lesion causing then to the flow below can.

15:29

And so the magic number,

15:31

if you remember from our prior lecture is 0.8.

15:34

0.8 is the relationship of the coronary flow to the aorta,

15:38

the thoracic aorta, and it should be 1.01 to one,

15:42

but if it's not, that is the flowing here is less than

15:44

what typically is associated with the aorta,

15:47

then we have a situation

15:48

where there's flow limitation or physiology.

15:52

So if this number is 0.8, 0.79, we'd have an issue.

15:57

Now, we get into some areas here, right? The RCA.

15:59

Now, the RCA is, um, is another lesion

16:01

that we're gonna review, um, shortly here,

16:04

but, um, I just wanted to have you guys take a quick look,

16:08

um, at what LED proper looked like and what then 50, 69% is,

16:13

and then what then that would look like under a functional

16:15

assessment if we start looking at them more at the lesions.

16:19

And I'll go back to the tear recon so we can confirm it,

16:21

but here's the tear recon, um, curve planer format

16:24

of the mid RCA, and we had another lesion there.

16:27

Um, in this telo ble we're at 50, uh,

16:30

that we're at less than 24,

16:32

or sorry, less than 50%, 24 hyphen 49% stenosis there.

16:37

Now you'd expect then, okay, so two centers from that lesion

16:41

that's proximal.

16:42

So that's somewhere right around here, two centers

16:44

below 0.85, right?

16:46

But what is this number, right?

16:47

And this is always the consequence, um, uh, of,

16:51

of a morphology or,

16:53

or, uh, a way of doing things, the results, right?

16:55

A methodology, these pins here indicate what is flow here,

17:00

but this is not, uh, indicative of a lesion above it.

17:04

This just means that flow at this area is low.

17:06

Well, we expect flow down below to be low flow,

17:11

and the reason is, is because it's a smaller vessel

17:13

and it has slower flow, smaller vessel, slower flow, right?

17:17

Okay. So it's okay that you'll see some pins

17:21

as it's called in that concerning range 0.8

17:25

and below as long as you associate,

17:27

and this is why we haven't been removed from it.

17:29

But as long as you associate the flow limitations

17:33

with an anatomic lesion,

17:34

then you know you're on the right path.

17:36

So we would take this pen here to that 25 hyphen,

17:41

49% s stenotic lesion right there

17:43

and see if there was any flow limitation.

17:45

Typically, as you'd expect, 25

17:47

to 49% stenosis does not have a flow limitation

17:50

or physiology associated with, so that's a very good example

17:55

of a lesion that has 50 to 69% anatomic

18:00

and no flow limitation

18:01

and a lesion with 25 40 9%, uh, anatomic

18:05

and no flow limitation, um, along in there.

18:09

Alright, so let's go back to Tara recon.

18:11

Any questions on that one?

18:12

That's a, that was a big chunk of, uh, of information.

18:20

Alright, so let's go to the RCA

18:25

and we'll just, uh, run out the RCA while we're still here.

18:29

So, uh, you just saw this image here, so there's

18:32

that mid RCA, uh, low attenuating plaque, uh, lesion.

18:37

Again, if we wanted to just straighten it

18:39

and just look at it, we can just already tell

18:41

that it's less than 50%.

18:42

If we added the contour lines to that, we can see that, um,

18:46

it's not touching the green yet.

18:49

Um, so we're good there.

18:50

If we wanted to do a plaque analysis, uh, we can then, um,

18:54

you know, estimate the RCA

18:57

and then do a, uh, coronary, uh, segment plaque analysis

19:01

and then get an idea of what that looks like.

19:03

And you can see then it's already, it's segmented

19:05

that region out there.

19:07

And so then therefore what you're seeing here in terms

19:10

of pixel, uh, analyses is associated with the plaque.

19:15

Okay, so questions on that? No. All right.

19:18

So how would you write this up,

19:20

Lawrence, how are you?

19:23

Very good. How are you doing?

19:25

I'm fine, thank you. Uh, just a question on

19:28

that stenosis in the, uh, left anterior descending, uh,

19:32

would you call it a napkin ring stenosis given

19:34

that low attenuation adjacent to the calcified plaque?

19:38

Oh, great idea. So morphologically speaking,

19:40

how do you characterize the plaques?

19:43

And so again, please excuse the, uh,

19:46

spatial resolution like I mentioned, CPR

19:49

and then straightened NPRs.

19:51

They don't do very well.

19:53

They just don't because they were not designed for that.

19:56

Um, so you would have to try

19:57

to evaluate this on the axial.

20:01

And so if we look at then

20:03

and try to find then high risk clock features, um,

20:07

as you mentioned that there are quite a few different ones.

20:10

So, um, in most cases, if you identify one out

20:15

of the four that are potentially available,

20:18

positive modeling, napkin ring stapled,

20:20

and the low attenuation, then you've met the,

20:25

uh, the intent of identifying

20:28

that this plaque is plaque that's vulnerable.

20:31

Now, vulnerable plaque is also the type of plaque that is,

20:35

uh, potentially can be changed.

20:37

So if we did sequential coronary CTAs pre

20:40

and post statin treatment as an example, we would see

20:43

that the amount of low attenuation in year would change

20:47

and decrease comparatively to the calcium component of it.

20:52

So, um, identifying all three

20:54

or all four, you know,

20:55

high risk plaque features not necessary.

20:57

If you identify one and indicate

20:58

that there is high risk plaque features, that's fine.

21:01

The overall movement into doing something

21:04

or not really isn't on the amount of plaque,

21:08

although Scott Hart too will probably show that you should.

21:11

What really is right now is defining management is the

21:14

amount of luminal stenosis.

21:16

Where this comes in is typically, um,

21:19

where statin plays a role,

21:20

and statin typically plays a role in the amount

21:23

of low attenuation, um, plaque

21:26

because it can remodel that out

21:27

to calcium plaque, um, and so forth.

21:30

So I like what you're thinking, like, well,

21:32

why don't we should be, you know, morphologically, um,

21:36

astute, but if you can identify one

21:38

of the, of the features, that's good.

21:39

Now, I do see some stipple,

21:41

or at least some calcification within there.

21:43

I typically call it per calcified plaque.

21:46

Um, I do mention if there is a significant,

21:49

or at least a qualitative increase in the amount

21:51

of low attenuation compared to high attenuation,

21:54

and then call that low, um, uh,

21:56

a vulnerable plaque for that reason.

21:58

Okay, with regards to, um,

22:02

cal staple calcification.

22:05

So I also, uh, describe it as either calcified

22:08

or noncalcified plaque,

22:09

but is there an objective measurement for the calcification

22:13

if you're seeing it like, uh,

22:17

less than two millimeters or is there any way to say

22:23

So? Um, this

22:24

is, It is a difficult

22:29

determinant, but there is ways of evaluat indicating clearly

22:33

that there's, uh, stip calcification

22:36

and where you're, you, what you're looking

22:39

for then is the absence

22:40

of this large chunk of calcification.

22:43

Okay? And, and if you have a low attenuating plaque, um,

22:49

that does not happen,

22:50

but then it has, um, absence of that large,

22:53

but then little areas just like even this here, then

22:57

that would count as being stifled.

23:00

Now that all that just means is

23:02

that we're catching this plaque

23:04

a little bit earlier in its evolution

23:06

to become then this area here.

23:08

So it's not a discreet, um, type of calcification.

23:13

It's temporally, an earlier calcification that is,

23:18

um, solidified.

23:19

That is, is that it, it's usually not a bother.

23:22

Um, so we're catching it early,

23:24

hopefully then we can do some OMT

23:26

optimized medical therapy for that.

23:28

Um, I will have some examples, uh, that we will probably go

23:33

through in the next couple of exams here.

23:35

The other great one that, uh, has good fidelity

23:40

across is the, um, CAD RADS two PDF.

23:44

It shows what's what it means by stippled

23:47

and it's just little dots of calcification

23:49

that are probably, like you said,

23:51

less than two millimeters, one millimeter.

23:54

The problem with arranging

23:55

or announcing a number two millimeter,

23:58

anything less than two millimeter calcification in

24:00

and around the area of, of plaque lesion is

24:02

that the spatial resolution changes it.

24:04

And then also the kilo voltage changes how much blooming.

24:08

So if you have an older machine, uh, the amount

24:12

of blooming would just essentially make all this look like

24:16

one large calcification.

24:17

Whereas if you had a newer machine,

24:19

higher special resolution, a lower lower kilo voltage,

24:23

you are not gonna have that much blooming.

24:24

And then you will see stifled plaque in there.

24:29

Okay, thank you.

24:31

Yeah, of course. Okay,

24:34

so the writeup on this one again is CADRAD three.

24:37

This had, um, high risk plaque features, um,

24:40

and severe amount of qualitative plaque.

24:43

If we did the quantitative assessment

24:45

of all the coronaries together, we would come up

24:47

with a number that we can pre

24:49

and post, uh, eval following treatment.

24:54

So, um, yeah, that's a pretty nice one.

24:57

Alright, so let's go to our next case here.

25:07

All right, let's get rid of this chest wall.

25:11

So the writeup on this guy was a 68-year-old male history

25:15

of recurrent chest pain, equivocal stress, ST

25:19

and t wave changes suggestive ischemia at peak exercise.

25:22

So under stress, they're having electrical changes,

25:24

but no evidence of ischemia on spec.

25:27

While SPECT is one of the worst ways, uh, in terms

25:31

of spatial resolution of evaluating, um,

25:35

disease from a functional assessment standpoint.

25:37

And the reason is, is because the low spatial resolution

25:41

hasn't really improved across, well, probably three decades,

25:46

um, at least three decades of time.

25:49

And so we have quite a few different, uh, studies

25:51

that have proven the, the comparative, uh, usage

25:57

and the sensitivity specificities

25:59

specificities according to gold standard.

26:02

Now, why do we still use it?

26:03

Why is it still, is there a penetration

26:06

of SPECT imaging across the enterprise?

26:10

Because it's cheap, the amount of services,

26:14

resources available, um, seems to be

26:16

that this is an extremely, um, capable system

26:22

and it does have a sensitivity that is, if it is negative,

26:26

it's gonna be negative.

26:27

Now, the problem is you have to choose the correct patient.

26:30

So if you pretest probability a 68-year-old male

26:35

and he's having currency of this chest pain, um, I,

26:39

I don't think functional is the right way to go.

26:41

I think anatomic. And so the anatomic is the right way.

26:44

So let's take a look at his anatomic.

26:47

Looks like we got a couple questions here,

26:49

and let me, uh, answer these real quick here.

26:51

Um, how do we classify the coronary arteries into large,

26:55

medium and small vessel?

26:56

That has to do with size.

26:58

Um, anything large than five millimeters is considered

27:01

large, um, or dilated

27:03

or maybe aneurysmal if it's somewhere around at seven,

27:05

which is a one and a half times the size

27:07

of a quote unquote normal.

27:09

So you'll typically see the LM somewhere around, uh,

27:13

five if it has a, an appropriate amount of, um,

27:16

of nitroglycerin.

27:17

Now, it doesn't obviously hang out at this, um,

27:21

high, uh, stage.

27:22

So here we got 4.9 millimeter, so five, um,

27:25

but it, it will react to that.

27:27

And so we are taking, um, an abnormal physiology

27:30

and saying that's the normal.

27:32

So five is the, the post NTG dilation of the vessel.

27:36

Now these vessels are typically at rest, they are dilating

27:40

and they are constricting,

27:41

but they're doing that with physiology.

27:43

So we could catch it at five if you're running

27:46

or just doing activity

27:47

or you're an 18-year-old male, for instance.

27:50

So five, um, millimeters or is considered large, um, three

27:54

and a half, you know, three to four is that medium size

27:57

and small is, um, anything less than three.

28:01

So three to 1.5 millimeter.

28:04

Um, because 1.5 is your cutoff for spatial resolution

28:08

for invasive coronary angiography.

28:10

So we may not be able to see 1.5 in terms

28:13

of our spatial resolution on, um, on coronary CTA.

28:17

Let's see what this vessel is.

28:18

This is probably, yeah, so this is saying that this is 1.5,

28:21

but would you feel confident in evaluating that vessel if

28:25

for, for disease?

28:27

I don't know. It depends. Probably not.

28:29

Um, keep in mind that this exam, I think I require this, um,

28:35

gosh, 20 18, 20 19.

28:37

So we're somewhere around five, six years.

28:40

Um, so that's a, that's a bit of time there in case one,

28:44

how do we differentiate between early

28:45

diagonal branch and ramus?

28:47

It's honestly not that big of a deal.

28:49

Um, but really the big thing would be is

28:52

that the ramus obviously comes off the lm so I'm looking

28:55

for a straight, if I see that the os osteon,

28:58

let's just take this one for an example here.

29:00

Um, if I see, um, a straight

29:05

of the OIA of whatever vessel, the branching D one

29:08

or whatever, then, then that's probably a ramus.

29:11

When I see the 45 degree angle of it, I believe, then

29:16

that's a branch and typically branches are 45, you know,

29:20

to 90 degree

29:22

and somewhere in there in terms of

29:23

what they're coming off on.

29:25

So this one here obviously is looks, um,

29:27

looks like a ramus to me.

29:28

And so I would, you know, I've said that in the report.

29:32

Uh, let's see. There were a couple other questions.

29:36

No, okay. Alright, well, so here we go.

29:39

So in this case here, 68-year-old male history

29:42

of recurrent chest pain, we're gonna

29:43

take the anatomic approach.

29:45

I always, again, I want, and maybe

29:47

because I like to tease the residents

29:49

and get 'em to kind of, you know, um, uh, you know,

29:53

just stand on their own two

29:54

feet and just tell me what it is.

29:55

So I I have them just kind of turn it around

29:57

and say, okay, come on, give me your,

30:00

your cad rads based on what you're seeing here.

30:02

And it could be shots in the dark

30:04

or it could just be seeing patterns of

30:06

how much disease here.

30:07

But if you look at the amount of disease before

30:09

and the amount of disease here

30:10

looks a little bit different, right?

30:12

Alright, so now we're gonna take a quick look at, at this

30:15

and see, and we find, um, find some disease that's,

30:20

uh, that's a bit of a problematic.

30:22

So, um, sinus of al Salva, um, left coronary cusp.

30:26

And so then we have to identify the osteo.

30:28

So if we identify the osteo, then um,

30:31

we have a problem here, right?

30:33

The problem here is that we have a osteo

30:36

or maybe sinus of el Salva plaque.

30:38

We got the calcification here, but we got this bad guy here.

30:41

So let's see what that looks like.

30:44

And we're just gonna come up over here. All right.

30:46

So I'm gonna make the, the bars disappear, uh,

30:49

because I'm pretty close to where,

30:52

where we can just take a look here.

30:55

Okay? Alright.

30:58

So that gives me probably, that's long.

31:02

That looks long. And this one here, we'll bring the,

31:05

the bars back here.

31:11

Uh, that one looks problematic, right?

31:15

Let's just bring that one up there.

31:19

Let's see if we can get a good view. Ooh, yeah. Am I,

31:30

this is why, um, being able

31:32

to do this on the fly is so fantastic.

31:38

I'll also plug that, uh, being able to evaluate

31:42

without post-processing is a learned technique.

31:45

It is absolutely not something that, um, we,

31:50

that you could just probably do effectively on your own.

31:55

Um, but it is, it is absolutely something to learn

31:57

because, um, if you do get cprs

32:00

and they don't show this, well then that's,

32:02

that's a bit of a problem, right?

32:04

And then if you don't know how to review it on the axial,

32:08

then that's also a bit of a problem here.

32:10

Okay? So once we're in line

32:12

with the vessel here in both long diameters here, we can see

32:17

that we have, we have an issue.

32:20

And this issue is right here.

32:25

So let's go take a look at this. Alright?

32:30

So we wanted to present a case where there was questionable

32:35

lm um, or osteo luminal stenosis

32:39

of par calcified plaque that was giving you the,

32:43

the heebie-jeebies, the one where there is 25 49

32:47

or something greater than 49%.

32:49

And see how many people decided to evaluate this.

32:53

Now, when, uh, I can re I remember this case, um,

32:57

I do recall having some difficulty identifying the,

33:01

like I just did here, the short, um,

33:04

axis and the long longs.

33:06

Um, but the individual did have disease

33:08

and it was persistent.

33:09

So what we ended up doing is, um,

33:12

because the follow-up, um, we did a,

33:16

a cardiac MR stress perfusion was also positive.

33:19

We sent the guy to, uh, to path, oh, I'm sorry, to cath.

33:22

And so when we sent him to Cath, what we noticed here is

33:25

that we were losing our spatial resolution

33:28

at the finest areas here.

33:29

So this is a five millimeter coronary artery,

33:31

and we're not quite sure if we're

33:34

making the proper diagnosis.

33:35

It looks 25 49, but it could be more.

33:38

So let's swing over to the, um,

33:41

to the invasive coronary angiography here.

33:45

Alright, so here's the lesion

33:48

and that is the problem right there.

33:50

And that's where we're looking at.

33:52

And then the concern here.

33:54

And so as we start looking at this, um, you'd probably,

33:59

you know, gloss it over.

34:01

And I think a, it's not uncommon for most of the classes

34:05

to gloss this one over,

34:07

but what the idea behind here is that this is a blind spot.

34:10

This is a spot where we have disease, uh, we have disease

34:15

that, um, is concerning.

34:17

And this is what they call the widow maker, mainly

34:20

because this is not identified, it's confused with, um,

34:24

with valvular or sense of al Salva calcification.

34:27

But this absolutely does affect the amount of, um, of,

34:31

of downflow obviously because it's the LM

34:34

and it's the osteo lm.

34:35

So if you look at this imaging here, um, it doesn't,

34:38

you know, look that bad right

34:40

there and then right over here.

34:41

But on the ICA, we absolutely have some, um, disease

34:45

and how they nosed it in there, that that's a problem.

34:49

But the vessel is much larger than that.

34:51

And so, but the writeup was, it was 50%, um,

34:55

and at 50% or greater.

34:56

And so that is, that's the problem.

34:59

I mean, and that's, um, you know, an,

35:02

an issue along in there.

35:04

So we threw this in

35:07

because we knew that a lot of people would miss it.

35:09

It's a very difficult lesion to, to, um,

35:13

triangulate down into.

35:15

And it's one that is very often, um, passed by.

35:20

Uh, I think when I start looking at this, um,

35:25

I start thinking, well,

35:26

what are the things that I could use?

35:29

One is, is that, and let's go back to the on the,

35:32

this volume rendering over here.

35:34

I'm just gonna kind of, okay, so

35:40

I have almost a collar, alright?

35:43

A collar is something that wraps around, right?

35:46

So I have almost a collar of persistence.

35:49

So top look, that's low attenuation, low attenuation,

35:52

low attenuation, low attenuation.

35:54

So I'm nearly 50% as I'm cruising from superior

35:58

to the mid to the inferior portion of that vessel.

36:01

That should make you stop, make you then pull out, um,

36:04

a long and try to find a short access evaluation here.

36:09

Additionally, I think the other clinical components were

36:11

that we had an individual who had a very

36:16

not good history on terms of the function.

36:19

Okay? So that's the other issue.

36:21

Now we've got disease all throughout this thing here

36:24

that just looks terrible, right?

36:25

I mean, this is really bad disease right here,

36:28

the osteo LAD.

36:29

And if we start making our way along in here,

36:31

we have this peppered calcium

36:34

that just looks the chronic portions of it here.

36:37

So there are a lot of reasons to be concerned for the,

36:42

what you're seeing in the LM

36:43

because of what is being, uh,

36:45

distributed across the remainder of the, of the vessels too.

36:49

Now one thing doesn't necessarily lead to the other,

36:51

but um, it is important to kind of assess

36:55

and aggregate what you're seeing in the coronary arteries.

36:58

So in this one here, we said this was the RADS four B,

37:01

we had the ICA to confirm,

37:04

although the initial, uh, writeup was that this was a, um,

37:08

was not a cataracts four B, this was the rads, um, three.

37:12

Um, but the ICA obviously for the higher spatial resolution

37:14

and like pairs did show that.

37:16

So that's a really fun one

37:18

because um, you have a big fat vessel, it's osteo.

37:22

It could be a lot of different things,

37:23

but there's some concerns.

37:25

So I like that one. Was anybody surprised when we came back?

37:30

Uh, and you looked at your, your, um, your report

37:34

and found that it was not what you thought it was.

37:37

Did anybody have any concerns about that?

37:42

No. Okay.

37:44

So the other thing of course here is

37:46

that this looks like this is around 50%.

37:48

Um, we will just follow, um, you know, this vessel

37:52

just a little weighs here.

37:54

And we can see then that there's, um, in the LAD,

37:56

proximal LAD that there's, uh,

37:58

probably 50% worth of stenosis here.

38:00

Alright, so we got a couple questions here.

38:02

Let's, let's see if I can answer a couple of 'em.

38:06

Nope, no questions. Okay. Alright.

38:10

So four B um,

38:12

is the take home point on this case here.

38:15

Uh, really fun case, uh, that really challenged everybody

38:20

and I like throwing that one in once in a while just

38:22

because we have an opportunity to kind of discuss

38:25

how do we lean, how do we know

38:27

that there's potential disease?

38:29

And then also, uh, what is our job here?

38:31

It's to rule out, it's not to be specific.

38:34

The specificity comes with improved spatial resolution,

38:37

which is a technological advancements.

38:40

And so, um, with a significant amount of disease here,

38:43

that collar of low attenuation, um, I,

38:46

I have my spidey sense of mouth.

38:50

Alright, page three,

38:54

case three is our 58-year-old male history of shortness

38:57

of breath exertion, underwent, arresting, um,

39:02

SPECT imaging, uh, that revealed inconclusive findings

39:05

of reversible ischemia on the basal

39:07

to mid anterolateral segments, okay?

39:10

Versus possible wall attenuation artifact. Alright?

39:13

So we think, um, that there could be base

39:17

to mid ant lateral, uh,

39:19

so ant lateral typically is associated with

39:22

what coronary distribution.

39:24

So it's dealing with this anterior wall here, anterolateral.

39:27

So we're probably dealing with LCX.

39:29

Alright, so we've got a little bit of information,

39:31

but the idea around here is that we're going

39:33

to do a due diligence to the anatomy.

39:36

Um, course termination looks pretty good, very nice, clean

39:39

and good of ification.

39:40

Even D one looks pretty nice.

39:42

That's gonna be our area of interest, um, which is LCX.

39:46

And then, um, RCA looks fantastic, right?

39:49

Not a lot of disease. Well, let's go to the tail

39:52

of the tape here and then just see what we find.

39:57

Woo, right? Already we can see

39:59

that there's a lot more low attenuation in this

40:02

individual than on the prior.

40:04

So if we're gonna use that, uh, top to bottom technique, uh,

40:07

of following the long, um, axis of the vessel, we can see

40:11

that there is um, uh, an amount of plaque here

40:15

that's 25, 40 9% in the distal lm,

40:18

distal LM is not. Yeah,

40:21

Dr. Lawrence, um, I think you need to switch to telecon.

40:26

Oh, thank you.

40:31

Alright, so thank you. Good.

40:33

Uh, so you can see then on this particular one

40:36

here, let's go back.

40:38

We're looking at then the, um, the,

40:40

the vessel here on the volume rendering.

40:42

And we can see that there's a great opacification

40:44

of the LAD, uh, in diagonal.

40:46

Um, looks fantastic, right? I mean, really not much.

40:50

Uh, I mean if you start quizzically looking,

40:53

you're going like, oh, what about that?

40:54

What about that? But everything seems pretty good.

40:57

We heard that ant lateral base, mid ant lateral,

40:59

which is an LCX distribution might be our area of concern.

41:02

So we'll take a look at that one.

41:03

Um, but again, kudos to the opacification team.

41:07

RCA also looks fantastic. No big issues here.

41:09

So if we're gonna take an axial approach to evaluate this

41:12

and doing that, um, superior to inferior on the long axis,

41:16

we identified the LM off of the LCC

41:19

and we can see then we have disease already starting here,

41:22

but we're in the mid segment.

41:23

That is this right here of the vessel.

41:26

We've got 25, uh, or 24

41:28

and less in terms of the amount of luminal stenosis

41:32

we've got, um, a bifurcation, right?

41:35

So we've got LAD coming across here

41:37

and LCX right along in there.

41:39

So let's take a quick look at the LAD.

41:41

We've got this, uh, essentially, uh, the proximal aspect

41:45

of this lesion having, uh, complete calcification

41:49

in terms of the amount of plaque.

41:50

And then we have the low attenuation plaque right behind it.

41:53

And this is at the area of, um, bifurcation of the diagonal

41:56

where there's um, there's a good

41:58

chunk of plaque right along there.

42:00

So 25, 49 maybe in that, um, in that,

42:03

as it makes its way there and we start looking at this

42:05

and just kind of scrolling here, we're trying

42:07

to find the mid portion of it.

42:09

So we, on the long axis, we can determine then how much

42:12

of that long is affected.

42:13

So that's probably 25 49 along in there too. Alright?

42:17

Um, the other things to kind of keep in mind,

42:23

we make our way, uh, usually the, the vessel starts taper,

42:27

so we wanna make sure that there's a good taper.

42:30

Um, there's not abrupt taper.

42:32

Um, and so I, I try to keep that in mind as I'm looking

42:35

through here, but, um, both D 1D two look pretty good.

42:39

Um, a little bit of flack along there,

42:42

but you know, not the really that, that difficulty.

42:45

So let's go back to the LCX again, that ant lateral, um,

42:49

perfusion was the, the concern here.

42:51

And so even on the long axis, we can see then that there's,

42:54

um, there's a significant amount of plaque

42:57

that's being deposited and then osteo LCX.

42:59

Um, and so there is a, uh,

43:02

couple different obtuse marginal branches.

43:04

There's a really tiny guy right there.

43:05

We probably won't count that

43:07

'cause it's less than 1.5, uh, in diameter,

43:10

but so we'll this will be om one, OM two,

43:14

then we've got this guy coming at superiorly OM three.

43:18

And then we make our way to the distal segment of the branch

43:21

as it cuts through the atrial ventricular group here.

43:24

Alright? So that's our, um, area

43:26

of concern if you wanted to look at that one.

43:28

That one there is, um, um, probably corresponding to that.

43:32

And so now let's identify it, uh, correctly in terms

43:37

of the amount of stenosis.

43:40

We can do a couple different techniques.

43:41

Again, some people like the long, long access

43:45

and so we're going to make sure that we've got a good view,

43:56

Okay?

44:00

Time consuming. Yeah. Yeah.

44:03

Alright, so we've got, uh, a 90 here.

44:08

We're looks pretty 90 long in there.

44:12

So this is the short axis.

44:13

And we can see then that this, in addition

44:15

to positive remodeling, this is taking, um, 50%

44:19

and more in terms of the, uh, the amount of, uh, lumen.

44:24

And so that does look like it starts

44:26

to narrow a little bit more there,

44:28

but there's also some branches.

44:29

So along in here, 50 to 69% is what we're finding.

44:33

So let's take a look at this in a couple other ways

44:36

and see if we agree.

44:40

So we're gonna take that and with terra recon

44:45

or any post-processing, you should be able to, um, point

44:48

to oops, point to any of the, uh, uh,

44:59

lesions.

45:00

And then you can see there, that's,

45:01

that's our area of concern.

45:03

So let's just come up here and, uh, and take a look at that.

45:07

Now again, we're gonna evaluate this

45:12

across, and you can see then that there's,

45:18

in addition to the, uh, the blooming artifact

45:21

that's going on in there, we're, we're probably close to

45:23

that 50 to 69% stenosis.

45:28

Now, I am not a big fan of these cprs.

45:31

The reason is, is because they can tell you

45:34

only what you wanna see.

45:36

They can't tell you what you, you know, more than that.

45:39

Um, they, they're often trimmed.

45:43

There's artificiality.

45:45

I'm not a big fan, um, uh, of them in terms of,

45:49

but they, a lot of people get, they love

45:51

to see the coronaries just displayed.

45:53

You know, they don't, the, the work behind it is just hard,

45:55

but, so, um, I'm not a big fan of them, but, uh, so,

46:00

but there is 50 to 69% Enos and,

46:04

and, uh, vessel when we start looking at it in terms

46:07

of the long axis as we saw in the prior one.

46:13

Alright, let's go to this vessel track.

46:16

I always want like to see if this thing agrees.

46:19

There's just not enough photons in here, right?

46:21

Oof just gets really ugly.

46:24

So let's just follow this one along in here. Yeah.

46:29

And so we're right about

46:30

right here where it's supposed to be.

46:31

And you can tell that that's low attenuating,

46:33

that's the positive remodeling there.

46:35

So this is the remainder of the lumen and,

46:37

and this is all plaque

46:39

and it's, I mean, it's, it's a guess, right?

46:41

I mean, you're trying to guess on it.

46:43

Maybe if you come up to here, you, you're able to see it.

46:45

But this is probably where the space re So I,

46:48

I'm not a big fan of when we tried

46:50

to reconstruct the reconstruct

46:51

of the reconstruction, as you could see.

46:54

So anyway, this one was a CAD rats three as well,

46:57

proximal LCX, the corresponds to the functional assessment.

47:01

Um, this one here probably, uh, could go two ways.

47:05

One at CAD rads two, uh,

47:07

one a cadrad rebo functional assessment.

47:09

So now the decision, this is the really important thing.

47:12

You had functional that was equivocal that said

47:14

that there was some ischemic changes, um, in that area.

47:18

And then you have 50 to 69%, uh,

47:20

that you were seeing anatomically.

47:22

So you have a positive functional

47:25

and you have a positive anatomy.

47:26

What do you do next? What's the next thing you do? Do?

47:33

Well, it turns out that from the ischemia trial,

47:37

what the next thing you could do is you can

47:41

optimize the medical therapy because

47:42

that is a non-inferior treatment modality to stent.

47:46

And we got that information from the ischemia trial,

47:48

which is that we can keep people in there

47:51

and we can keep them going on.

47:54

So I think that's a very considerable way of doing it.

47:57

Again, positive anatomy,

47:59

positive functional stent is not only the,

48:02

the only way to do it.

48:04

Now, that is one way of looking at it, another way

48:08

of definitive, which is we put a stent in there

48:10

and then the stent has a definitive, um, you know, therapy.

48:16

And I think that's an another interesting, you know,

48:19

good way of doing things too.

48:20

So what I think is, as you, as the imager,

48:24

the diagnostic imager can get out of this is that

48:27

we should always know what the endpoint is and could be.

48:31

And so then therefore we can change things.

48:33

Do I believe that this is stent?

48:35

Do I believe this is 70, 99% stent?

48:38

You know, um, level of osi? Absolutely not.

48:41

Do I have a, a, a very squirrely SPECT that says,

48:44

unequivocally there is some functional issues here,

48:47

or it could be gut, you know, some gut crosstalk

48:49

or Yeah, do I see have an anatomy that yeah, it's,

48:53

it's kind of there, but not quite.

48:55

Yeah. So this is for me,

48:57

this is an optimize the medical therapy and evaluate

49:00

and see how the progression of plaque is.

49:02

Um, so I like to add those conversations

49:04

because we are part of the team.

49:06

And so your input in terms of,

49:09

because the ranges are so big, right?

49:12

The 70 to 99% range is crazy big in terms

49:16

of the clinical outcome behind that.

49:18

Is it closer to 70 OMT? Is it the 99%?

49:21

Are you telling me this guy's gonna die?

49:23

That's a different story, but it's in the same bucket.

49:26

So I find that same conversation at the CADRAD four A

49:30

or four B, um, is occurring at the CADRAD three, which is,

49:34

are you telling me it's 70%?

49:36

Are you telling me it's 50%?

49:38

And so I think being able to confirm that is very useful

49:42

for some of our funds.

49:45

Okay, so on that case here, we were trying to show

49:48

that there's a correlative to functional

49:51

and anatomic anatomy

49:52

that we can make an adjudication on this,

49:54

but it's not quite definitive.

49:56

And that's where the cat, uh, the guidelines are useful

49:58

because they could say, you can watch this,

50:00

you can do optimized medical therapy,

50:02

or you can go into an in, in an evaluation.

50:05

And what you could do in the evaluation,

50:08

the stent evaluation is, is, uh, cross the lesion

50:11

and then do an, uh, an invasive FFR.

50:14

So you're doing then a blockage

50:16

and seeing then what kind of flow limitation is occurring

50:18

with the, with the pressure wire.

50:23

Alright? All right. Fun. Fun, right?

50:25

Okay, so, uh, let's see if we can get

50:28

through the, this next one here.

50:30

rads, uh, let's see, week three, case four.

50:35

Do, do, do. Okay, it looks like we're still recon. Perfect.

50:39

Alright, so 54-year-old female with a history

50:42

of hypertension, family history, uh,

50:44

and she's got a new onset of chest pain

50:47

with exertion request for CCTA.

50:49

Alright, so you're starting to see that, uh, the, the,

50:53

the clinical, uh, demographics don't really change too much.

50:58

We can see a good opacification,

51:00

but what is one morphologic finding here that we are seeing,

51:04

uh, in some other ones, the squirrelly, uh, vessels.

51:07

What does that have to do with high resistance increase in

51:10

the surface area of the vessel, um, by

51:13

creating more tortuosity.

51:15

Um, so we do have longstanding

51:17

or definitive systolic hypertension.

51:20

Um, the major or the epic coronaries of the top here.

51:23

Um, you know, I would say probably what, what would you say?

51:27

Uh, three out of the, out of the, the four major,

51:31

the biggies are, are probably affected in terms of the,

51:34

uh, technique and quality.

51:35

We've got, uh, the majority

51:37

of the contrast on the left side of the system.

51:39

That's a very good way to go.

51:41

Um, so let's go ahead and review this one.

51:44

Um, um, lemme make sure my notes look good here.

51:50

Ah, yeah. Okay.

51:57

So what I think is always fun is as we're kind

51:59

of looking at this, and I'll just take one more, um,

52:02

one more review for you guys, great.

52:04

Opacification, right?

52:05

So does opacification to the distal coronaries indicate

52:10

that there's no obstructive lesion?

52:12

No, it doesn't because all we're seeing here is the,

52:17

um, endpoint of, of flow.

52:21

We are not seeing how that flow is occurring.

52:23

So we might have retroactive, we might have

52:28

contralateral, we might have parallel flow.

52:32

Flow is not always in series that is from LM to LAD

52:36

to all the way to the distal end and so forth.

52:38

So, and that's a good thing, right?

52:40

We want a system that's designed to have multiple channels

52:44

and a microvascular system in

52:47

between these larger vessels here that's allowing

52:49

for flow to occur.

52:51

Okay? So, um, don't get too excited

52:55

that you can see opacification to the distal tips

52:58

of the coronary arteries

52:59

and think, ah, there's no lesion here.

53:02

Um, because that's, that's, uh,

53:04

that's always a problem here.

53:05

Okay? So, uh, LCC lm very good, um,

53:11

uh, appearance of that, but what are we seeing here?

53:14

It's like the, you know, shoulder sign, the cutoff sign,

53:17

the, uh, you know, uh, reverse beak.

53:20

There's so many ways of describing then a, a stenotic

53:25

or a change in the contour and the caliber of a vessel.

53:28

Um, and that post stenotic dilation.

53:31

So it's not gonna be too hard to determine then

53:34

that this is our area of interest

53:36

and thankfully, you guys all got this one, correct?

53:39

I mean, this was not hard here.

53:40

So now we gotta decide where are we in terms of percentage.

53:45

Now, I would argue this amount of low attenuation,

53:49

no calcification in the osteo

53:51

or proximal part of the LAD, this is a do not go,

53:56

uh, do not pass, go, do not go anywhere.

53:59

Get this to a functional evaluation, um,

54:03

for potential stent.

54:04

And the reason is because it's not gonna get any bigger

54:07

or better and it's not going to, um, reverse that

54:12

amount of luminal narrowing, uh,

54:15

with any other thing other than, um, intervention.

54:19

So I'm, I don't think you need anything more other than

54:22

to see that if you start from the superior

54:24

and you make, make your way to the inferior,

54:26

you're still left with this tiny, tiny channel here, right?

54:29

And with the post NOAC dilation, um, to the remainder

54:32

of the LAD into the D one

54:34

and the septals, um,

54:36

there's really nothing else you need to do, right?

54:39

I, I think other than just indicating any, uh,

54:42

sequela from having that, now we do have, um, you know,

54:47

anomalous origin, uh, that, um, RCA, um, off

54:50

of the cyt tubular junction as opposed from the RCC.

54:54

Uh, but that's inconsequential, right?

54:56

LCX looks pretty good.

54:58

It's the, uh, looks like it's got a very nice

55:01

om and that goes out there.

55:03

So was there any disease anywhere else? Absolutely not.

55:05

Was there a disease here that was pretty easy to find?

55:09

Absolutely. Let's go to then another eval, uh, way

55:11

of looking at this just so we can

55:13

confirm what we were seeing.

55:16

And, uh, even without the, uh, the need for,

55:20

for too much in terms of regulating this appearance, uh,

55:24

I mean that's, that's pretty, pretty good, right?

55:27

So, uh, this wasn't too

55:31

different than, um, her ICA

55:34

and her ICA showed then that similar sort of, um,

55:38

cutoff sign as you can see right there.

55:40

So that's a, that's a severe lesion

55:42

that ended up being stunted.

55:44

So very exciting to see the,

55:47

and satisfying to see the correlation of, um,

55:50

different types of a modality, um, with this disease here.

55:54

Now we are seeing low attenuating plaque deposited in the

55:58

osteo LED, no calcification.

56:00

This is, um, she was how old? 54 years old.

56:04

So your question should be why?

56:07

What, and you know, where

56:12

that is, where why the wear of the LED right there

56:18

and the, hopefully if we take virtual,

56:20

there is a disturbance

56:21

and irregularity to the laminar flow, there is inflammation,

56:26

um, and there's potentially then, uh, vortal flow in

56:30

that space that's causing then endothelial damage.

56:32

Okay? O other potential things could be, um,

56:35

that typically at branch points is

56:37

where we're gonna see more of the damage.

56:39

Um, maybe not necessarily being hypercoagulable,

56:43

but she's got thicker elements in her

56:46

blood compared to somebody else.

56:48

And so this is rapid onset

56:51

of plaque deposition occurring in a very, very, um, um,

56:56

difficult area to improve with just, um, medical therapy.

57:01

So this would obviously require them

57:02

that invasion invasive therapies.

57:05

Any questions on that one?

57:10

Okay, last case, see if we can do this.

57:13

One quick 69-year-old male with a history of hypertension,

57:17

mixed hyperlipidemia

57:18

and pre-diabetes, new onset of shortness of breath.

57:21

Okay? So a lot of, um, personal risk factor there.

57:24

Um, males can, uh, can go a while here

57:29

in terms of, uh, deposition of plaque,

57:32

and so we can see a significant amount

57:34

of calcification VI guy.

57:35

You can see then that there's a bit more

57:37

quantum modeling around here.

57:39

The noise index looks a little bit, uh,

57:42

higher than the other individual who didn't have such an,

57:45

uh, uh, high degree of, uh, anterior posterior diameter.

57:49

Um, so the main thing, uh, to get across with this one is

57:52

what well, uh, that we've got, um, an evaluation

57:56

that requires them, um, astute EE uh,

58:00

evaluation for many different things.

58:03

Um, and so let's take then, then LCC

58:08

to the lm and let's just take a quick

58:10

look at what that looks like here.

58:12

So tiny bit of, um, positive remodeling, calcification,

58:15

plaque disease along in there at, um, you can say

58:18

that's at the distal LM right before the LED.

58:21

We've got, um, a few focal areas here

58:23

where there's an irregularity of the lumen

58:25

and part calcified plaque, little bridge,

58:28

but, um, it's a superficial bridge, um, not deep

58:31

and no luminal stenosis along there.

58:34

And then it pops up pretty well here.

58:37

Okay, if we take a look at the, um, LCX,

58:42

oof, that looks bad, right?

58:43

Not a good and not a happy LCX.

58:46

And then we've got some disease going along in here too.

58:49

So, um, this is certainly one

58:51

that does require some further characterization.

58:54

Uh, and so then we're gonna do that,

58:56

but we're just getting, uh,

58:58

I haven't given you your stake yet, right?

58:59

We're, we're not quite there yet.

59:01

So let's now take a look at this guy.

59:03

So RCA off the RCC, we can see then there

59:07

that we've got a significant degree of low attenuation

59:11

that is blocking the, uh, proximal segment.

59:14

Um, what do you guys think of that one? Bad, not so bad.

59:19

No big deal. Okay, big deal.

59:21

Well, if you weren't surprised by that

59:23

or that wasn't a big deal, look at down here.

59:26

Now this is always the trouble spot here,

59:27

and I'm gonna spend just a bit of time here

59:29

because the P-D-A-R-C-A-P-D-A junction is

59:32

oftentimes ripe with motion.

59:34

It, this is a difficult area to find

59:36

and everybody figures that this is gonna be the boogeyman.

59:39

They're gonna miss the PDA lesion.

59:41

Well, this is the PDA lesion that everybody's afraid

59:43

of missing, which is this low attenuation, uh,

59:46

complete non opacification of the osteum of the PDA,

59:49

um, as you can see here.

59:50

So we're gonna go to the superior aspect of it,

59:53

inferior aspect, and that low attenuation just stays there.

59:56

This is a non-Pacific cataracts five right at that, uh, PDA

60:01

as it makes its way there.

60:03

Um, the PLA looks pretty good.

60:05

There's just a little bit of plaque along there.

60:07

So why is it that all the plaque non-Pacific wise went

60:12

to the area with the lowest, uh,

60:14

or one of the smallest diameters, slowest flow.

60:18

Why did it collect there? Why is it occurring right here?

60:21

The why, why, why?

60:23

I've got some thoughts on it,

60:25

but I'm always interested in seeing

60:27

what everybody else's thoughts are.

60:28

But, uh, essentially we have a deposition in

60:32

the areas that are vulnerable.

60:33

Vulnerable areas are areas where there is tortuosity.

60:37

Vulnerable areas are the areas where there is slow flow,

60:40

irregular flow, or that there is flow, um, that um,

60:45

that's not quite, uh, capable in meeting the needs.

60:49

So by that I mean that we have regions proximal

60:52

disease in the LAD.

60:54

So we're shifting probably the overall amount of flow,

60:57

not just from here, but probably over here

60:59

because this can't unfortunately get any larger.

61:02

So a lot more flow is gonna go into the RCA than typical.

61:06

So our at, um, axiom that the PDA

61:10

and the distal RCA gets a slow flow, low flow situation

61:14

goes out the window when you had disease in the other areas

61:17

and you have to put more flow into a

61:20

contralateral uh, schema.

61:22

So here we've got the RCA, we've got the proximal 50,

61:24

69% here, another, uh, focal lesion here,

61:27

but it's really right here at the PDA, um, uh, interface

61:32

that I want, uh, gets your eyeballs on.

61:34

So distal RCA in here.

61:36

And so I'm gonna remove these lines here just

61:38

so you can just follow this right there.

61:41

And unfortunately, regardless of how much twist turn we go,

61:44

that plaque just stays there completely occluding.

61:47

We can do our, um, our long

61:49

as long access diameter and see them.

61:51

That's a similar sort of thing here.

61:53

So this one was a CAD RADS five,

61:54

this is our first introduction in it.

61:56

You might see foot stomp,

61:58

foot stomp some more CAD RADS five in

62:00

the next week's lectures.

62:01

Um, but this is absolutely one that we should be catching

62:05

regardless of all the difficulties in terms of noise index,

62:08

bigger person and some of the other things.

62:11

Um, this is the one unfortunately that a lot

62:13

of people over call,

62:15

but at the same time, um, don't find, so

62:18

we're introducing this now.

62:19

So you can take a look at it, play with it, enter recon,

62:22

and see how would you be able to find physiologically,

62:25

why would this situation be set up?

62:27

And if you remember what I just said, I think the,

62:29

the movement of flow to the RCA from the LAD secondary

62:32

to all that chronic plaque in there was why there's more

62:35

flow in there and therefore more endothelial disease.

62:38

Alright, I'll stop right there.

62:39

Um, I apologize going over time,

62:41

but if you have any specific questions,

62:43

please, uh, let me know.

62:45

Um, or email me. Hi

62:47

Dr. Lawrence. Yeah,

62:48

Uh, can I ask a few before we jump off?

62:52

Let's go. Okay.

62:55

Um, so just I, in terms of quality of the study, uh,

62:58

there's less opacification of the left ventricle

63:01

and the coronary arteries compared to the previous case.

63:04

It's still, um, uh, it's still fine for reporting.

63:07

However, I wanted to know are there any hard limits we

63:10

should take, uh, for non-diagnostic study

63:13

or we should just go with theq value all the time,

63:16

Right? Yes. So

63:17

you have a, a household unit value, 2 50, 2 30,

63:21

somewhere around there to indicate a good of ification.

63:24

It is also useful to have a discriminatory where most

63:28

of the contrast, like you said, is in the left system

63:31

as opposed to the right.

63:33

That is unfortunately not enough, um, in terms

63:37

of when you have a non motion artifacts,

63:40

uh, coronary system.

63:42

So if there's no motion in the vessel

63:44

that typically has the most motion

63:46

because of the swing apical swing long here

63:48

and you can see it pretty well, unfortunately

63:51

we're on the hook for evaluating this now we're getting

63:55

to the point where the spatial resolution of two millimeter,

63:59

um, you know, 1.5 millimeter comes into play.

64:02

So as I've sat on reviewed some of these cases that some

64:06

of my colleagues, including myself, has missed in the past,

64:09

when we get down to that two 1.5 millimeter, I don't think

64:13

that we're held to that standard as if we missed it,

64:17

you know, at the, at the osteo

64:20

Mm-hmm. Including

64:21

then the use of the term n which is, um, unable

64:25

to be, um, evaluated.

64:27

I see too many people utilizing

64:29

that in the PDA distal RCA distal LCX

64:34

to describe them, that it's a low resolution

64:36

spatial resolution system.

64:37

That's not the case. The idea behind the n are unable

64:40

to be evaluated, um, in terms of that moniker is

64:43

that in a normal segment to be normally evaluated,

64:48

you can't see it because of motion

64:49

or some other opacification issue artifact or whatever.

64:53

Um, so unfortunately we wouldn't be able

64:56

to use an end on this

64:57

because there's no motion that would be

64:59

typically expected for this.

65:00

And unfortunately, I believe the size

65:02

of this looks like it's gonna be two millimeter

65:04

to two and a half millimeter.

65:05

So we should be able to then to agree

65:08

that at least it meets the spatial resolution of evaluation

65:11

for coronary CTA.

65:13

Okay. And uh, lastly regarding the complete occlusion

65:16

of the PDA, uh, there is a distal opacification

65:20

beyond that occlusion.

65:22

So is that opacified via collaterals

65:25

or is there still some contrast getting through?

65:28

Absolutely. That's the, the, the finest thing to take out

65:32

of this is that, and I I,

65:34

and I hit upon this maybe two times in this lecture here,

65:37

uh, in the discussion, is that

65:39

what we are seeing is the epic coronary,

65:41

as the end all be all

65:42

of the coronary system is completely false.

65:45

We are probably seeing less than 20%

65:47

of the total vasculature of the heart, 80%

65:51

of it is at a resolution at as a connect dome, as a,

65:55

as a network that we're not imaging yet huge opportunities

65:59

for all of us to, to innovate in that space.

66:03

But just because it's large doesn't mean

66:04

that it's the totality of it.

66:06

And in fact, these are, uh, in series vessels.

66:11

So in series from proximal mid to distal, when you get to,

66:16

um, to parallel where then the parallel of,

66:20

of how this interacts with this branch and this branch

66:23

and all that branch and all this all

66:25

around in the microvasculature, that's, that's what we're

66:29

should be mon uh, mentoring and discussing and stuff.

66:32

And we're not even there. We're not even imaging you yet.

66:34

I mean, it's so fantastic

66:35

that we think we're doing coronary evaluation when we're not

66:38

even seeing 80% of the coronary tree. I love it.

66:42

Okay, With that, um, I appreciate your guys' time.

66:45

Thank you so much. Uh, please keep, you know, working hard.

66:50

You guys are doing great. We're,

66:51

I think we're in week four right now,

66:53

so you guys are, you guys are doing great.

66:55

Keep it going. Uh, keep going strong.

66:58

Okay. Yes. Thank you. Thank you Dr.

67:00

Lorenz, and for staying on a little

67:01

long to answer questions.

67:02

Um, I do see we have one more question, the chat,

67:04

but I will email that to you, Dr.

67:06

Lorenz if you're able to answer.

67:08

Um, don't wanna keep you past the time.

67:10

But thank you again, everyone, this is being recorded

67:13

and will be made available

67:15

to you within the next couple of hours.

67:17

I'll be emailing it to you individually. So thanks again Dr.

67:20

Lorenz and everybody. Have a good rest of your day.

67:23

Take care. Bye.