0:00

Hi, everybody.

0:01

Thank you for joining us today

0:03

for the second lecture with Dr.

0:05

Lorenz for the cardiac CTA online training course.

0:08

Just a reminder, if you have any questions, you can ask Dr.

0:11

Lorenz directly.

0:13

Um, you can also use the hand raising,

0:15

um, uh, hand raise emoji.

0:16

We will call on you, or you can also put your question in

0:19

the chat chat.

0:20

So, Dr. Loren, whenever you are ready.

0:24

Great. Hi guys. Hope everybody is well, thanks again.

0:27

Sorry, I was, um, I was in the lecture too,

0:30

and, uh, I'm sorry,

0:32

office hours too, instead of lecture two.

0:34

So got a little mixed up here, but here I am.

0:36

And here we go. So, one

0:38

of the nice things about having at least two weeks under

0:41

your belt is, is that, you know,

0:42

you can understand the anatomy, you understand the basics

0:46

of CT and acquisition.

0:48

Now it's gonna be the, um, can you talk the talk,

0:51

which is being able to then to describe why we're doing it,

0:54

what is the accuracy, the benefits,

0:57

and as well as the limitations.

0:58

And so what this, that's what this, um,

1:00

presentation in the next 45 minutes is going

1:02

to help you, uh, do.

1:05

So, um, what is CT angiogram?

1:09

Um, what is CT A or CT angiogram of the coronary arteries.

1:14

And so that's one of the components behind strengths,

1:17

which is that being able to have a high spec resolution

1:19

examination of a moving structure.

1:21

So not just something in the neurovascular bundle

1:24

for neurovascular, um,

1:26

or down in the, um, abdomen that it's, yes, it's pulsitile,

1:30

but it's not this kind of pulsitile.

1:32

So here we're gonna, uh, dive into that.

1:34

We're gonna talk about the accuracy

1:36

and then also some of the results, um,

1:38

that we can then conclude from in terms of

1:41

how this test changes management.

1:46

So, uh, strengths, that's obviously one of the big things

1:49

that we always want to, uh, get across here.

1:52

Uh, so one of the things with, uh, with that is then,

1:57

um, the sensitivity.

2:00

Um, so sensitivity, being able to say

2:02

that something is not there, right?

2:04

So getting it out.

2:05

So is the chest pain due to coronary arteries? Yes or no?

2:10

Well, um, that is one of the basis behind this examination,

2:14

and it is so good, so strong

2:17

and so useful that it has a level two a, uh,

2:22

recommendation in terms of, um, of meeting, uh,

2:28

determination of that the coronary disease is part of the,

2:33

um, problem of chest pain.

2:35

But in terms of sensitivity instead of in, in terms

2:38

of getting it out, that is saying

2:39

that the coronary arteries are not the problem.

2:41

It's a one A, which means it is the first line,

2:45

the best thing to confirm

2:46

that the coronary arteries are not.

2:48

So a lot to unpack there,

2:50

but we'll get into that in a few, in the few next slides.

2:53

The main thing to remember is sensitivity.

2:55

Saying something is not the causative

2:58

factor behind something.

2:59

So causative.

3:02

This has the best, the anatomy of the corneal arteries

3:06

and what you are able to see in terms

3:07

of origin course termination,

3:09

and then luminal blockage, gen noses and so forth.

3:12

This is one A, this is the best thing you can do

3:15

or we can do right now.

3:17

Um, and so that has a lot to go with it.

3:20

So that's the powerful prognostic portion of it.

3:23

The safe and effective, of course, as you

3:25

and I know reading a hundred coronary CTAs a day is, is

3:29

that the amount of dose that is given to an individual

3:32

by this examination is not even close to any other type

3:36

of do type of dosing exam.

3:37

By that I mean our functional nuclear imaging, um,

3:41

and some of the other types of testing, SPECT and PET and

3:44

otherwise, okay.

3:47

So a lot has happened, um, in this world.

3:51

And so we're going to talk about, um, some studies

3:54

that have occurred from 2008 all the way to 2022.

3:58

Now, new data continues to operate in this area,

4:01

but there's actually been a paucity

4:03

of data recently in the last two years.

4:06

Uh, can anybody under, uh,

4:07

gimme a good reason why we haven't had so much good, um,

4:11

data come out in the last two years, uh, related

4:15

to coronary CTA angiogram?

4:16

Anybody want to give a guess?

4:19

One of the reasons actually is Photon County.

4:22

There has been such a change in the spatial resolution,

4:24

in the temporal resolution capability of being able

4:27

to bend every single photon

4:29

and get rid of the noise that is involved.

4:31

Um, that used to be involved in sation

4:34

incitation absorption.

4:37

Now, it, it's getting to the point where we have

4:39

to reassess, um, individuals based on the new technology.

4:44

And I ran into this recently in an informed

4:46

consent, and I'll get into this.

4:48

Uh, and this is why it's important to kind

4:50

of look at the trials and particularly the informed

4:52

consenting is the do know a horn portion of it.

4:55

And are you necessarily increasing somebody's harm now

4:59

by standard convention or conventional, um, dosing

5:02

and conventional, um, acquisition?

5:04

The second and third generation CT scanners

5:07

that are out there absolutely are considered conventional

5:10

and standard, uh, of care.

5:12

And that would fall under, again, that one a sort

5:14

of evidence in terms of being able to provide

5:17

that spatial and temporal resolution.

5:19

But photon counting is, and I'm not a spokesman for them,

5:22

but the photon counting is such a complete change

5:24

in the amount of dosing.

5:25

It is such complete change in the spatial resolution.

5:29

We actually have had to pause

5:30

and determine what kind of additional harm could we be doing

5:34

to individuals who are not, um, who are not receiving

5:38

that type of exam.

5:39

And they're are receiving a different type of exam.

5:41

Now, it, it's, again, it's more than theoretical,

5:44

but at this point, and yes,

5:46

it is a statistically different significant

5:49

and different dosing,

5:50

but it's still following the standard of care

5:53

and the convention of acquisition.

5:55

So we can't get in too much into just saying, well,

5:57

everybody must have a photon counting.

5:59

But it is something you may want to look at this data

6:02

and determine as we progress from 2008

6:04

and the type of dosing and the type of spatial resolution

6:07

and how well it made a change there to then.

6:09

Now, the new revolutionary change was occurred now

6:11

with this new technology and how well that's making things.

6:15

So put that in the back of your head.

6:16

But let's talk a little bit about some of these trials here.

6:19

So these trials from 2008, uh, to about 2017, uh,

6:23

and broken up into columns of sensitivity

6:26

and specificity, negative predictive

6:27

and obviously positive predictive values.

6:29

And then what the, what the gold standard reference was.

6:33

Main one should be obviously invasive coronary angiogram,

6:35

obviously because of the spatial resolution in there.

6:37

And what you find is that sensitivity is gonna be the

6:40

main component behind that.

6:41

The specificity is going to fall apart comparatively to some

6:45

of the functional imaging,

6:47

but obviously to invasive coronary angiogram,

6:49

it's just not gonna hold as well, right?

6:51

Just because of the line pair resolution comparatively to

6:55

how ct, um, spatial resolution is.

6:58

So on a per patient basis, coronary CTA identified stenosis

7:01

of equal or greater than 50%

7:03

with high sensitivity across everything, 85 to 99%,

7:07

if you're above that 80, you know, 85%, uh,

7:11

threshold range in terms of sensitivity, that is,

7:14

that's a, that's the positive, right?

7:16

That's the odds ratio. That's the, that's the, the p value

7:19

that we're looking for is 85% on on that standpoint there.

7:23

The negative predictive, um, takes an unfortunately, uh,

7:25

a wider interval.

7:27

So then, uh, unfortunately you can see sometimes a dropage

7:31

behind that, but essentially in terms of the sensitivity

7:34

to the negative predictive value,

7:35

but essentially it should correlate right, high sensitivity,

7:38

a very high negative predictive value behind it.

7:42

Okay, in histogram form here,

7:44

we've broken it out as you can see.

7:46

Um, and then again, using something such as FFR

7:50

for instance, we can see then

7:52

that there's a significant sensitivity

7:54

and specificity as well.

7:57

So I think I might have shown this last week, um,

8:00

because this is kind of a, an important way

8:02

of demonstrating then that technology does make a change in

8:06

terms of the improvements in spatial resolution, in terms of

8:11

how the net correlates into sensitivity and specificity.

8:14

So always be looking for the better newer technology

8:19

and seeing how it could potentially change clinically your

8:22

sensitivity and specificity.

8:24

And so, um, coronary CTA,

8:26

obviously the sensitivity sensitivity's great.

8:27

And so this number here, this is the one that I'm kind

8:30

of hinting at, is going to be a, a change in terms

8:34

of the specificity with the new photon counting systems.

8:39

Okay? So performance, uh, sort

8:42

of chatted about this a little bit in terms of, uh,

8:44

non-invasive imaging modalities.

8:46

And so this is a comparison, comparison

8:48

to non-invasive to non-invasive.

8:50

And you can see then very, very high marks here, again,

8:53

for sensitivity in terms of usage

8:55

of coronary CTA compared to everything else.

8:57

The specificity, again, non-invasively has, uh,

9:01

utilizing then 28, uh, 2008 to 2018 data, uh,

9:06

when this paper came out.

9:07

That's the drop there.

9:08

And we can explain that we've got a range of 10 years worth

9:13

of innovation change in scan technology, um, that, you know,

9:17

um, has not changed.

9:18

What's interesting is that, um, some of these, uh,

9:21

technologies haven't budged at all dependent, uh, regardless

9:26

of how, you know, how much time has, uh, occurred.

9:30

So in, if you look at invasive coronary angiography,

9:34

if you look at PET

9:35

or spec, regardless of the amount of time, the sensitivity

9:40

and specificity had not changed.

9:42

So that should give you kind of an idea, well,

9:44

what is the cost effectness of something, um,

9:47

in terms of a technology?

9:48

Now, I'm not just ct, obviously, like you, I read, you know,

9:53

PET and spec and, um, MR.

9:56

And, and, and everything else.

9:57

So it's really interesting how some areas

10:00

of our ecosystem have improved in 10 years

10:03

and others have taken a much longer period of time.

10:07

Okay, so we're coming back to the F-F-R-C-T now.

10:11

And so F-F-R-C-T is a computational fluid dynamic

10:15

that is an an, uh, uh, an evaluation

10:19

utilizing synthetic, um,

10:20

and non-synthetic data resources available on the coronary

10:23

CTA and making assumptions of

10:26

what then the flow rate limitation is before and

10:30

after a, a lesion, and we call that then the delta.

10:34

And on a number of patients, um, uh, per patient

10:37

and per vessel, um, the usage of F-F-R-C-T obviously,

10:42

um, is as an additional improvement in that sensitivity

10:47

and specificity and a lot of different, um,

10:50

diagrams have shown this, this is the number one.

10:52

And, um, and then we can get into then how that's flown.

10:56

But before we move into F FFR CT

10:58

as a novel innovative technique, let's go back then

11:02

to the usage of coronary CTA.

11:04

That is the normal, just an anatomy behind it.

11:08

And so we have some really recent data that has come out,

11:11

and that's shown then why then,

11:13

and how this translates into saving lives.

11:17

So some of the really important data

11:18

that came out is in terms of interventions.

11:21

And so ischemia trial did show some really great ways

11:25

of intervention and interventional, um, outcomes

11:28

that is into reducing major adverse cardiac events.

11:32

So that was the main, um,

11:34

endpoint was major adverse cardiac events by, um,

11:37

interventions by utilizing standard

11:39

or non-standard, um, conventional diagnostics.

11:44

The non-standard conventional,

11:45

or the non-standard diagnostics was additional use

11:48

of coronary CTA as opposed to a functional approach,

11:51

which was the ECG, um, uh, spect

11:55

and then the ICA.

11:57

So if we were to just focus on their primary endpoint, then

12:00

what if you're, if you know, standard non-standard, um,

12:04

diagnostics, but then what is the endpoint?

12:06

We found that, um, medical therapy was,

12:12

had no negative, uh, comparatively to, um,

12:16

outcome in terms of, um,

12:19

reducing major adverse cardiac events compared to invasive,

12:22

um, therapies such as, uh, stent placement.

12:24

And that's obviously there's some caveats behind that.

12:27

We can carve out many different things

12:28

for the different subpopulation groups,

12:30

but the main message is, is

12:32

that medical therapy essentially will do a great job.

12:34

So what that means is, do you really need

12:37

to invasively move into therapeutics stents, um,

12:41

or cabbage or so forth?

12:43

Well, again, caveat out

12:44

that there are subgroups were absolutely 100%, yes,

12:47

it did show improvement,

12:48

but for the majority of, uh, patients all comers, um, no,

12:51

in fact, medical therapy did extremely well.

12:54

Okay. So if you are not looking to place then, um, a stent

12:58

or make a huge intervention, then perhaps then

13:01

how is the diagnostics going to change that?

13:04

That is if you fall into the categorization of, um,

13:09

functional assessment and then invasive coronary angiogram,

13:11

how does that comparatively change then outcomes

13:14

to then the non-standard care

13:16

where you did then an anatomic approach.

13:19

And what we found was that there was a change in outcome

13:23

that is individuals who received

13:25

a coronary CTA had a reduced major adverse cardiac event

13:29

output comparatively to those.

13:31

Now, there's a lot to tease out of that al versus corollary,

13:35

but I think as we've reviewed this data, a lot

13:38

of people have assumed then have come to the conclusion

13:40

that, uh, and an anatomic non-invasive approach

13:44

reduces the potential outcome

13:46

of stent placement in the diagnostic

13:49

to therapeutic transition in the ICA room.

13:52

So there is potentially

13:54

that if you can avoid being in the cath room

13:56

for your diagnostic,

13:58

that then potentially you can avoid then the conversation

14:00

of having stent being placed.

14:02

And so there's a lot to do with that.

14:03

A a lot of informed consenting in terms of diagnostic then

14:06

to transition to therapeutic catheterization, uh,

14:09

in the informed consent, um,

14:11

in some of the other techniques.

14:13

Now, um, let's move back here.

14:15

So what does this mean for us in terms of an imager?

14:18

If we do the coronary CTA evaluation,

14:21

we are actively changing the outcome at major adverse

14:25

cardiac events for our patients, mainly

14:27

because of we're doing a non-invasive approach

14:29

to determining the degree of plaque

14:31

and the degree of stenosis outside

14:34

of the cath room potentially,

14:35

or we are highlighting the role of early plaque

14:40

diagnoses so

14:41

that medical therapy potentially can then be utilized

14:44

to reduce down the Kaplan Meier curve for those,

14:47

um, individuals.

14:48

I think that's probably what it is, we're just preventing

14:51

and catching earlier as opposed

14:53

to maybe the invasive coronary angiogram.

14:55

That's what I like to think, but

14:56

ischemia really did show that.

14:59

Okay, so let's break down the data here.

15:01

Um, and so by a per vessel,

15:03

and then also by a per patient, there was, um,

15:06

very good strong evidence that showed agreement

15:09

between the coronary CTA

15:10

and obviously the invasive coronary

15:12

angiogram and LM stenosis.

15:13

So can it do it in terms of, uh, predict, uh, of evaluation?

15:17

Yes, it can. Okay, so that's great.

15:20

And so that's what we wanted, that's

15:22

what we wanted to see in that one.

15:23

Okay, so let's break it down into, uh, one vessel,

15:26

two vessel, and three a vessel and then disease,

15:28

and then, um, concordance versus

15:30

overestimation and underestimation.

15:32

And so what we found is, is as you would expect here, um,

15:37

that the coronary CTA is, um, had very good, um,

15:43

concordance in that, um, that, uh,

15:46

that one vessel in that two vessel, uh,

15:49

and potentially that three vessel component there.

15:52

It's when we started getting into areas that, um,

15:54

are much more difficult, um, in, in terms of the evaluation.

15:58

So smaller, um, um, vessel size, um,

16:02

and then potentially then motion

16:04

and some of those other things there.

16:10

So obviously there are variables that you

16:12

and I, um, run into every single day in terms

16:15

of the coronary CTA, um, that we have to just adjudicate.

16:19

That means be able to determine, use weights in our own, um,

16:23

experience, determine if this is appropriate or not.

16:26

Um, and a lot of this unfortunately, is things that you

16:29

and I just, um, if, if we're just starting our journey into

16:32

assessing, um, a structure in the body that MO moves,

16:37

and then being able to look at the picture of the movement

16:40

as opposed to into the actual motion

16:42

and then be able to do it, these things should not

16:44

become a surprise.

16:45

One of them, of course, is penetration, uh, so morbid, B,

16:49

CD, um, irregular heart rhythms, uh, rapid heart rates,

16:52

and, uh, presence of severity of coronary calcification.

16:55

Obviously the blooming effect is something

16:58

that is exacerbated by, um, uh,

17:01

spatial resolution, uh, septations.

17:03

And so then, um, there are some technological overcomes

17:07

behind, um, that component there in the, in terms

17:11

of affecting accuracy, which is again,

17:13

the specificity portion of it, not the sensitivity.

17:16

Okay, so contraindications, again, just a, a real quick,

17:19

just over draw, um, overview behind that.

17:22

Um, and you can see those there really, it, it's nothing

17:27

different than anything else.

17:28

I would highlight then that there are some medications, um,

17:31

that are soft calls, and so we,

17:33

we can potentially get into that.

17:35

Um, essentially what we wanna brew this down to,

17:37

and this is why ischemia continues

17:39

to be such a big importance in, in our world,

17:43

cardiovascular imaging,

17:44

and then obviously cardiovascular disease is finding the

17:47

right test for the right question and for the right patient.

17:51

And so there is a lot of

17:54

work in this pretest probability, um, pretest, um,

17:58

prediction and algorithmic prediction and guideline based,

18:02

and that derives from that.

18:03

And so we have a couple different types of chest pain.

18:06

Um, the,

18:07

and these terms obviously have changed, uh, recently

18:10

with the new, um, guidelines, but, uh, cardiac

18:14

and non cardiac, um, angina.

18:16

Um, and then, um, you know, angina that is, uh,

18:20

potentially then, um, you know, exacerbated

18:24

by other conditions.

18:25

Uh, so we can get into that,

18:27

but we really wanna find the right patient, um,

18:31

for this test or the other way around,

18:33

use this test for the right patient.

18:34

And so there's a couple different things

18:35

that we'll get into this caveat on this.

18:39

The evidence, again, for most in all comers, um,

18:42

is an anatomic approach, and that's a one a, um, evidence.

18:47

So this absolutely has its place

18:50

among all chest pain comers,

18:51

but you know, we then have the opportunity to dial down

18:56

to the right patient population.

18:58

Are they utilizing this test, again, those contraindications

19:01

and soft, um, concerns that we had before,

19:04

and then how that would affect then our, um, our accuracy,

19:12

Uh, to, to draw it out of this essentially is

19:15

as you get older and there's more calcification, then, um,

19:18

our, our prob pretest probability drops off

19:21

at being as an accurate test.

19:22

And that's essentially what these, um,

19:23

trials had indicated in the past here.

19:27

Okay? So not gonna draw too much into this other than, um,

19:31

that there are some, um, biomarkers

19:35

that are extremely impo important.

19:37

And so, um, the usage of some of these biomarkers

19:40

that we've, I just previously hint at F-F-R-C-T, um, plaque,

19:45

um, and some of these other ones

19:47

that are peri coronary can be utilized as well.

19:50

Okay? Pretest probability based on calculators.

19:54

And these calculators take on non-imaging calculations of,

19:57

um, sex age, uh, the type of symptoms and risk factors.

20:01

All these can be fed into an algorithm.

20:02

The algorithm can then be useful in determining then a

20:06

pre-test probability.

20:08

But basically with the low dosage

20:11

and with everything else, I don't think we're in the age

20:14

of pre-test probability anymore.

20:16

I think, um, coronary CTA should be consideration

20:19

as your frontline test for essentially everything.

20:21

But here are the numbers, um, in, in, in, uh,

20:25

in the agreement in terms of, uh,

20:27

confidence interval and so forth.

20:37

Okay? So identification of low risk, um,

20:42

in versus high lifetime risk.

20:44

Uh, one of the things that we, we can use this for is

20:48

what we call the warranty period.

20:50

And you may have heard about this.

20:52

The warranty is essentially that the, um,

20:55

pathologic accumulation of plaque calcified

20:58

and noncalcified in your coronary arteries take some time.

21:02

And so if you have a flash evaluation of the anatomy,

21:05

then you can give a warranty period of how, um,

21:08

those coronaries may not be involved in future

21:11

or symptomatic, um, anginal, um, uh, events in the future.

21:17

And so I, I find that, um, what this essentially means is

21:20

that if you don't have much plaque

21:23

and you've already seen it anatomically,

21:25

then you can just say then any future concerns of

21:28

of chest pain are not related to the coronary arteries.

21:30

And so that's what this, this essentially,

21:32

this histogram is trying to show.

21:34

And this correlates extremely well, as you can tell,

21:37

it becomes more 10 more tenuous

21:39

and more difficult to make those kind of assumptions, um,

21:43

in the future in terms of, um, increased stenosis

21:45

because of the amount, um, of vulnerability

21:48

that these plaques are undergoing across time

21:51

and across situations.

21:54

Okay? The prognostic

21:55

and advantage, um, from this Kaplan-Meier, you can see then

21:59

that if you had no coronary artery disease, uh,

22:02

essentially there's no risk of coronary artery disease, um,

22:06

relating in terms of relating then

22:08

to your major adverse cardiac events, uh,

22:10

whereas obstructive disease

22:12

and non-obstructive disease, um, have, um,

22:15

different Kaplan mires.

22:16

So let's focus on this yellow line here.

22:18

Essentially what we're trying to say here is, is

22:21

that if you make the call

22:22

of obstructive coronary artery disease, you are putting

22:25

that person in the, in the spiral, in the loop, in the,

22:29

in the component of let's continue to value this individual.

22:32

Now, keep in mind that the pathology of accumulation

22:36

of plaque in the accumulation of, um,

22:38

disease is a long-term event.

22:41

But if you have disease already there, the disease

22:43

that's in there is vulnerable.

22:45

And so we made some assumptions, um, on the lecture, uh,

22:50

last week and then in this lecture in about two hours,

22:53

I'll talk a little bit more about this,

22:54

but features that can make your disease,

22:59

whether it's obstructive

23:00

or not move into that, um, that there's a corollary

23:04

and causative from corollary

23:06

to causative is based upon those, um, those features

23:10

that we talked about in terms of the plaque.

23:11

And so there was a four of those features,

23:13

we'll talk about 'em a little bit,

23:14

but basically if you've said obstructive disease, so 50%

23:18

or above in terms of the stenosis

23:20

or high risk plaque features, then you are saying,

23:23

let's watch that individual a little bit more.

23:25

Whereas if you get to that individual in terms of 25

23:29

to 49% luminal stenosis, um, you know,

23:32

no high risk features,

23:34

then you are essentially saying the coronary arteries are

23:36

not a big deal, and you can use that for several years.

23:40

Okay, so what was the follow-up time

23:43

and the prognostic advantage?

23:44

Well, it depends on the type of exam, um, trial

23:47

and then what were the inclusion

23:49

and, um, exclusionary, um, components behind that.

23:53

I like confirm. I think that, um, was more of a,

23:55

a newer data, uh, that came out.

23:58

And, uh, so three years is probably a good call there.

24:01

I think some of these other ones here that, um, uh,

24:05

basically you can see the, the total population here.

24:08

Um, but I, I think some of these are a little, um,

24:11

not correct and mainly

24:12

because I'm seeing different changes in the coronary

24:16

arteries, uh, due to recent events

24:17

that we hadn't seen before.

24:19

Um, so I don't know if this amount

24:22

of follow-up data is something

24:24

that you should cite in your report

24:25

and say that, you know, coronary to clean, no need

24:28

to see you for another 11 years.

24:30

I think the three to five years probably

24:32

where most people are gonna lie.

24:33

And so we'll see that. But basically

24:34

what you're saying you're seeing here is that

24:37

what is the event rate?

24:38

If you did call it at that period of time

24:41

and less than 1%, you and I will absolutely take that.

24:44

Um, nobody would find you out of standard

24:47

of care if you were to indicate then, you know, three year,

24:50

um, follow up for a coronary CTA,

24:53

you know, and everything's fine.

24:56

Okay, event rate annualized, um, across populations, again,

25:01

um, based on the type of modality, the main thing again

25:03

to look out here is how well

25:06

the coronary CTA did in terms of the other modalities.

25:10

And so obviously the modalities

25:12

that are not an atomic base are gonna have a worse, um,

25:16

where, uh, histogram bar comparatively.

25:19

So we, um, we obviously don't want to lean on those as much.

25:24

So if we aggregate all of what we've talked about so far,

25:28

anatomy first, anatomy has preventive as well as prognostic

25:33

determinants into major adverse cardiac events.

25:36

A lot of that is in terms of the high sensitivity

25:40

and negative predictive value.

25:42

Those things are coupled to

25:44

and directly with spatial resolution.

25:47

The more you can see, the more you can say.

25:50

And so I think about this in terms of

25:53

what modalities in this

25:56

bar graph talks about this very cleanly

25:58

and well, what modalities are un undergoing the greatest

26:01

amount of innovation and improvements.

26:04

And so if you look at the improvement of technology

26:08

as a tool, prognostic tool tool in terms of itself,

26:13

you want to utilize the, in, uh, the innovation

26:17

as your leverage to get to the better type of examination.

26:22

And so, um, that's really, uh, what you and I

26:25

and everybody could do is we can say, what type

26:27

of examination or tool has undergone

26:29

the greatest amount of innovation?

26:31

Well, that's probably gonna be a better tool. Tool, okay?

26:36

So plaque burden is obviously one of those things, um,

26:38

that we've talked about in terms of, um, risk.

26:42

Um, and so you can see then the incremental improvement, um,

26:46

advantage there, that is,

26:47

if we can tease out the plaque burden, um, there is, um,

26:51

obviously an anatomic finding behind that,

26:53

but it also has, as you can tell, a,

26:56

a hazard risk associated with that.

26:58

Um, the other risk factors that are combined into, um,

27:02

here are those, um, family history, social history, smoking,

27:06

non-smoking, diabetic diabetes,

27:08

and so forth that are associated with it.

27:10

So we can see then that, um, that there is absolutely some

27:15

marginal improvement in the usage of plaque burden, um,

27:17

to determine then disease.

27:19

So if we could quantify it out or at least say it.

27:23

Okay, uh, we'll skip this one here

27:26

'cause we sort of chatted about ischemia already.

27:30

Coronary CTA, how does it directly, um,

27:33

move into improving outcomes?

27:35

Uh, it's essentially a 50% reduction in coronary vascular

27:37

disease and mi

27:39

and that's what that kapler mind, uh, curve, um, in, uh,

27:43

delta is right along in there.

27:45

So we have now evidence that shows that the utilization

27:49

of coronary CTAs by patient

27:51

or by population improves outcome.

27:54

That is, it's a reduction of myocardial infarction

27:56

and the overall reduction

27:58

of coronary heart disease related deaths.

28:04

So it is the first line test one a,

28:06

it is the cath lab gatekeeper.

28:08

I think we've sort of chatted about that in terms of how

28:11

that could affect, um, the outcomes in terms of, um,

28:15

major adverse cardiac events, risk stratification,

28:17

and prognostic capabilities.

28:25

Uh, any questions related to that one so far? No.

28:30

Okay. So I have one more that I'm gonna do a quick little

28:36

thing on if you'd like.

28:38

Does anybody have any questions so far on the,

28:41

the literature, the trials,

28:42

and in the, the, the talk portions of behind this

28:47

before we go into one more lecture?

28:50

Okay. So hopefully we're sharing this one here. Okay.

28:52

So let's talk a little bit about the novel technologies.

28:56

Um, the things that are constantly gonna improve.

28:59

Oh, looks, I haven't got a question here.

29:00

Role of CT angio in pediatric. Oof, I love it.

29:04

Yes, you're moving into the right direction here. Why?

29:07

Because there's a populational crisis in terms of per

29:11

cardiovascular, um, issues, right?

29:14

Obesity, hepatic steatosis, um, demineralization, uh,

29:19

lack of, uh, vitamin D

29:21

and all those have cardiovascular,

29:22

no neuro cardiovascular related things.

29:25

So where is the role of coronary angiogram in terms

29:27

of chest pain for that population?

29:29

But in terms of then the overall things that we're seeing

29:31

as risk factors associated into achieving for, um,

29:35

CBD related, um, disease?

29:38

Great question. I wish I could say that it, um, that it,

29:43

the, this data falls into that one A for the, um,

29:48

pediatric population, but it does not.

29:50

And why? Because nobody is willing to dose kids.

29:53

Now that is, um, that has to do with the informed consenting

29:58

and with the guidelines considering a difference in the,

30:04

the informed consenting capability of a child to an adult,

30:07

even though the BMIs are the same,

30:09

even though the penetration, the spatial resolution, um,

30:13

is the same there, uh, there potentially is then, uh,

30:17

a consenting to, uh, for a child

30:20

that is markedly different than an adult.

30:22

Now, the other thing to consider is what are the life years?

30:26

Um, and the interval, I would argue

30:29

that a child has more, um, population risk value.

30:34

That is how many quality

30:36

or, um, um, quali, you know, the Q-A-L-I-Y,

30:40

that many amount of years of valuation economically and,

30:43

and then socially and then ethically to, um,

30:47

to the population compared to an adult,

30:49

because obviously they should be living longer.

30:51

That should then be a considerate to then

30:55

coronary evaluation.

30:56

Now, let's be honest here, would,

30:59

do you expect coronary disease in a 13-year-old?

31:03

No, you expect some of the other things

31:05

that potentially are attributed,

31:07

so would then the number needed to treat that is how many

31:11

treated in avoided, um,

31:15

pediatric coronary related disease results in, in output?

31:20

It's gonna be a very high number.

31:22

So mainly

31:23

because we don't have as many children yet

31:26

with coronary artery disease.

31:27

Now that's gonna be a very difficult time in our world, um,

31:29

population in sister, when we do get

31:31

to there, is it gonna get there?

31:33

Oh, gosh, I hope not, but that's a great question.

31:36

So in terms of how we would look at this as an imager,

31:40

I would not turn away an individual who is at

31:43

that 16, 8 18, 20 year, you know,

31:48

um, age as long as a informed consent.

31:52

And as long as there is then a, um, a correlative in the BMI

31:55

and then the penetration so forth, do I expect that

31:59

to be a low risk exam?

32:00

Absolutely. Now, how can I do this?

32:02

I am leveraging CAC score evaluation.

32:04

So now I'm doing coronary calcium scores on the daily

32:08

of individuals who are there in their twenties and thirties.

32:10

And I'm finding disease, I'm finding calcified disease,

32:13

which should be a later biomarker compared

32:16

to noncalcified disease.

32:18

So I know it's out there,

32:19

but I think the number needed

32:20

to treat is gonna make this an expensive endeavor.

32:23

And because of the, um, dosage concerns,

32:26

which are not necessarily concerns

32:28

anymore, that's gonna be another thing.

32:29

But I think more importantly,

32:30

it's gonna be the informed consenting.

32:31

So hopefully that answers your question, but great question.

32:33

I love it. Okay, so let's talk a little bit about, um,

32:36

what is on the horizon here.

32:38

Again, this busy slide sort of talks about

32:40

where coronary CTA, um, plays a role into different types

32:44

of acute chest pain, known or unknown.

32:46

Um, and so we won't really have to worry about that one.

32:54

Okay, moving on. Moving on.

32:58

Okay, so let's talk about high risk plaque features

33:00

here, um, very quickly.

33:02

So high risk plaque, what is this?

33:04

And so we chatted a little bit about this.

33:06

This is the amount of plaque that occurs in, in

33:09

around the vessels,

33:10

and it occurs in, there are three layers, right?

33:13

So there is the endothelial layer, this, the,

33:16

the mid layer, and then the roal layer.

33:17

So this, um, vaso Zora where there is blood vessels, um,

33:22

there's arterials there, there's smooth muscle in there.

33:25

Those are highly perfused, highly, um, regulated areas

33:29

of the vessel that have monetization and surveillance.

33:33

That is, um, immune cells and, um, items that are moving

33:36

and directly working together to, uh, keep

33:39

that working well.

33:41

And they are highly attuned.

33:43

That is the nitric nitric oxide, um,

33:47

concentration in one portion of that vessel comparatively

33:49

to the, another portion of that vessel,

33:51

maybe five millimeters down the road, um, is very,

33:54

very discriminatory and very heterogeneous.

33:57

So in that milieu of, um, of an ecosystem here,

34:02

we have inflammatory changes that can occur,

34:04

inflammatory due to the cells being involved in there,

34:07

or items being, um, exposed.

34:10

Um, and so in the conventional way of evaluating it,

34:14

what this means is that there's too much of a good thing,

34:17

such as triglycerides, cholesterols, um,

34:21

and so forth that potentially are just within the blood pool

34:25

and they are seeping through

34:26

or causing a damage to the endothelial layer

34:29

and then seeping through and being absorbed

34:30

or, um, placed into storage

34:33

or, uh, causing them the inflammatory changes.

34:36

You can see as in terms of remodeling an accumulation in

34:40

that portion of the vessel, there is some very good evidence

34:43

that indicates then that this has to do with vi's, um, um,

34:47

principle discoveries that, um, at areas of, um,

34:52

high resistance, um, with low velocities, so stagnation

34:57

and then, um, coag, coagulability, hypercoagulable states.

35:01

Um, so inflammatory states is potentially then

35:03

where you're gonna see this occur.

35:05

And what do you find when you are

35:07

reading your coronary arteries?

35:08

Um, so far it seems to be at bifurcation points, it has

35:11

to be at areas that are high flow or low flow

35:14

or areas prior to, um, or at high resistance.

35:18

And so it's not uncommon then to see, that's

35:20

where we're going to find then the deposition of plaques.

35:24

There's a lot more science that needs

35:25

to be done into evaluating this area here from a

35:28

pathophysiological standpoint.

35:30

But, um, if we were to compare, you know, populations,

35:34

essentially the ones that accumulate, um, uh, more

35:37

of this in their blood pool seems to be more at risk,

35:40

IE the, uh, lipid, um, theory, uh,

35:44

and cholesterol theory behind disease, that more of it

35:46

that you have floating around, um, potentially then

35:49

that's the cause of nature behind this.

35:51

Uh, the potentially there, there are some very good evidence

35:53

for that and strong, strong associations,

35:56

but there's potentially more behind that.

35:58

So I don't want to put all my eggs in that basket.

36:01

Um, funny because eggs have a lot of cholesterol, uh,

36:04

but you know, 80%

36:06

of your cholesterol is created by your liver.

36:08

It's endogenous. Um,

36:09

and several very important mechanisms of your body

36:13

at several different times of, of, um, an animalism.

36:18

So that is the functional growth of from, for instance, baby

36:21

to then, um, to toddler

36:23

and then, um, adolescent and then so forth.

36:26

Those functional areas

36:27

of an animalism need more cholesterols need more

36:30

of those things components on there.

36:31

So it's not, um, a,

36:34

a linear regress curve in my personal opinion.

36:36

And we've seen this with the u-shaped, um, odds ratios

36:39

of too low

36:40

or too high of cholesterols both le LDLV, LDLs and HDLs.

36:44

Okay, so let's move on to this area here.

36:47

What are some morphologic features of some of this plaque,

36:50

um, and, and so forth.

36:51

And what we find is that positive remodeling the IE,

36:54

that 1.5 diameter greater than another area here

36:58

that's positive, um, spotty calcifications

37:01

where there are components of calcified material

37:04

that's being turned around, turned over, um,

37:06

the low attenuating plaques,

37:07

and you can see the examples around the here

37:10

and then the napkin ring

37:11

where we have then an accumulation in a

37:14

curva linear deposition.

37:16

The, uh, core, as you can see is made up

37:19

of various densities, um, from a low attenuating core to,

37:23

um, calcified core

37:24

and then fibro fatty fatty, which is the end stage typically

37:28

of any disease scar.

37:30

Um, but that also applies in, in the vessels as well.

37:37

So the Kaplan Meyer obviously is that, um, the presence

37:40

or absence of plaque makes a huge, uh,

37:42

determination in, in, in death.

37:45

And so, um, adverse plaque in this case, um, is associated,

37:49

uh, you can tell with this delta with a significant, uh,

37:52

degree of, um, mortality associated with it.

37:55

And we can see that across, um, time, you know,

37:57

from two year mark to the, um, um, adverse plaque.

38:01

Um, so if you had it, um, you know, at, uh, you know,

38:05

two year versus, um, um, you know, five year,

38:09

and then what that does in association

38:11

with the luminal stenosis.

38:12

So this is a nice histogram that shows then

38:15

luminal stenosis obstructive 50 to 69% stenosis

38:18

and above, and then plaque.

38:20

And so if we took those two biomarkers

38:22

and we plotted them in our report

38:25

or coronary CTA report, we then would hopefully be able

38:28

to catch these groups of individuals here.

38:31

So it's kind of funny that the CAD

38:32

rads, that's exactly what we do.

38:34

We talk about plaque and we talk about AL stenosis, okay?

38:38

Um, the usage of coronary CT

38:40

and high risk plaque features as a combinator, um,

38:45

evaluation of biomarkers that we can see

38:48

with any coronary CTA is extremely important.

38:51

And so that's what we're talking about here.

38:52

So the significant stenosis in high risk plaque,

38:56

so obviously what we don't want is a combination of two,

38:59

and we saw that in the prior histogram.

39:03

Uh, low attenuating plaque is a very interesting thing

39:06

and by itself.

39:08

So we, I think we saw a case of this, um,

39:10

this la this week here where we had a, um, CAD reds one,

39:15

so a less than 24% stenosis,

39:17

but we had a P two, which is a significant amount of plaque

39:21

that was, and then that was also low attenuating.

39:24

So we inverted it, right?

39:26

And what was interesting, uh,

39:27

you can see from this Captain Meyer here, is

39:29

that the low attenuation burden is a big deal, right?

39:32

It appears to be a big deal in itself, a distinct

39:37

and discrim marker for disease.

39:39

And so I find that to be the most important thing.

39:43

When did that come out? 2020.

39:44

When was our spatial resolution able to post to, uh,

39:48

you know, 2016?

39:49

2018 is when the, the, um, um,

39:54

you know, the secondary, uh, the second degree, um,

39:57

CT scanners started coming out, right?

39:59

I mean, when we were seeing like 16 centimeter panels, um,

40:03

you know, resolution one heartbeat acquisitions, you know,

40:06

that was around that 2016 time period.

40:08

Now we're eight years past that.

40:09

And so what are we seeing now?

40:11

We're gonna see even higher resolution,

40:13

even higher performative plaque characteristic evaluations,

40:16

and that's gonna probably make this number

40:19

and this delta increase even more.

40:24

Okay, so let's take a quick look here.

40:27

Patients not taking statin.

40:28

Statin obviously has a role in the pathophysiology

40:30

of laying down cholesterol depositions within certain areas.

40:35

I think it's more nuanced than that,

40:36

but, um, that's a very good way of looking at it.

40:38

And then patients taking the statin, you can see then

40:41

that the degree of stenosis, which is characterized

40:44

by the plaque deposition, um, has, uh, has, uh,

40:48

changed markedly.

40:50

Interestingly, statins also tend to stabilize plaque.

40:54

And so sometimes you'll see the, the coronary calcium

40:58

quantification go up post statin use.

41:00

And so, um, that's kind

41:02

of an interesting nuance that you wanna be aware of.

41:07

Okay, so coronary CT and fractional flow.

41:09

What are the combinations behind this

41:11

and what are the considerations?

41:13

A lot of this is based upon invasive fractional flow,

41:17

which is the delta behind pre and post, um, lesion.

41:21

And how then if we measure the pressure,

41:23

which is then related to the flow,

41:25

we can then determine then, um, if there is, uh,

41:28

downstream flow that is, um, worrisome.

41:32

And so, um, FFR guided, um,

41:35

percutaneous interventions versus just the anatomic

41:38

guidance, we can see then that the, uh,

41:40

Kaplan Meier does show then a significant,

41:43

uh, degree of change there.

41:44

So FFR guidance is important.

41:47

The problem is if you are going to plug up, um,

41:50

a already an occluded, uh, lesion,

41:53

that obviously has risk and concerns.

41:56

Um, so if you can do it non-invasively

41:59

and it correlates extremely well with this, then

42:01

that would be, uh, an extremely additive feature, right?

42:04

So let's go with that for just a second here.

42:09

What we find then is from a typical coronary CTA angiogram

42:13

is that we can then determine utilizing computational fluid

42:16

dynamic, which is the evaluation

42:19

of flow based on attenuation, council attenuation

42:23

starting here all the way here.

42:25

What is the dynamic, um, probability assessment throughout

42:28

that tree, that vascular tree.

42:31

And so then the iterative, um, evaluations are then, um,

42:37

remodeled over and over,

42:38

and we're able then to acquire then a synthetic, um, dataset

42:42

that we can model

42:44

that then works extremely well comparatively to

42:47

as if we were gonna do it invasively.

42:49

So we use the same, um, F-F-R-C-T utilizes the same pressure

42:54

of the coronary to the pressure of the aorta guideline here,

42:57

which is that if it is a 0.8, um, degree difference, um,

43:01

so it's not one to one,

43:03

but it's a little bit less than that 0.8, um,

43:05

or less, then that is considered then limiting flow.

43:09

So 0.8 is your number of choice, 0.7.

43:12

If you wanted to be even more sensitive behind that, um,

43:15

you know, is, is concern here.

43:17

So we can derive then that number,

43:20

the F-F-R-C-T peak flow, um, um,

43:25

from the, from the dataset.

43:27

And so this is a really important thing.

43:28

What does that mean in terms of prognostic?

43:30

And then, uh, and, and how that changes then the sensitivity

43:34

and specificities that is, if we were

43:36

to compare the non-invasive then

43:38

to the invasive, what does it do?

43:39

Well, it's this blue thing here.

43:41

It gets us higher to that in that au

43:44

where we're high top, high, right?

43:45

Where we're all the way up here in terms of, um,

43:48

that one-to-one specificity and sensitivity.

43:51

So way higher better than anything else

43:54

that we have available in terms of

43:55

that comparatively to ICA.

44:00

And as you could imagine, the Kaplan Meyer, um,

44:03

differential is significant.

44:05

And so there's a change in the major adverse cardiac event

44:08

rate when utilizing FFR CT

44:12

as you can see here, and being able to evaluate

44:16

that individual, um, for that less than 0.82, the 0.8,

44:21

it obviously corresponds to

44:22

what we had seen with that earlier.

44:24

Um, Kaplan-Meier with um, f uh, IFR invasive,

44:29

uh, fractional flow reserve, um, and, and PCI.

44:33

So this is exactly what we wanna see

44:35

trending in the same way.

44:37

Okay. Um, while shear stress, this is another, um,

44:41

very interesting modality that utilizes, um,

44:43

the relationship of, um, deposited energy into the system

44:48

and how that could either inflame, degrade

44:51

or reduce the capability of the walls to elastically respond

44:56

to, um, to flow, being able to give more flow,

44:59

less flow depending on what the situation is at real time.

45:03

And so we can then do this, um, with a kilo pascal.

45:06

We can do this, um, through a couple different ME measures,

45:09

but essentially the idea behind here is that we are trying

45:11

to identify less movement or less sheer stress capabilities.

45:16

So there's an, um, an ultrasound way,

45:18

there's a cardiac MR way,

45:20

there's also a CT derived way that we can do this too.

45:26

Uh, while sheer stress, um, in terms of how it works in,

45:31

um, and, um, in data comparatively

45:34

to something like F-F-R-C-T, essentially the wall,

45:37

your stress, um, if it's, it is positive here,

45:41

it should correlate to then, um,

45:43

to a dramatic change in the velocity pre and post.

45:47

And so that's what we're finding here then is

45:49

that there should be less elastic motion, um,

45:52

because there's a higher pressure going through there.

45:58

Other biomarkers have been looked at if you're looking at

46:00

the coronary, um, artery.

46:02

Um, so we've looked at the flow within,

46:04

we've looked at obviously lumal stenosis

46:06

and then the, um, morphology

46:07

of plaque deposition in the layers of the,

46:11

of the coronary artery.

46:12

We've now looked at, um, the flow, uh, through F-F-R-C-T

46:16

and then the sheer stress.

46:17

So the, how the wall accumulates, um, a capability

46:20

for elasticity or not.

46:22

So this here is talking about what is going on

46:25

around the vessel and is that important?

46:28

Well, the idea behind this is that there is a crosstalk

46:31

and that is that, um, structures nearby each other,

46:34

so are supportive, uh, in terms of, um, being able

46:38

to provide signaling, um, and are protagonistic

46:42

or antagonistic to then working, um,

46:46

and able to then provide signaling.

46:48

So what we find here is that the fat changes density

46:52

that is becomes more EDUs when there is a situation that

46:56

that is occurring within the system

46:58

in the coronary arteries.

47:00

And so what we find is essentially is that the relationship

47:03

of lipid to, uh, water is changing in terms of

47:08

how much accumulation of plaque

47:11

and then, um, uh, luminal stenosis and sentimental events.

47:15

And so some really nice work done out of, um,

47:17

Oxford was showing then how you can real time, um, do, um,

47:22

quantitative assessments of that peric coronary, um, fat

47:26

and be able to do then an attenuation, um,

47:29

evaluation quantitatively or from an index.

47:32

And so it's very interesting

47:33

and you can see that this low inflammation state

47:35

to a high inflammation state.

47:37

How then, as you can imagine edema is then the biomarker

47:42

of choice that we're looking at here

47:43

and how we can then be able to see that in terms of, um,

47:47

housefield unit change.

47:48

And that's where that, um,

47:49

that's utilized in this image analysis, uh, matrix.

47:55

So we can create then very nice trees of evaluation

47:58

and then be able then to do, um, a heat map evaluation

48:01

by pixel and be able then to find them the areas of

48:04

that correlate into high edema and low edema.

48:08

Um, and that's a very fantastic, um, usage of a,

48:12

a coronary marker that's sitting there.

48:15

How does it relate? Well, it's extremely well, um,

48:18

to then high risk plaque features.

48:21

And as you can see then that in this where the, um, uh,

48:25

fat attenuation index was very high, um, in how that related

48:29

to high risk plaque features is that we had then, uh,

48:32

cardiac mortality also increase as well.

48:35

So in obviously if you had a low FAI

48:38

and no, um, high-risk

48:39

plaque features that there's no disease.

48:41

So it's a really, really exciting additional marker, um,

48:45

that's utilized, uh, the, the system of that there is a

48:50

more than just the, um, discrete elements here

48:53

of coronary disease and coronary coronary luminal stenosis.

48:56

And why is this important?

48:58

Well, what is an invasive coronary angiogram? It's a lumino.

49:01

You are able to see in very high spatial resolution

49:05

what is occurring within the lumen.

49:07

Unfortunately, you cannot see what's in the vessel, which is

49:11

where, um, the use of ultrasound, for instance, in

49:14

that methodology can work, um, or CT

49:17

or in the case what's around the vessel,

49:18

which in this case would then be the FAI.

49:21

And so all those types of biomarkers can be, um, obtained

49:24

through a ct.

49:28

So the way forward first line test coronary CTA, absolutely,

49:32

absolutely great way plaque analysis, ffr, ct

49:35

and the new emerging factors

49:37

and, um, novel biomarkers to include, um, FAI, um,

49:41

shear stress, um,

49:42

and then obviously profusion in the myocardium.

49:45

So, um, this leads us into thinking about

49:49

what do we do with all this technology?

49:51

Well, one of them is that just

49:52

because we can see it doesn't mean that we can do something

49:55

with it in terms of the clinical guidelines

49:57

and the clinical therapy,

49:59

but what I want you to kind of consider is

50:03

what modality is highly innovative, is continually to change

50:08

and increase, and is that where you want to be

50:10

or do you not wanna be there?

50:11

And so for me, my answer is yes, I wanna be there.

50:13

Yes, please, please. I wanna be there

50:15

and I wanna be able to know these things so

50:17

that I can be able to offer them.

50:18

And so I personally was working with, um, the FAI

50:22

and some of this per coronary fats

50:24

and some of these other components in plaque analyses from

50:26

20 16 20 18 when it was offered through some,

50:29

um, software vendors.

50:31

But that doesn't mean that it's translated into guidelines

50:34

or into my reports, it just means that I'm aware of

50:36

that the entire system.

50:37

So as you, as an imager as you're moving along,

50:40

what I want you to consider is, is that these biomarkers

50:43

that you were evaluating on your exam, on your image,

50:46

on your, uh, in putting down your report,

50:48

they will be there whether you mark on them or not.

50:52

And so there are some really interesting things of,

50:55

of working with your colleagues to determine if,

50:57

if this is a marker that you want to continue to work with

51:00

and to figure out as being useful in a

51:02

prognostic or long-term way.

51:04

And so I worked with a couple other, um, places

51:06

and we've decided to do some of that stuff

51:09

and it's actually come out to be really useful.

51:11

As you had mentioned in your, uh, question about the role

51:13

of, um, CT angio in pediatric populations.

51:16

There are some very definite biomarkers in the pediatric

51:19

population that we now watch

51:20

because the field of view is so important that allows us

51:24

to watch 'em in the pediatric population.

51:27

And so those are very exciting things.

51:29

Anyway, um, I want to thank you for your time, um, and,

51:32

and for, uh, your opportunity for listening to this.

51:36

So I've got another question here, sir.

51:38

What is your opinion regarding optical coherence, OCT

51:41

and coronary angio, specifically plaque evaluation,

51:44

coronary dissection?

51:45

It's a fantastic high spatial resolution,

51:48

but with anything that has a high spatial resolution such as

51:51

that, immense detail, there is a, an inverse relationship

51:55

to the penetration, so how deep you can go with it.

51:59

And then also what is the, um, the invasiveness

52:04

or the capability behind it.

52:06

So those trade-offs are areas of innovation.

52:11

I've logged OCT for a very long time.

52:13

I've tried to get involved in that in terms

52:17

of using like F-F-R-C-T-A surrogate, so it's not OCT

52:22

invasively in the coronary arteries,

52:24

which would not be appropriate,

52:25

but it's a surrogate marker of OCT results

52:29

that can be acquired conventionally

52:31

and at the edge of ct, um, capability and resolution.

52:36

So absolutely, I think it's a great way,

52:38

it's the highest spatial resolution you can get

52:40

much more than ultrasound.

52:42

It does provide then, um, levels of detail

52:44

that are within the normal electromagnetic spectrum,

52:48

but also things that are beyond that.

52:49

And why that is important is

52:50

because we know from some novel, uh, research that

52:56

light spectra that is outside

52:58

of the electromagnetic spectrum, so near infrared redd, um,

53:01

infrared ultraviolet

53:03

and so forth, they play a role in disease

53:06

and in pathology as well as health.

53:08

And so if we can see, see some of that with other mod, um,

53:12

modalities, then potentially we can then comment on it

53:15

and then be able to make it.

53:16

So, oh, I'm the big fan of it.

53:18

I just haven't been able to translate that in terms

53:20

of a surrogate or in terms of a marker yet.

53:23

But, um, I would love to use it more for the,

53:26

like I mentioned, the electromagnetic spectrum portions

53:28

of it that we can't quite see right now, um, in terms of,

53:33

um, our modalities.

53:34

But that's a great question. Love it.

53:36

Any other questions you guys have?

53:38

Um, hello? Yes.

53:41

Yeah, hi. Actually in that, uh, uh, case evaluation,

53:45

you have mentioned that, uh, uh, to rate P one,

53:49

P two according to plaque distribution.

53:51

So I was just, uh, uh, wondering that on the software,

53:55

is there an option to see the calcium score

53:58

or anything so that we can write it in the report

54:01

or that whether it's P one, P two,

54:03

or Yeah,

54:06

That's a great question because well, so my answer is no.

54:11

I, um, the, the coronary CTA should not technically

54:14

have a CAC score.

54:16

Um, it should be a luminal

54:18

and plaque evaluation as opposed to the calcium evaluation.

54:21

Calcium has a very, very stringent,

54:24

very clear role in risk prediction.

54:26

Once you get into symptomatology IE chest pain, then we,

54:31

we, um, we should not be using a calcium

54:33

because it doesn't work as well in terms of that dataset.

54:37

Now, do we do a calcium

54:39

with a coronary CTA acquisition in some,

54:42

in a lot of my centers, yes.

54:44

Um, we do. And some of my centers, no, we don't.

54:47

So I, unfortunately I say all that to just caveat

54:49

that typically a, a CAC score is not part

54:51

of the CTA acquisition.

54:54

Now what can we do in terms of quantitative

54:58

or qualitative assessment of the plaque

55:01

by utilizing the CAD rads and then what, um, the software

55:05

or what our eyes are doing, the cad rads uh,

55:09

reporting says you can do qualitative or quantitative.

55:13

So a qualitative would be a, a system that is agreed upon

55:17

by you and by your peers that says there is a mild,

55:20

moderate, or severe amount of plaque, um, burden.

55:25

The distribution that is, how much of it where it is,

55:28

is it all plugged up in the LM

55:30

and the proximal, you know, osteo LID

55:32

or is it all at the distal aspects of the LCX?

55:35

That is a completely different thing

55:36

that it does not talk about,

55:38

which will be needed in the next iteration, of course,

55:41

as we say then there.

55:43

But you can see then the problem right now is

55:46

that it's CAD rads 1, 2, 3, 4, 5,

55:49

and then it is a, uh, a P one, two,

55:52

and then there are the modifiers, right?

55:54

So then we have all the different modifiers.

55:56

So we're getting into a, an alphabetical

55:58

and numerical soup

56:00

where we're constantly then adding more to that.

56:03

And while that level of, um, we call 'em loins,

56:07

L-O-I-N-C, while those levels of, um, being able to

56:12

objectively measure a, a characteristic

56:14

and then be able to send that out,

56:16

and then it should hopefully be used for objective measures

56:19

and then algorithm training, it, we lose a little bit

56:22

of our soul and herself, right?

56:24

I mean it, to do a soup like

56:25

that is just too much craziness.

56:28

So what I would suggest for you to bring it all back

56:31

to your question is, um, mild, moderate,

56:34

extensive amount of plaque.

56:36

Um, I, I think cat rats does say something a little bit

56:38

different in terms of their qualifiers, um,

56:41

or decide to use a, a system, a software system

56:44

that does break down the plaque into a quantitative system.

56:50

Those are costly,

56:51

those can potentially then have inter radiology

56:54

or inter imager variability.

56:57

So I try not to do that, but, and so to make it just three

57:00

or four words is probably the better thing.

57:03

I hope that answers your question.

57:05

Thank you. Of course.

57:10

Well, terrific. If we don't have any other questions, Dr.

57:13

Lorenz, thank you again.

57:15

And just a reminder here, in about one hour we'll be, uh,

57:18

coming back to do, uh, week two case review again with Dr.

57:22

Lorenz. So if you have any questions, then just let us know.

57:26

Uh, Dr. Lorenz, thank you,

57:27

and we will see you in about an hour.

57:30

Thank you. Everyone. Can't wait to see you all again.

57:32

Um, um, yeah, I'm gonna get a quick lunch

57:34

and then we'll be right back at it. Okay,

57:36

Thanks again. Bye.

57:37