0:00

Hi everybody, and thank you for joining us today

0:03

for week one Office Hours for the Cardiac ct,

0:07

a online training course.

0:08

We're here with Dr. Lorenz.

0:09

Um, he is going to review each case

0:12

and answer any questions you may have.

0:14

Um, if you have a question, um, you can ask Dr.

0:17

Lorenz directly. You can put your question in the chat,

0:20

or if you wanna use the hand ra raising emoji next

0:23

to your name, um, we'll call on you.

0:25

So, uh, Dr. Lawrence, whenever you're ready.

0:28

Cool. Hi everybody. Hello.

0:30

Hope you're doing well in whatever locale that you're at.

0:34

I'm in the Pacific Northwest of the United States

0:36

and it's beautiful fall weather

0:39

and, uh, so yeah, had a lovely time going over your cases.

0:42

Really, really wonderful you guys.

0:44

Fantastic job, um, going through them. So thank you.

0:49

And, uh, extra kudos

0:50

and thank you to the individuals who, uh, did a complete,

0:54

uh, radiology review of that.

0:56

So that includes, you know, uh, findings, impression,

0:59

and then obviously extra coronary, extra cardiac, um,

1:02

components there, because this is a chest pain evaluation.

1:05

So you will find breast cancers, you will find,

1:08

obviously the hial hernia and then the lung cancers

1:10

and stuff that will be causing their pain too and so forth.

1:13

Um, so as you can see, uh,

1:15

I'm gonna share just this really quick, um, slide

1:18

and hopefully it's, it's picking up well,

1:19

but there are segments to the coronary tree.

1:22

There are approximately 17 plus

1:24

or minus, if you include Rams, intermedius.

1:26

But, um, the idea behind here is

1:29

that if we can segment a piece of anatomy,

1:32

then we can assign weight to it in terms of its, um,

1:37

overall, uh, importance,

1:39

but also we can assign then a perfusion.

1:41

And so you're gonna hear me a lot throughout our,

1:43

my lecture components.

1:44

Talk about perfusion, why?

1:46

Well, the radiologist eye can perceive the differences in

1:50

hounsfield attenuation and perfusion extremely well.

1:54

Um, and obviously there is a correlative

1:57

to the quantification perfusion

1:59

that will be taking place either at your institutions

2:03

or with, um, with, uh, other components.

2:06

And there are CPT codes to be associated with that.

2:08

So this does break it down.

2:10

Essentially, there are four components

2:13

for the RCA left main is one specific segment two,

2:17

and then the, um, LAD of course is proximal mid distal

2:21

with the diagonal branches being part of that.

2:24

Circ has, um, a proximal, um, and a distal branch.

2:28

And then the obtuse marginal, uh, plus

2:31

or minus a secondary Optus marginal.

2:33

And then, um, a, uh, a marginal PDA component if, uh,

2:37

and if it's present there, uh, B, BB,

2:41

and that's really about it.

2:43

Uh, so there's usually at, at most about 17 of them.

2:45

But the idea behind there is that you're going to,

2:48

uh, start signing it.

2:49

So now let's break it up into binary.

2:52

So we take the full components.

2:53

Now let's binary into left tree and then right tree.

2:58

And as we kind of talk about here in, in terms of, um,

3:02

overall coronary blood flow

3:05

and how would you get a coronary blood flow?

3:07

How would you do an evaluation of the distribution

3:10

of coronary blood flow?

3:11

Well, quantitatively you can use, um, these techniques such

3:15

as, uh, SPECT imaging and um, uh, pet imaging.

3:19

You can also then look at the size of the,

3:24

the coronary tree following NTG.

3:27

And so the reserve coronary blood flow is a good, um,

3:31

informal and indirect measurement of the amount

3:34

of coronary blood flow that's gonna be in that tree too.

3:36

So how plumpy is the LM LAD compared to the RCA?

3:41

And if you start seeing discreet changes in pro in proximal

3:45

to mid and distal segments,

3:47

those are actually gonna correspond to, um,

3:49

symptomatic changes in the patient.

3:52

Um, not only at work, but also at rest

3:54

and also with microvascular disease.

3:56

So we actually can qualitatively

3:59

evaluate microvascular disease based upon those changes too.

4:02

But getting back to a binary left and right coronary flow,

4:07

and as the, as you can see there,

4:08

there is a significant amount of flow

4:11

to the left side of the system.

4:12

So if we're talking about chest pain

4:14

and the symptomatology of a lack of,

4:17

or a dysfunction of perfusing, a portion of the heart,

4:21

you are talking essentially the left system.

4:24

And we see this, um, obviously in terms of the types

4:27

of treatments that are gonna be offered when there is not

4:30

just, uh, chronic obstructions,

4:33

but then obstructions that are

4:35

of multiple vessel segments in the left side

4:37

of the tree compared to the right.

4:40

So don't get lost in the weeds of, um, of the segments.

4:44

Don't get lost in the percentage, just know

4:47

that you're playing a binary game of left or right

4:51

and how much of it, and then we can go from there.

4:55

Uh, one other thing to note is, if you had looked at the SEC

4:59

template, um,

5:00

or some of the other templates, there is a percentage

5:03

of grading from 0% luminal stenosis

5:05

to a hundred percent luminal luminal stenosis.

5:09

And the SCCT guidelines

5:11

and the CAD RADS two guidelines talk about

5:14

how at some point from zero to, you know, 50%,

5:19

that's essentially a non-obstructive lumen.

5:22

And then when you get to 50%

5:24

and above that, it is an obstructive lumen.

5:26

Well, we all know that that came from, uh,

5:29

a different data set that's from the invasive coronary

5:31

angiogram evaluation where line pairs

5:34

and high spatial resolution was allowed for that type of,

5:38

um, specificity here with coronary CTA, particularly

5:43

with the 2016 and 2018 dataset,

5:47

that high spatial resolution was not available.

5:49

So, you know, you have an interval range.

5:51

What that means, again, is that anything up to about 50 to

5:56

even 70%, um, of

6:00

luminal stenosis on your coronary CTA with a machine that is

6:04

around 2018 or less is probably not gonna be very accurate.

6:09

And that's fine. Um, if you're going to, uh,

6:13

be conservative in terms

6:15

of getting things into a functional assessment.

6:19

The other way is to look at it is

6:21

that you've got a lot of room, right?

6:23

Zero to 70% of the lumen can be supposedly obstructed

6:27

or affected by plaque or, or stenosis,

6:31

and you're really not gonna do anything from a

6:33

management standpoint.

6:34

And I'll get into this in a PowerPoint here.

6:36

So speaking of that, let's just jump right into just

6:39

a few quick things here.

6:40

Um, accuracy of the coronary CTA,

6:44

this is a really important thing

6:45

before we start on some of the cases here.

6:48

Uh, what we're dealing with is two numbers under the, um,

6:51

uh, the area under the curve sensitivity and specificity.

6:55

So when it's coronary CTA, it is a sensitivity test,

6:59

rule it out, right?

7:01

Not specificity. That means give me the specific number

7:04

of stenosis, gimme the specific number of, of, uh,

7:07

of effect on the lumen.

7:09

Um, but get those individuals

7:12

and say the coronary arteries are not the problem.

7:14

And so you can see that it has one

7:16

of the best sensitivities across modalities here.

7:19

This is from, again, 2018.

7:21

So we're dealing with, um, uh, second generation ct,

7:25

coronary CT angiogram protocols

7:27

and spatial resolution detectors,

7:31

and that type of detector system.

7:33

So this is pre natoma and photon counting.

7:37

And so the resolution obviously wasn't accounting for, uh,

7:40

those types of systems that are now gonna be part

7:42

of the newer evaluation.

7:44

So what that would mean is, you'll see this number here in

7:46

specificity pop right up here.

7:49

So the takeaway is by utilizing 2020

7:53

and 2024 data with post on counting,

7:57

this number is just gonna actually get better.

7:58

But right now, sensitivity is what coronary CTA is useful

8:02

for rolling it out in terms of ischemia

8:05

or functionality or the function.

8:08

This is not where you're gonna put a lot

8:10

of your money, as you can see here.

8:11

Uh, what you're gonna put it to is those functional tests.

8:14

So we see the functional tests,

8:17

the functional assessments still being with those

8:19

nucleotides, so like spect, pet ct,

8:22

and of course stress, uh, CMR

8:24

where there's a signal intensity change,

8:26

uh, pre and post work.

8:28

Now, this signal intensity change

8:29

is actually getting better.

8:31

Why? Because of higher spatial resolution, as you

8:33

and I all know with, uh, 1.5 and three T systems,

8:37

but also that we're able to detect, um, more subtle changes

8:41

in terms of what is the paramagnetic properties

8:45

of oxy hemoglobin and deoxy hemoglobin.

8:48

And this sort of what we call a blood oxygen

8:50

or bold type evaluation can be done

8:53

with contrast and without contrast.

8:55

So there's some really great evidence

8:56

and some good research that's being done.

8:58

We did a little bit and dabbled a lot, uh, a little bit,

9:01

well, I won't say a lot, but a, a little bit

9:03

of it in the Department of Defense.

9:04

And he was fantastic stuff too.

9:06

Um, there are some Matthias Friedrich

9:08

and some of the other guys in Europe, um,

9:11

do wonderful job on bold, uh, in stress, cardiac

9:15

and mi i, they, they fantastic stuff.

9:17

Alright, so not gonna get too deep into this stuff,

9:20

but just talk about here some really quick.

9:22

Captain Meyer. Obviously if you have no cad, um,

9:25

things are great, but, uh, uh,

9:27

the more progression you get in your coronary organ disease

9:29

in terms of plaque as well as luminal stenosis,

9:33

it gets worse, uh, for you.

9:35

And so we find this, um,

9:37

play out prognostically coronary CTA has an absolute

9:41

wonderful, um, work ethic.

9:43

And so you can see then

9:45

that a negative test is always gonna be a good thing on a

9:48

coronary CTA comparatively

9:50

to a negative test on something else

9:52

that's not gonna do such a great job.

9:53

IE these guys right over here, okay?

9:56

Uh, several trials including Scott Hart promise.

9:59

Um, and Scott Hart too had shown

10:02

that coronary CTA involved in your standard evaluation

10:06

of coronary artery disease absolutely

10:08

makes money difference.

10:09

It's a huge difference, uh, in a player.

10:11

So that's why we're obviously doing this course right now

10:14

to learn how to take advantage of coronary CTA, um,

10:18

in making that difference.

10:20

I think you've all seen this.

10:22

Um, this is a decision tree based upon acute chest pain,

10:25

intermediate risk, no known and known it.

10:27

Uh, the main thing I want to just stress here is

10:29

that it absolutely has a role to play.

10:31

It's a two A in terms of its, um, uh,

10:35

data in terms of evaluating, uh, for, uh, for disease.

10:40

And so it's a huge player when we add the functional

10:42

assessment of FFR ct.

10:45

So fractional flow reserve from a CT standpoint

10:48

or stress, we do have an additional component

10:51

that's functional to get the specificity back up too,

10:54

as we were kind of chatting about before.

10:56

Alright, so enough of that, uh,

10:58

unless you guys have any questions specific

11:00

to theory on why we're doing coronary CTA,

11:03

how about we jump into a couple of cases?

11:05

All right, so I'm gonna change, um, over here.

11:10

Let's share that screen. So

11:11

hopefully you're seeing my screen.

11:13

Anybody have any specific issue on Terry Recon right now

11:17

that we solved before we can jump into some cases?

11:21

Nope. Alright, so this is case one.

11:25

Uh, case one is a 38-year-old male, uh, with a history

11:30

of MV mitral valve prolapse, intermittent chest pain,

11:33

increased physical exertion, uh, the treadmill stress test,

11:37

which obviously Bruce protocol for the 38 year mild who can,

11:40

who can run walk, uh, did show some limiting chest pain.

11:44

So some symptomatology, but normal ECG on stress.

11:48

So the mets and the amount of, uh,

11:50

electrical changes were normal, right?

11:52

So what is going on with this individual? Anything?

11:55

Well, the way

11:56

to evaluate then a coronary based evaluation in terms

12:00

of the chest pain is to ensure

12:01

that the coronaries are not part of the decision tree.

12:04

So we have to rule it out, right?

12:06

So the sensitivity, the best sensitivity tests that we have,

12:09

that the coronaries are not involved as the coronary CTA

12:13

or the an anatomic approach.

12:15

So here, uh, we've got our multiplanar, um, review

12:19

and we have axial coronal and sagal.

12:22

And, uh, here we're just gonna remove out the 3D volume

12:25

rendering so we can get a quick look at the tree.

12:28

Now I personally, I like looking at the tree

12:31

because it gives me, again, that perfusion evaluation of

12:35

in the anterior in ventricular space, the LAD

12:38

and all of its branches, the RCA and its branches.

12:44

And if we go along here, the, uh,

12:45

left a atrial ventricular groove and the LCX.

12:49

So things look pretty good here.

12:51

You can, um, absolutely look at, uh,

12:55

things along this way

12:56

and get a really good idea of

12:58

where then there's gonna be a perfusion, asymmetry, uh,

13:02

left side, right side and so forth.

13:03

You can also do that on a, um, on the anterior, I'm sorry,

13:07

the axials and do a good job of that too.

13:10

So we're gonna pull up the axial.

13:12

Now, if you remember what I said, we match well in terms

13:15

of spatial resolution.

13:17

You wanna match the evaluation, the qualitative evaluation

13:21

to then how it was acquired.

13:22

So if we're acquiring on an axial,

13:24

that is supine positioning, take a slice, move the patient,

13:28

take another slice, move the patient.

13:30

Your highest spatial RESO resolution is gonna be

13:33

this axial image here.

13:35

And when you start adding the multiplanar reforms,

13:38

the three, uh, and the curve planar reforms,

13:40

and then the 3D reforms,

13:42

that's when you start getting some spatial resolution loss

13:45

because those pixels in 2D have

13:48

to be shared in three dimensions.

13:50

Okay? So, um, this is called the trifecta where you have,

13:55

um, all three vessels.

13:57

So we're in the mid, um, mid LAD, um, proximal ready

14:02

to move on over to the, to the mid RCA

14:04

and then LCX over here, prox, LCX moving on over here.

14:08

So when you have your trifecta,

14:09

you can see then you can actually put a household unit

14:12

here, here, and here.

14:14

And if the household unit is in plus

14:15

or minus, you know, five household unit, you know

14:18

that you have an instantaneous perfect transmission of blood

14:23

into your three arteries at the same time.

14:26

And then therefore there should be a really excellent

14:29

perfusion, very little perfusion anomaly,

14:31

IE no CES or plaque.

14:33

So this gives you a really good

14:35

idea of what you're dealing with.

14:36

And I typically use this on my 50-year-old females

14:40

for microvascular disease.

14:42

I use this in some of the, um, zibo, uh, cases.

14:47

Um, and some of the other things that are potentially post,

14:50

um, myocarditis to see if there's a microvascular disorder.

14:54

Um, so as we're kind of looking on here,

14:56

then there are a couple different ways of doing

14:59

what we call the, um, the, uh, the evaluation,

15:04

uh, your, your decision matrix

15:06

of how you're gonna evaluate it.

15:07

You can use A SVC down to the right atrium

15:11

to the right ventricle and come on back to the MPA eval.

15:15

Or you can just go right into the thoracic area

15:17

and follow the tree and then finish up there.

15:19

Either way is fine.

15:21

What I would like to impress upon you is getting down

15:25

your search pattern is,

15:28

is gonna be the most important thing.

15:29

So whatever comes natural to you, I I,

15:31

and I'm purposely trying to stay stray

15:34

and stay away from in giving you my search pattern

15:37

because I don't want you it to be something

15:41

that you take on if it didn't feel right for you.

15:44

So if you immediately went to the sinus

15:47

of al Salva in your coronary treat, totally fine.

15:49

If you took, um, a search pattern that did right

15:52

to left side of the flow

15:54

of contrast, that's totally fine too.

15:55

Either one, it doesn't matter.

15:58

Okay, so LM off of the LAD, uh, ramus

16:01

and then the LCX, we'll just follow LAD first.

16:04

We can see here that LM has, um, a,

16:07

a very nice appearance to it.

16:09

This is approximately five millimeters.

16:11

Um, and so we're getting about four and a half on this here,

16:14

but if we measure there, obviously five.

16:16

So, um, very nice plumpy appearance to it.

16:19

Very good coronary blood flow.

16:20

And then similar here, five, um, to three,

16:24

then, then to two.

16:25

And then that should be about when we get down to about 1.5,

16:28

which is somewhere around here is where, um, we start

16:32

to lose the spatial resolution.

16:35

That is gonna be beyond chance or probability.

16:37

So anything less than 1.5 on a ct, um, anything around,

16:42

you know, 2016, um, CT chest, uh, equipment,

16:47

then you start getting into probability where index

16:49

and noise and stuff can play a role into

16:51

how the hounds filled units are, are, are due to something

16:56

inside the, um, the artery are not.

16:59

So we have a couple branches, as you can see, uh, three,

17:02

two, uh, one.

17:04

And, uh, so the diagonals look great too.

17:06

Ramus again, looks f fine, no issues here.

17:09

And this has a pretty good profusion amount there.

17:13

And then the LCX looks really great.

17:15

So what's this vessel here?

17:17

Um, somebody had considered this an anomalous, um, vessel.

17:21

Um, no, it's, it's actually what, it's an av,

17:26

um, branch.

17:27

And so we have our AV node, um,

17:30

along here on the anterior aspect and the left atrium.

17:33

And that's, um, uh, a sino node.

17:35

We also have them the sino atrial node along in here,

17:38

and typically we'll see a little branch come off of that,

17:41

um, maybe right around there.

17:44

Yep. And this is obviously conus

17:47

branch that comes off of there.

17:48

Um, and then, so mid RCA to the PDA

17:53

and then this is a PLA

17:54

that marches along the posterior aspect of the left, um,

17:58

atrial ventricular groove if they don't go

18:01

directly down in this way.

18:03

So that is, they take a more lazy approach

18:05

that's called a marginal, just know that

18:07

that's nothing different, it's just that it just decided

18:10

to branch off a little bit earlier.

18:12

But as you can see, it's nearly a complete wrap

18:15

around the left.

18:16

Um, the LAD, uh, to the posterior in ventricular groove

18:20

and the PDA meeting that up there,

18:23

you'll see some branches come off here that go

18:25

to the esophagus, go to the, uh, left hepatic lobe, uh,

18:28

that go to other structures such as the cardiac, uh, segment

18:32

of the, of the, uh, proximal stomach.

18:35

Um, the anatomy is fantastic and wonderful.

18:38

Sometimes you'll even see bronchials, um,

18:40

from the thoracic aorta making some sort of shunt to, uh,

18:44

to some of the vessel components

18:45

and cardiac structures longing here.

18:47

Okay, so what do we have? We have a normal opacification

18:50

normal origin course

18:51

and termination of the coronary arteries.

18:54

We have, uh, normal opacification, no luminal disease,

18:57

no stenosis, no uh, plaque.

19:00

I have a little bit of thickening, um, at late diastole.

19:03

So this, we know that this is real.

19:05

It's a little bit of thinking corresponding

19:07

to the individual's history of mitral valve prolapse.

19:10

Obviously with that, what we wanna make sure is

19:12

that there's mitral anular calcification plus

19:14

or minus, any kind of sub aortic membranes, um,

19:17

calcification along the LVOT

19:19

and then, um, potentially, um, a mac, right mitral handler,

19:23

um, calcifications or, um, some sort of prolapse

19:28

or anything else, um, associated with, um, those types

19:31

of disease program of the, of the valve.

19:34

Okay. Um, I usually look at, in this case here,

19:39

the profusion.

19:40

And so, um, I don't get too, you know, too hard and,

19:45

and difficult about, um, evaluating,

19:48

but sometimes I will take, um, a quick little,

19:51

um, evaluation here.

19:52

So we'll just take this little circle, ROI

19:55

and just eval what we got.

19:58

Uh, so, uh, it's about 68 household unit right on in here.

20:02

And then we can just, you know, take this guy and,

20:04

and just bring it along

20:05

and just see where we are at 60 there.

20:08

And, and then 115 down here, maybe 94.

20:12

And then, you know, and just kind of see just

20:14

how the perfusion is.

20:15

Um, there was a really great evidence on CT

20:18

perfusion and it's getting there.

20:19

It's gonna get better. We've got some, you know,

20:21

dosing issues that we're gonna get around,

20:23

but, so this is a cadrad zero.

20:26

And so this, uh, exam should then potentially evaluate

20:30

for the anatomy, uh, with no disease, uh,

20:32

in the coronary arteries.

20:33

No other issues along in here.

20:35

What was the chest pain related concern here?

20:37

Well, it's not coronary related

20:39

and it doesn't appear to be myocardial.

20:42

Um, muscle related, potentially.

20:44

There's a little bit of redundancy in the, um,

20:47

serosal vessels, um, at this, um, uh,

20:52

thickened, uh, esophagus and then small hidal hernia.

20:55

So potentially there's some esophagitis or,

20:57

or some other issues here.

20:58

So that's probably what's going on.

21:00

Um, hard to tell, but I usually toss it in you

21:03

and I probably will see this more often than coronary

21:05

heart disease to be honest.

21:07

Alright, so I have questions on this

21:09

One. Yeah, Dr.

21:10

Loren. Um, there is a question from Dr. Yeah,

21:22

Hi, Dr. Lorenzo.

21:23

Hi, uh, is there a bridging

21:26

of Rams branch on, uh, left side?

21:31

Say that one more time. Is there myocardial

21:36

bridging of, uh, ramus?

21:40

Um, so no, uh, usually, um,

21:46

the bridging will only affect

21:50

the main coronary arteries of the,

21:52

so L-A-D-L-C-X and RCA.

21:55

It is extremely common for diagonals,

21:58

which this is probably a progenitor two

22:01

and of, to then make its way into the, um, myocardium

22:06

as you can see along here and here obtuse as well.

22:09

So we wouldn't call that a bridge.

22:12

Typically, the, it is gonna be a, like in airways,

22:16

there'll be a res, uh, a component,

22:19

typically the terminal component that will need to dive in

22:22

to become then the microvascular chart,

22:24

as you can see here and here and here.

22:26

So we wouldn't call that it's when it's a conductive portion

22:29

of the, of, of the vessel.

22:32

So if it, for instance, this were

22:34

to dive in right now into the myocardium

22:37

or to another structure,

22:39

then you could potentially call that a bridge.

22:41

But because it's conducting,

22:43

but uh, when it's a terminal like this

22:45

and down over here, no, we wouldn't call that a bridge,

22:48

just a normal physiology of, uh,

22:51

shaping down into just a normal microvasculature.

22:56

Thank you. Yeah, yeah, good question though. I like it.

22:59

There is and will always be some sort of bridge

23:03

and I don't know, and I haven't received a really good

23:06

reason why, um, that that is.

23:09

But do you all know where is the origin

23:12

of the coronary arteries?

23:13

Everybody typically says, well,

23:15

the origin is is right here, right?

23:17

That's why we call it the origin

23:18

of the coronary arteries right here, right,

23:19

right off the sinus, sinus of al Salva.

23:23

Actually no embryologically.

23:24

What occurs is, is the micro vasculature is the pro gentine,

23:29

um, vasculature.

23:31

So it starts in the sub endocardial, makes its ray

23:34

mid wall endocardial, um, myocardium,

23:37

and then it comes out of the epicardium

23:40

and sniffs through chemokine to then find

23:43

the sinus of Val Salva.

23:46

So when it doesn't do that is when we have an anomalous, um,

23:50

course and termination, but we call it the origin

23:53

because it was thought to be the origin, um,

23:57

until they actually mapped it out.

23:59

So, um, it for a reason, the LED always seems

24:04

to have a bridge right

24:05

around this mid segment right in here.

24:07

Why? Well, because this is the thickest portion

24:10

of the muscle that takes a, a few weeks later than

24:13

where then this vessel starts to sniff

24:15

and find its way in this inner ventricular groove here.

24:19

So you'll always find a bridge there.

24:20

I always think that also it has some sort of way of milking

24:24

in terms of pushing blood flow down into the other, um,

24:28

into the deepest portion of the LAD two.

24:31

Um, there are some really interesting respiratory, uh,

24:35

mechanisms that are used to stunt, um, myocardium

24:39

because there isn't, you know, obviously, um, uh,

24:42

a chemical, uh, contractility that occurs with some

24:45

of the components along the septum, right?

24:47

To, you know, those Perkin g fibers.

24:50

But interesting, I I just, I think

24:51

that there's also a respiratory component too,

24:53

and you can see this respiratory motion,

24:55

not just the vasso chemical of Perkin G you know, you know

25:00

that stuff, but anyway,

25:01

you always see the bridge always right in there.

25:03

And there is, and I think I might have mentioned this

25:05

to some of you all in your discussion about bridging,

25:08

there is a definitive definition about bridge, um,

25:13

the length, the depth,

25:14

and then how much stenosis involved in it.

25:17

And so the physiologic bridge, um, has

25:21

to meet a criteria

25:23

because you will always see an anatomic intra myocardial

25:26

bridge, and that's considered no problem.

25:29

I mean, everybody has that.

25:31

So anyway, we got a little sidetracked,

25:32

but we'll, we'll get into that one on the next one.

25:37

All right, so case number two, let's chat about this one.

25:42

So this is the 47-year-old male history

25:44

of prior tobacco use, onset

25:47

of intermittent substernal chest pain,

25:49

increased physical exertion, coronary CT angio

25:54

for the A evaluation, right?

25:55

So again, um, not too uncommon to find then,

26:00

uh, you know, that, uh, birds

26:02

of a feather like to hang out together.

26:04

So if you smoke or if you, you know, have other issues, um,

26:09

like family history, blood pressure

26:10

and stuff that you're gonna have, then chest pain.

26:12

And then that chest pain is gonna have a certain amount

26:14

of risk and that certain amount

26:16

of risk when you look at in calculator, it's gonna say,

26:18

well, it could be then related to, to coronary disease,

26:22

or there could be also coronary disease.

26:24

So you stop all that potential risk

26:27

and clinical risk prediction

26:28

and then you stop all the functional evaluation to just,

26:30

let's just take a look at the coronaries

26:32

and see if the coronaries have an issue.

26:34

So here we are with the coronary A CTA.

26:36

So as I mentioned before, I take a look at the volume

26:38

rendering just to kinda get a quick idea not only

26:41

of normal anatomy,

26:42

anterior interventricular groove having a very strong large

26:45

vessel being the LAD with a branch coming off of it.

26:49

You can also lift off, um, you know, some

26:52

of the other structures to take a quick look at the LCX

26:54

and um, obtuse margin along there and then the RCA

26:59

and making sure that it has a nice appearance

27:01

to to that as well.

27:02

So do the vessels look pretty good? You look about the same?

27:05

Yeah, I would say so.

27:06

Alright, so in this particular case here,

27:08

we're gonna take a look at it both in axial

27:10

and then also in the curve planer

27:12

or the multiplanar reforms curve,

27:14

planar reforms in the short axis and see what we get.

27:16

So as I said, there's a couple different ways

27:18

of doing your search pattern.

27:20

You can follow then the, the attenuation of the contrast

27:23

of SVC down to the right atrium, right atrial appendage,

27:27

and then, uh, to the right ventricle.

27:29

There's always a little bit of, um, gutter, uh, contrast

27:33

that hangs out down here

27:35

that doesn't obviously make its way independently even

27:38

with contraction into the MPA to to the pa,

27:42

but it is good to get a good search pattern down

27:44

and make sure you, um, see those things.

27:47

So what is the difference in unit from the PA to the LA

27:50

that's approximately through what, one second one

27:54

and a half second in a normal papillary bed

27:56

of the pulmonary arteries, if you see it later

27:59

and you could potentially even, you know, take a look at it,

28:02

that just looks a little bit brighter than this.

28:04

There potentially is some slowdown or some issues.

28:06

So what did we have on the history with this guy smoker?

28:09

What does smoking do? It absolutely vasso constricts

28:12

capillaries, particularly in the lung, uh,

28:14

parenchyma in the lung bed.

28:16

So that's potentially the delay in the ville unit here

28:20

as opposed to the prior exam where it was just a young guy

28:23

who was deconditioned, um,

28:26

and he had absolutely similar attenuation in his PA,

28:30

L-P-A-R-P-A in his la in pulmonary veins.

28:34

Okay, so, um, LA um,

28:38

and left a trim.

28:40

Looks fine. Left atrial appendage looks great.

28:42

Let's get on down here to the left ventricle.

28:44

That looks pretty good. And now we're in the sub aortic LVOT

28:47

area and uh, now pop off here into the LM

28:52

to bifurcate into the L-A-D-L-C-X.

28:54

So we're just gonna take a quick look here.

28:57

I always start at the top of a vessel,

29:00

so I make the vessel disappear and then I make my white in.

29:03

Why? Because this is probably one of the most important

29:07

real estate areas ever.

29:10

Why? Because this is what I mentioned in terms

29:13

of coronary blood flow.

29:14

This is the spigot.

29:15

If you block this thing, you're done, right?

29:18

And we all know that you and I know that too,

29:20

but how do you determine that it is blocked or not?

29:23

Well, you have to go to the top and see it.

29:26

Now obviously a big red flag is a calcium up top here.

29:30

Now is this not, um, lm, could it be,

29:35

uh, aortic valve?

29:36

Could it be sinus valve salvo calcification? Absolutely.

29:40

How do you tell? Well,

29:42

I think there's a nice little inlet along in here

29:45

that is useful to tell.

29:47

Um, you can see this also on calcium scoring here,

29:50

but in this case here, we had to go all the way to the top

29:53

and see that it is right in line with where the LM is.

29:57

So we have osteo LM

30:00

par calcified plaque that is less than 24% stenosis.

30:05

Now we're gonna take a quick look at, um, at, uh,

30:09

it on multiplanar.

30:10

So the curve planar reformance.

30:12

But what I want to do is,

30:13

do you see the thoracic a r right here,

30:15

the descending thoracic virta?

30:17

Let's just imagine for instance, that the LM is a

30:21

and this is a long cut and we just did a shortcut out here.

30:24

So that calcification

30:26

and that plaque is at the top here, right?

30:29

We can all imagine it.

30:30

And as we are slicing through,

30:31

we're in the midsection right here,

30:33

we're in the midsection right here.

30:35

Well, I want you to try

30:36

to think about this organizationally, is

30:38

that you can then scroll through on the axial,

30:42

remember highest spatial resolution

30:44

and be able to then determine the percentage of effect that,

30:49

of lumen that that amount

30:50

of plaque has if you think about it.

30:52

So here we had, uh, obviously less than 24%

30:55

because we're at the 50% that is halfway through

30:58

where we can see the, the, the vessel in fonts.

31:02

And we can see that we should be right along here

31:04

and we don't have a plaque here.

31:06

So obviously it's less than, um, it's not 25, it's not 45,

31:10

uh, 25, 40 9%, it's less than that.

31:13

So it's 25% or less

31:15

and it would probably be only 5% at most here.

31:18

So we can use this sort of infos

31:21

and then, uh, short access view to kind of get an idea of

31:25

how much plaque is there, which when we go to the NPRs

31:28

and the cprs is gonna be really useful.

31:30

Okay, so speaking of, let's just go to that one real quick.

31:33

We're gonna just move this on over here

31:36

and then find our vessel again, that's a shift technique,

31:45

okay?

31:45

So even on here on the curve planers, we can already tell

31:48

that there is just a tiny bit

31:49

of plaque right here at the ostia.

31:52

And it's, um, although you, you, you can see

31:55

that clearly it's not to the full width half max

31:58

where the green line is.

31:59

So that's approximately 50%. So it's less than that.

32:03

It's less of the less. So if this were 25%,

32:06

um, it's even less than that.

32:07

So it's around 10 to 15%.

32:09

You can take these little calipers and and do that,

32:11

but it starts getting really wonky and,

32:14

and not really accurate.

32:15

So it's saying it's 30%, I don't believe that

32:17

because there's a little bit of, um, uh, uh, of loss

32:21

of caliber of the main,

32:23

the the left main with that sort of thing.

32:25

But as we kind of twirl it around, we can see that it's,

32:28

it's there, it's well within the ostia.

32:30

And so having a good mechanism to go

32:33

through is very important.

32:34

Let's go to short access view

32:36

and you can see then similarly

32:38

as we make our way along in here, um,

32:41

where the gray is right there is where we can see it.

32:45

In some cases this is useful. Um, in some cases it's not.

32:49

And so here we can see then that

32:51

as we make our way into the vessel here, we have this amount

32:54

of plaque, 30%, 20%, 25%

32:58

or last, somewhere around there is where we start seeing

33:00

that low attenuation and the calcification along in here.

33:04

So all in all, we could have probably figured that out

33:08

just on this view.

33:10

Um, you know that there is a tiny

33:12

bit of plaque along in there.

33:13

Again, something similar

33:15

to just the little top hat portion along that

33:18

'cause we all don't see it at the 50%,

33:20

which would've been right there

33:22

and then clearly it didn't extend down to 75% of the vessel.

33:26

So do you need

33:27

to do N-P-R-C-P-R short access view and everything?

33:31

Absolutely not. Is it useful?

33:33

Eh, sometimes it can be very useful.

33:36

Is my job here to teach you a lot of different methodologies

33:38

so that you can be fast and accurate at the same time?

33:42

Absolutely. That is my job.

33:44

So I'm, we're gonna come on back over here

33:46

so you can get an idea of what that looks like in this view.

33:49

And you can see similarly on this view without doing

33:52

that other one, um, that we have, you know, 25%

33:57

or less, um, by doing then the double oblique technique.

34:01

Okay? So, um, we will finish up

34:04

and see if there's any more plaque anywhere else.

34:07

LAD uh, has a tiny bit in the prox segment here.

34:10

Similarly, again, if we go to the top of the vessel,

34:14

so here's the top of the vessel, whoop,

34:16

and then we're gonna come on down.

34:17

And so we're about midway through right here, so at the mid,

34:22

mid vessel portion of it

34:24

and we can see that it's only taking up, uh, less than 24%

34:27

of that, uh, vessel length as well there.

34:30

So that's again, something that is

34:32

probably just affecting this top portion, the, uh,

34:35

of the vessel if we were to cut in short access

34:38

and how can we, uh, be sure of that?

34:42

Well, we can always then do our double oblique again.

34:45

And so then we're gonna just gonna bring that down there,

34:49

look at it that way, pop, pop, pop

34:51

and then come on over here to the one that's showing it

34:54

and boss, oops.

34:56

Alright,

35:01

that, that.

35:01

Okay. And then come to this one

35:03

and then, yeah, then you can see then just a very tiny

35:06

amount affecting that, that vessel right there too.

35:12

Alright, so less than 24 at the oste.

35:15

LM less than 24 at the proximal LAD.

35:18

And if we make our way along in here, we can see then

35:21

that there's very little plaque at the rest of the segment.

35:23

Looks really great as it curves along

35:27

distal LAD looks wonderful.

35:29

Uh, while we're down here, we'll just take a quick look at

35:31

the marginal PDA

35:33

and um, uh, uh, PLA branch there.

35:38

And then RCA looks fantastic for the remainder of it.

35:41

Let's not forget LCX.

35:43

So we got a quick OM that comes off there

35:46

and then the LCX continues on in the atrial ventricular

35:50

groove and continues along the lateral aspect

35:52

of the, of the left ventricle.

35:54

So, uh, all looks pretty good, right?

35:58

Yeah, and that was just a little oblique off

36:00

because we had done our double oblique

36:02

technique utilizing that.

36:04

So three different ways of looking at it.

36:06

Um, do you need to do all of them? Absolutely not.

36:08

If you have a center, um, that acquires this,

36:12

there's an an engine

36:13

and an automatic engine that will find your,

36:18

um, your coronary trees

36:20

and it will automatically process it.

36:23

So once you open up the case,

36:25

you'll have these green lines already there.

36:27

This is super easy on care recon, other post-process

36:30

and softwares will do the same thing too.

36:32

And you can just immediately come in here,

36:34

click on the green lines, that will be on all of the,

36:37

the vessels and uh, and just evaluate it that way.

36:40

So you can, if you wanted to do the straight view

36:43

and just see then, um, that you add a little bit

36:46

of plaque there and then a little bit

36:47

of plaque right there at the p um, or the proximal segment.

36:51

Um, this is obviously RCA,

36:53

but if we were to mon over here, similar right there

36:56

and then, uh, just a little tiny bit right along.

37:00

Okay. So, uh, lots

37:03

of easiness I in my personal practice and I,

37:06

and I'm sorry, I'll tell you about my personal practice

37:08

as opposed to my search patterns in my personal practice,

37:11

what I, I do not have them do this extra work.

37:14

I try to read off of the axials

37:16

'cause again, highest spatial resolution

37:19

and very few cases will I come in

37:21

and start doing this on my, uh, pre-procedural days

37:24

where we're doing, um, you know, mvs and uh, T mvs

37:28

and some of these other things then and ta TAVRs.

37:31

Yeah, absolutely. I'll,

37:32

I'll probably spend a bit more time in,

37:34

in this particular program just to make sure that I'm,

37:37

you know, seeing things, um,

37:39

and then having the quantification available.

37:41

So, uh, what was the writeup on this one?

37:43

This is a CAD rads one, right?

37:45

We have less than 24% and the LM and the LAD.

37:49

So just because we have less than 24% in two vessels,

37:53

three segments, four segments, five segments, whatever,

37:56

it's still a RADS one

37:57

because the highest degree of luminal stenosis is

38:00

what drives your CAD rads categorizations such as similar

38:03

to, um, birads, um, and RADS and so forth.

38:08

So, uh, the highest stenosis will be there.

38:12

Similarly, we could then quantify the amount of plaque

38:16

that's associated with this.

38:17

So we can just take this little guy there

38:19

and then come along here.

38:21

And at the handlebar, I'm just gonna right click here

38:25

and do a plaque analysis.

38:27

And so it will then just drive, as you can see here,

38:29

a plaque analysis program, um, to then evaluate those pixels

38:34

between my two, um, ROIs from the red to the blue.

38:38

And then give me then a breakdown of the amount of pixels,

38:42

what is their attenuation, the volume of them, so forth.

38:45

This is a poor man's clearly, or everything else.

38:47

I mean, this is free and super easy.

38:49

It gives you kind of an idea of

38:51

where then the attenuation is along there.

38:54

And as you can tell, it certainly did find, um,

38:57

all the important ones here.

38:58

So, um, you know, obviously we would wanna clean this up,

39:02

just make sure it looked, you know, appropriate and stuff.

39:04

But plaque analysis,

39:06

absolute can be done here if you wanted to and get an idea.

39:09

You can also do, if you wanted to epicardial attenuation fat

39:13

and then evaluate that up.

39:14

I mean, there's so much easiness around here,

39:17

so we can just do a fat analysis here

39:19

and then redraw, you know, what it is that we wanted,

39:26

you know, and just redraw then and,

39:28

and recalculate the amount of visceral to, uh,

39:31

to parietal fat and so forth.

39:33

So lots of really fun things. Are they useful?

39:36

Nah, some of them are. What is, where are the guidelines?

39:39

What is, what are, where is treatment, right?

39:42

Where is treatment, where are the guidelines?

39:45

What can we quantify? What can we see?

39:50

And, and then, you know,

39:52

where do we wanna lean forward and, and so forth.

39:55

So there's a whole lot, I mean a ton of biomarkers

39:59

and I don't need to tell all you guys, all them.

40:01

Um, but anyway, so we can talk about all that stuff.

40:04

So any questions on case number two?

40:07

Cadrad one, two locations. Osteo, LM and proximal LAD.

40:15

Alright, let's go then into cad, uh, to case number three.

40:20

So this is a 58-year-old male with a history

40:22

of intermittent chest pain exertion, so it's intermittent,

40:25

doesn't say anything about associated with work.

40:28

Uh, patient has a family history, so early coronary disease,

40:32

so father with myocardial infarction at age 65.

40:35

So if we were to plot this into a, a typical calculator, um,

40:40

we would have family history and um,

40:44

and that looks about it.

40:45

Nothing about his hypertension, smoking history

40:48

or any, um, other concerns.

40:50

Alright, so we're gonna do the same thing as you can, uh,

40:54

imagine we're gonna do an anatomic evaluation evaluating,

40:58

so let's get rid of the,

40:59

the chest wall there and that could be automated.

41:01

I'm not sure why on this particular one it's not automated,

41:05

but it, uh, anterior in ventricular groove, we have an LAD

41:08

with a couple different branches,

41:10

looks pretty good all the way down to distal LAD.

41:13

And then we have, that's probably a, a lima

41:15

or some other vessel coming along there.

41:17

LCX with a very stout, um, obtuse marginal

41:20

with some good branching going on there.

41:22

And then RCA very nice strong vessel.

41:25

Look at that with a good conus

41:26

and a couple branches along in there.

41:28

So what's the attenuation round here?

41:29

It looks really good, right? I mean,

41:31

really nice looking vessels.

41:32

So are we gonna, um, see some disease?

41:35

Well, let's find out, right?

41:40

Okay, so we'll just start immediately into the, uh,

41:43

left main and then what do we see here?

41:45

Well, we're seeing some disease right now.

41:49

The main thing is to determine is this real or not real?

41:51

What could it be? It could be confounding motion,

41:54

it could be, um, epic coronary fat.

41:57

It could be a couple other things

41:59

that could be involved in here,

42:01

but if you're not seeing a lot of motion on any

42:02

of the other sequences or in the other segments,

42:05

and it probably isn't so

42:06

that this is very sharp along this edge here,

42:09

very likely means that it's gonna be sharp, it's supposed

42:12

to be sharp on this edge, the no motion.

42:15

So this is probably a low attenuating plaque.

42:18

So this is low attenuating plaque

42:19

with a little stipple o calcification

42:21

as you can see at the top portion, superior aspect of it.

42:24

And when we do our double oblique, we'll take a look

42:26

and be able to see that a little bit more.

42:28

So less than 24% stenosis at the osteo LAD or proximal LAD.

42:33

And then when we continue on,

42:35

branching looks pretty good, right?

42:37

D one looks great, D two very strong large vessel here.

42:40

We do have a bridge and we'll uh, take another look at that.

42:43

And so that was mentioned, uh, and so we'll take a look.

42:47

Uh, distal LAD looks fantastic.

42:49

All right, let's pick up our, um,

42:51

our PDA right along in here to distal RCA

42:56

and work our way back and really great, right?

43:00

I mean, no motion. Usually you have a lot

43:02

of motion right here as it does its atrial kick

43:05

and that looks fantastic.

43:06

So good control. And here's that av, um,

43:10

that we were chatting about before.

43:12

So we have a sino atrial node right there,

43:14

and then we have then this av, um, branch

43:16

that goes along in there.

43:18

Conus branch coming along there. So no disease.

43:21

Um, normal origin course and termination of the RCA

43:23

and no dis luminal disease here.

43:26

Um, bifurcation to LCX

43:29

that travels within the atrial ventricular groove.

43:32

We have an obtuse marginal, um,

43:34

and then another obtuse marginal

43:36

as LCX continues on in the posterior aspect along here.

43:40

So this is, uh, looking pretty nice and good.

43:44

Alright, great. So only a little bit of disease there.

43:47

Let's just characterize this a little bit more.

43:49

How could we have found it if we didn't do

43:51

this axial technique?

43:52

Well, there are a couple different ways.

43:54

Um, again, we can, um, found it if we had, um,

43:58

our vessels set up in this way.

43:59

And so we can then see then that there's, uh, a little bit

44:02

of disease in that branching region.

44:06

And you guys pick it up. Yeah, right there.

44:11

We can straighten the vessel

44:12

and then we can just twirl it on its edge

44:14

and we can see that there's a little bit

44:16

of positive remodeling, low attenuation.

44:18

I'm just gonna bring this up here

44:20

so we can just take a quick look.

44:21

My apologies, I'm going a little bit fast on here, it's kind

44:24

of an old hat situation for me.

44:25

But we can see then this sort of irregularity to the lumen,

44:29

very sharp clean lumen on the LM over here, proximal LED.

44:32

But we can see that there's a little irregularity,

44:35

we call it the rat bite appearance.

44:37

And you can almost just see that right along there,

44:40

right rat bites, little, little, little n*****s, uh,

44:44

nibbles out there, um, in there.

44:46

So that is the early onset of those foam macrophages,

44:51

the inflammatory change,

44:52

and then the embedding of, um,

44:55

not only just cholesterol laden

44:56

but triglyceride laden material within, um, the second layer

45:00

of, of that vessel.

45:02

And so we can twirl it along in here

45:04

and see that it does make just a tiny indent along that, uh,

45:08

the, that aspect along in there.

45:10

Let's see if the plaque analysis, um,

45:12

picked it up, probably did.

45:14

So we'll just do here.

45:15

And then again, I'm gonna go to one

45:19

of the handlebars and then twirl around.

45:20

You can see that there is an, um, uh, a contour abnormality,

45:24

uh, little positive remodeling associated with there.

45:26

And then this low attenuating plaque.

45:28

Red means that it's low attenuating,

45:31

and so I picked it up as well.

45:32

Okay, so we have multiple ways of proving that we have, uh,

45:37

low attenuating material in the, uh, in

45:40

that portion of the vessel there.

45:41

We can also then do, let's just come on back over here.

45:44

We're gonna do then another view, which is, um,

45:47

our double oblique.

45:49

Uh, so some of you are, are fans of this.

45:52

I, again, I I'm not, this obviously is

45:56

a long drawn out process

45:59

and I'm a radiologist, so I like to be quick and fast

46:01

and, uh, and so yeah, this is, this is, uh,

46:04

a little too long for me, but that's okay.

46:06

We gotta learn how to do everything.

46:08

And so if we look at it from this standpoint,

46:10

we can see then that little, um, half moon

46:12

or coline shape there, uh, of low attenuating plaque

46:15

with a little stipple of, of high, um, degree

46:18

of calcified material along in there.

46:20

So we'll just kind of disappears and then ramp, there it is

46:25

and then it just disappears again.

46:27

Okay? So yeah, we got a little bit

46:29

of material right along in there

46:30

and we can just follow along there

46:33

and in case we didn't believe it that way, not

46:35

to worry there's another, uh, way we could do it.

46:37

And that's the vessel track

46:38

and we can see it in this way here

46:40

and then see that exact same thing right now.

46:44

You can see this is pixeling, um, obviously

46:46

because it has, uh, less amount of information

46:49

that it's using to fill in this space three dimensionally.

46:52

Um, so again, uh, something to consider.

46:56

Alright, so what is the writeup on this one here?

46:59

This is a CAD rads one less than 24% stenosis in the osteo

47:03

LAD secondary to low attenuating plaque.

47:06

What plaque has more of a, of a risk predictor,

47:10

or at least what are some of the conditioning things

47:12

that we look at in terms of risk?

47:15

Uh, of the, uh, features of plaque?

47:17

Look at the stapled calcific.

47:20

So little tiny bits of calcium as opposed

47:22

to big chunks of calcium.

47:24

We look at low attenuation.

47:26

The more low attenuating,

47:27

the more vulnerable the plaque is, right?

47:30

Napkin ring, uh, where there is sort of a ring of

47:33

that material around there

47:35

and positive remodeling where there's an extension,

47:38

a little hat that, uh, remodels the, the vessel outward.

47:42

So those four different biomarkers are used

47:45

to characterize plaque negatively

47:48

and there's a worse outcome in terms

47:50

of major adverse cardiac events with them.

47:53

So, um, why is that important?

47:55

Because the Scott Hart trial showed that for whatever reason

47:58

around that 25 to 49%, so our ca rads two,

48:02

we have a lot more death associated with individuals

48:06

as opposed to interestingly, the Cadrad three

48:09

and cadrad four.

48:11

Why? Well, because it, it appears

48:13

that the vulnerable plaque, the low attenuating plaque,

48:15

which is laying down, is laying down silently at

48:19

that cadrad two, which is typically not picked up

48:21

before corner ct.

48:23

Um, and it has the opportunity to crack or inflame or break

48:28

and then results in a call to thrombin, right?

48:31

And a call to thrombin is not good

48:33

because then it can create then an occlusion event

48:36

and that occlusion event we call an acute coronary syndrome.

48:39

And so that can lead into an infarct

48:41

and then, um, into depth.

48:44

So Scott Hart was really in informational in telling us

48:47

that it's not just the amount of stenosis,

48:50

but it's also the plaque features.

48:53

And so that's why we call out the plaque features, um,

48:56

in our current cab rats two.

48:58

So any questions on that? That's a pretty nice case, right?

49:06

Okay, moving on. Moving on. Case number four.

49:11

This is a 48-year-old male, uh, history of chest pain

49:14

and mixed hyperlipidemia.

49:16

So we have, um, some, uh,

49:19

abnormal calculator risk associated with the HLP

49:23

and so we're going to take a look

49:26

and see if any of that is landed in his coronary artery.

49:31

So, uh, good control,

49:33

good opacification, very strong.

49:36

Um, LAD with good branching here, it's a little torturous.

49:39

So what does tortuosity in the large epic corn

49:42

coronary arteries means?

49:43

Typically it means hypertension

49:45

or longstanding, um, uh, resistance in the vascular flow.

49:50

And so there are a couple different mechanisms

49:51

that could cause that microvascular disease, um, as well

49:55

as then hypertension.

49:56

So, so if you see a significant amount of that, um,

50:00

as you can see here, hypertension can be involved in there.

50:03

And so why is that important?

50:04

Well, if you have an increase in the vascular resistance,

50:07

you then have the potential for inflammatory changes

50:10

to the endothelial lining.

50:13

So if we remember back to the virtual,

50:15

what were the three things that caused an issue?

50:17

Well, po stagnant flow, inflammatory change, right?

50:22

And then, uh, thickening some sort of thrombosis, uh,

50:25

thrombotic capability within the material

50:28

that's sliding through those vessels.

50:30

And so then hypertension obviously can cause that.

50:32

So one of the bigger things in my personal opinion

50:36

that needs to be evaluated is hypertension

50:39

that we can find in our, in our anatomy as opposed

50:43

to waiting for it

50:44

to show up silently on a blood pressure measurement.

50:48

So we have the opportunity to change that.

50:50

So let's just take a quick look here

50:52

and see where we are with the coronary tree.

50:55

Um, and so we have,

50:56

and then the LM arising from the posterior aspect,

50:58

the left coronary cusp, a good bifurcation right there,

51:02

got just a tiny bit of disease

51:03

as you can see right there at the osteo LAD

51:06

and we'll just follow that LAD down.

51:09

So good septal branches as well

51:11

as diagonal branches coming off on both ends.

51:14

Um, and it looks very nice, uh, good ification, right?

51:18

We call this our trifecta where we can see all three

51:20

of them at the same time

51:22

and see that then the attenuation qualitatively is the same,

51:25

um, but that tortuosity, um, looks,

51:28

you know, ominous, right?

51:29

Alright, let's come on back to LCX.

51:32

So we had the normal course, um, uh, normal origin,

51:36

normal course and normal termination with a little bit

51:38

of luminal disease right there.

51:40

Uh, partial ified plaque less than 24% LCX in the atrial

51:45

ventricular groove and that looks pretty good.

51:48

A couple little tiny branches coming off there

51:50

and as, um, LCX continues on the lateral aspect

51:52

of the left ventricle, we'll pick up the PDA right here.

51:55

Um, and you can see then the PDA has a little bit

51:58

of tortuosity to it and then there's PLA

52:02

and it comes along here.

52:03

Torturous, torturous, torturous,

52:05

but no significant disease,

52:07

at least at this spatial resolution.

52:08

Right? And that looks pretty good.

52:11

So our call, um, here at the,

52:13

at the impression would be a cataracts one

52:16

with less than 24% stenosis at the osteo LAD secondary

52:20

to partial calcified plaque.

52:22

And um, are there any other high

52:23

risk features assisting with it?

52:25

Not really, although there is, um, a little, you can see

52:28

that dot of calcium here.

52:30

Let's, um, do this here.

52:32

You can see that little dot of calcium,

52:34

you can see also the low attenuation above

52:37

and beyond it here and,

52:39

and there's, there it is right there.

52:41

And so there is some low attenuating features,

52:43

but the predominant, um, makeup of this is that this is,

52:47

you know, uh, more, uh, more calcification than not.

52:50

Alright, so here's a little bit of rat bites.

52:52

So there's a bit of disease in there, um,

52:54

but that, um, that, you know, probably not, not the biggest,

52:59

greatest, uh, deal comparatively to everything else.

53:02

Alright, so any questions on this one?

53:05

I like these cases

53:06

because these are, you know, simple, easy to read.

53:10

There is, um, a good amount of, you know, sat

53:14

satisfaction in reading this in younger people.

53:17

And so I, I find that this is are really nice cases, um,

53:22

and you could really do something for them.

53:24

Would this have been picked up on a functional assessment?

53:27

Well, I mean it didn't sound like they went that direction

53:30

to start it, but, um, would this,

53:33

would doing a functional assessment change anything?

53:36

Absolutely not. I mean, it would probably have registered

53:38

depending on what kind of unit they were using a spec

53:40

imaging or not, it probably wouldn't have registered.

53:43

Um, so it's, you really can get somebody started on reversal

53:48

of disease if you then find the anatomy related changes

53:52

that are associated with it.

53:53

So anatomy first, right?

53:55

Anatomy first, that's the way to go.

53:57

Now how and what would you do in terms of mentioning the,

54:00

the tortuosity?

54:02

I typically mention tortuosity associated, um,

54:06

tortuosity in the coronary arteries, uh, correlate

54:09

for, um, hypertension.

54:10

And so I think that's a really important thing to kind

54:12

of call out because that's really, he's 48

54:16

and that's really gonna change the difference if you allow

54:18

this to go along for another 10 years, um, without, um,

54:21

disease modification.

54:24

So any, uh, questions on case number four?

54:29

Okay, so case number five.

54:33

We have quite a few different, uh, ways to evaluate this.

54:36

We have our best diastole, um, both

54:41

this looks like, uh, these are the same,

54:42

so we'll just disregard there,

54:44

but we have a couple different things here too.

54:46

Um, and they're at different, uh,

54:49

times in the cardiac cycle.

54:52

Um, we have also some, a couple of different things here.

54:55

So you can obviously, you know, get really crazy

55:00

with the amount of breakdowns

55:02

and breakouts of your, um, of your, of the type of exams

55:07

that you want to do and what you wanna send to the packs,

55:09

what you don't and stuff like that.

55:11

But remember that the most important thing

55:14

to read is the one that has no motion

55:16

and has good a ification.

55:18

And that's typically your diastole.

55:20

Diastole again is somewhere around the 60 to 70%

55:25

or late diastole somewhere around the 60 to 70%.

55:28

If you get later than that, like 80%,

55:30

then you're gonna get into um, you know,

55:32

some more motion along the edge.

55:34

If you go a little bit earlier, like 40, uh, 30

55:37

and 40%, then there's motion too.

55:40

There's a great emphasis now these days on, um, considering,

55:45

um, early systole as well

55:47

because we can time it pretty well to get them, um,

55:51

you know, uh, good look at the coronary arteries.

55:53

And so there's some really great papers about that.

55:57

Interesting thing about, um, early sly is

56:00

that then you don't have to then do heart rate modification.

56:04

You can actually just give nitroglycerin as a patch

56:07

and then go, alright, so for this one here,

56:09

this is a 66-year-old male with a history

56:11

of chest pain with activity.

56:13

Okay? Patient has a history of hypertension, mixed

56:17

hyperlipidemia and DM two.

56:19

So we've got a lot of different things from the risk

56:21

prediction standpoint, why is risk prediction important?

56:24

It gives us that pretest probability determination then

56:27

that there's gonna be something going on, um, or not.

56:30

So here, extensive coronary tree with a lot of branching.

56:34

Um, and, uh, so in the, a atrial ventricular groove here,

56:40

I'm sorry, the anterior interventricular groove here,

56:42

we've got the coronary artery here,

56:44

and then we have this overlying vessel here.

56:45

This is the LCX coming across here.

56:48

Um, so what looks bigger?

56:49

Um, well the LCX looks bigger

56:51

as it makes the way down here got some irregularity

56:54

of the mid and the distal aspect

56:56

of the LAD diagonal looks pretty good.

56:58

If we look along the RCA very nice robust vessel here.

57:02

So remember, where did most of our coronary blood flow

57:05

and the coronary blood flow reserve, um, end up in terms

57:09

of the vessel wasn't in the LCX, wasn't in the L-E-D-L-A-D

57:12

or the RCA, well it was the LAD, the LM to LAD.

57:16

So we're not seeing a really good plumpy appearance just on

57:19

the volume rendering of the LAD.

57:21

Then this is potentially

57:22

where we're gonna have some disease.

57:24

So the pretest evaluation of the anatomy is you can use this

57:29

to your advantage and evaluate it.

57:31

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

57:36

Very nice strong vessel. Again, in terms of, um,

57:39

the reserve, it should be around five.

57:41

So this is a little bit bigger. Uh, is that bad?

57:45

No, it's not bad. So oftentimes, uh, on the amount

57:49

of nitroglycerin you can get an enlargement of it.

57:51

Um, but if it's seven millimeters, eight millimeters,

57:54

and that's potentially dilation or aneurysmal.

57:57

So in this case here, LN looks pretty good.

57:59

We've got a nice bifurcation right there.

58:01

And then we already have then, um, some concerns

58:04

for disease right along in there.

58:12

And then let's take a look, uh,

58:15

at the LCX, since we're right here.

58:16

LCX looks pretty good.

58:20

Nice again, plumpy vessel, right? Plumpy plumpy.

58:24

So LCX plumpy vessel gives off

58:26

that obtuse marginal, but looks pretty good.

58:28

So what's the dealio? Why is it plumpy?

58:30

Well, maybe because of this guy.

58:32

Look at this post stenotic dilation, right?

58:35

We see this in some of the other vessels,

58:37

potentially the mesenteric vent vessels, um,

58:40

where there is an area of stenosis.

58:42

And then at following it, we have this dilation, right?

58:46

So this is unable to dilate. Why?

58:48

Well, the mechanism behind vasoconstriction

58:50

and dilation is associated with nitroglycerin.

58:53

It's the reactivity.

58:54

Um, nitrous oxide is the, um,

58:57

endogenous form of nitroglycerin.

58:59

And so nitrous oxide is released with breath,

59:02

breath in, breath out.

59:04

And then the endothelial lining, um, absolutely is able

59:07

to contract and dilate based on it.

59:10

So if nitroglycerin's given

59:11

and it's not able to contract like this is,

59:13

it's very likely due to some sort

59:14

of constriction associated with disease.

59:17

And so here we have the luminal disease

59:19

affecting this portion of it.

59:21

And then we have the, the post stenotic

59:22

dilation going along there.

59:24

You see this in the mesenteric vessels like celiac

59:27

and SMA trunk and sometimes the carotid arteries.

59:29

And obviously, um, CCO Willis. Why do you see that?

59:33

Well, because there's more neuroactivity associated

59:35

with those areas, right?

59:36

There's much more, um, neuroactivity.

59:40

And so you should see that potentially

59:42

around the coronary arteries too, right?

59:45

Well, there's some interesting evidence related

59:49

to the parasynthetic, um, innervation

59:51

of the coronary arteries,

59:52

and we haven't quite figured out yet if there's a lot of it

59:54

or a little bit of it or if it's the moment

59:57

that we're seeing it that it's already been damaged.

59:59

So there's a whole discussion on neuro cardiovascular, um,

60:04

uh, mechanisms and so we can't get into that today,

60:07

but it's absolutely is a really important thing.

60:10

Okay? So main thing to take away from here is that, um,

60:13

this looks disease.

60:14

Let's just go ahead and finish this, uh, last case up here

60:17

and get an idea of how much disease is going on

60:22

and then we can then, then take a break here.

60:24

All right, so then in our double ogle technique

60:27

where we're just gonna take a quick look, uh,

60:33

we'll just come down here and you can see then that there,

60:36

um, absolutely is at least greater than 25%

60:39

of the vessel positive remodeling low attenuating plaque.

60:41

And if we're gonna follow this along here,

60:45

we'll just continue on marching.

60:46

And this is again, why I'm not a big fan of the march,

60:50

march, march, but you know some,

60:52

and I'll learn some of this sometime.

60:55

So we're just gonna march along in here

60:59

and you can then see then that that's a significant amount

61:02

of, uh, low attenuating plaque.

61:03

If we were to look at it from, uh, curve planar reforms,

61:06

which come off the computer,

61:08

we'll just straighten this bad boy here.

61:10

So we can take a quick look if this green line is our, um,

61:13

full width half max, so 50% here,

61:16

we can see that it's pretty close.

61:18

Um, it's absolutely greater than 25%. It's not 50%.

61:21

So it's 25 40 9%,

61:23

and that's positive remodeling, low attenuating plaque.

61:27

So for case number five, this is CAD rads two with 25

61:30

and 49% stenosis in the proximal RCA secondary

61:33

to low attenuating plaque.

61:35

Some tortuosity a good reserve,

61:38

but as you can see associated with this here,

61:40

there's some inly dysfunction.

61:42

Uh, so this is a chronicity associated with, uh, the amount

61:46

of, uh, time he's been laying down plaque.

61:48

All right, it's two o'clock. I will stop there.

61:50

So if you have any questions, please ask

61:53

or send, um, questions to me via email or chat,

61:57

and then we can get 'em, um, answered for you.

61:59

But I'll stop talking now so you guys have an opportunity

62:01

to ask questions if needed.

62:04

Uh, Dr. Lorenzo? Yes.

62:07

Yeah, hi. Actually, my terracon, uh, player is not, uh,

62:11

really working too fast.

62:13

It's, it's really stopping

62:15

and you know, it's very difficult to, uh, yeah.

62:19

So can something be done about it? Like, uh,

62:25

We can get a technician to take it.

62:27

Just make sure that there's a, a really, you know,

62:29

that you've got a good strong internet speed.

62:31

But yeah, we can um, we can get a technician

62:34

to look at it. Yeah, it should be

62:36

Alright.

62:38

Absolutely. There's a question related to the length

62:40

of the plaque as mentioned here.

62:42

So we have handlebar, uh, one and handlebar two,

62:45

and the length of the plaque is, uh, 27 millimeters.

62:48

In this particular instance here, I tend

62:50

to use this only in, um, interventional cases.

62:54

So if I have an obstruction that I know is 70 to 99%, um,

62:58

then I will measure actually where the inlet is,

63:01

so the ostia to then the origin of the plaque.

63:05

So somewhere like that. So five millimeters, uh,

63:07

from the osteum of the segment is where the, the lesion

63:12

of interest begins.

63:14

And then, yeah, I think it is kind of nice to measure

63:17

the length of it too, mainly

63:19

because you wanna know how much wire to extend beyond that.

63:23

Now most cases the wire is gonna be three x the length

63:28

of your coronary artery.

63:30

So it's not really that big of a deal,

63:32

but it's kind of nice to know that,

63:34

that the agreement in the coronary CTA pre-procedural wise

63:38

to the invasive coronary angiogram is about the right.

63:41

So I do tell 'em, um,

63:43

but I think what's more important is how far from the origin

63:47

is than the beginning point of the plaque.

63:59

Of course. You're welcome. So I want

64:01

to thank you all very much.

64:03

Uh, your cases have been fantastic.

64:06

Continue to send them and continue to work

64:08

with the template provided.

64:09

If you have any questions, please, um, email, um, Courtney

64:13

or myself or Dr.

64:15

Fin, and hopefully we, you guys are still learning.

64:18

Yeah, thank everyone.

64:19

Thanks everyone for joining today

64:21

and this raw footage will be sent out here within the

64:24

next hour or so.

64:26

Um, take care everyone, and we'll see you next time.