0:00

Well, thanks everyone for joining us today for, uh,

0:04

week four office hours.

0:05

Dr. Loren is here. Um, Dr.

0:07

Lorenzen friends, we'll be here to review week four cases.

0:11

Um, as usual, if you have a question,

0:14

uh, feel free to ask Dr.

0:15

Lorenz directly. You can also type it into the chat

0:18

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

0:21

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

0:24

Great, thanks everyone.

0:26

I, um, love how you guys are, um,

0:31

evolving as cardiac imagers.

0:33

It, no joke that week four is kind of the, um, it's,

0:37

if you remember, it's the biochemistry, uh, month

0:40

of medical school, right?

0:41

Where we're gonna hit hard.

0:43

We're gonna just see how you do under the stress.

0:46

There is no right or wrong in terms of

0:49

how many you're getting, right?

0:50

And, but it's that, can you take the cases,

0:53

break them down methodically,

0:55

and see where there are areas for the improvement.

0:58

And for most of you, um, that the identification

1:02

of the amount of stenosis is not your area

1:05

where you need to improve upon.

1:08

Um, that's area's fantastic.

1:10

So that is, um, I hopefully are comments, um, are,

1:15

are useful to you guys.

1:17

I'm going to, um, go over this case here.

1:21

This is our first case, um, one.

1:24

And so let's pull this one up here.

1:25

And this was, uh, for 49-year-old male history

1:30

of hyperlipidemia, family history,

1:32

early coronary early disease, okay, new onset

1:35

of chest pain with exertion.

1:38

So right here, we should already have an idea,

1:41

pretest probability of what we should expect to find.

1:45

Now, a 49-year-old is, um, in terms of the biological

1:50

or the chronological age progression,

1:53

this should put 'em into the moderate amount

1:55

of coronary artery disease deposition, potentially, um,

2:00

or on the lighter end of it, um,

2:03

we won't see the extensive disease, so nothing greater than,

2:06

you know, uh, 3, 4, 5, or 600 biogas and scoring.

2:10

Now, all these additional factors, if we were

2:13

to plot 'em into a calculator, so would, uh, encourage us

2:16

to believe that there is an increased risk,

2:19

but the risk isn't because of a chronicity.

2:22

The risk is because of low attenuation

2:25

or vulnerable plaque

2:26

that's being deposited faster than it can be, uh, formulated

2:31

by the body to not affect lumen and lumen stenosis.

2:35

So we're dealing with the low attenuating plaque.

2:38

So if I see a young age with this, this amount

2:41

of symptomatology, which should put 'em in a higher pretest

2:44

probability of risk, I gotta think low attenuation,

2:46

which means then for us from an imaging standpoint,

2:50

higher space resolution and,

2:52

and a higher discernment value in my mind.

2:56

And for looking at the low attenuation

2:58

at the bifurcation areas.

2:59

Okay? So in this case,

3:01

you can see we don't really get the greatest

3:03

facial resolution.

3:05

Um, we've got a, a modeling effect that's occurring here

3:08

because of the individual's, um, AP anterior

3:12

to posterior chest dimensions, which, um, that

3:16

probably limited the, um, the amount of, um,

3:21

of mass, uh, that, uh, that we were able

3:25

to do under typical guidelines, right?

3:27

I, I mean, we don't, we can't absolutely, um, irradiate, um,

3:31

there you can do an admire, um, override on Siemens

3:34

and then ge similar sort of thing

3:36

and just go above what the milli amperage kv to size

3:41

of the patient is on that scout

3:43

and really get a genuinely beautiful picture.

3:46

Um, oftentimes you're not gonna get that

3:48

because you're not at the, at the scanner,

3:49

but if you are, my rule of thumb is do a test image.

3:54

Do a test image, um, on your, on your, uh,

3:59

scout or on your CAC score,

4:00

and just see if you see that

4:02

that AP diameter is greater than 30 centimeters,

4:05

um, or they're thicker.

4:06

There is a significant amount

4:07

of soft tissue involved in here.

4:09

Your quantum modeling is gonna go up now

4:11

with the third generations, that is the photon counties,

4:15

we've already been to each photon to get rid of that step.

4:18

So that's what you're paying the extra million dollars for.

4:22

Um, by the way, they go for about 2.8 to 3.1 million ish.

4:25

So in here we didn't, and we don't.

4:27

So we have to make assumptions, um, for, um, for that.

4:31

So let's go through this and see what we can do here.

4:37

All right, so as we look at this examination from a quality

4:40

standpoint, we look at motion and we look at opacification.

4:44

So we've got most of the opacification

4:46

of this bolus in the left side of the chambers.

4:49

We're in late diastole, right? 70% is late diastole.

4:53

Um, and we have pretty good motion control.

4:57

Uh, really you're able to then, uh, cruise through

5:00

and see, uh, the vessels without a lot of motion on this.

5:03

Now, if you do have access, obviously to other padding

5:05

or other, um, portions of the cardiac cycle, um, at areas

5:09

where there is some concern, you can certainly review that.

5:12

Okay, so at the lm, we have a part calcified plaque, uh,

5:15

positive remodeling here at the bifurcation.

5:17

So that's less than 24% right there.

5:20

Always go up and down through the o osteo.

5:22

The lm right widow maker, certainly don't wanna miss that.

5:25

And in the osteo slash proximal LAD, we have that bridging,

5:30

um, per calcified plaque.

5:32

But within, we also have this,

5:33

this component right along in here.

5:35

So that's less than 24%.

5:37

Now, when we get to the, uh, mid LAD, which is

5:40

after the first diagonal branches here, we're dealing

5:43

with this, um, component right here,

5:45

and we can see that it, um, has a per calcified component.

5:50

There is a little stipple of calcification there.

5:53

And then right there, and

5:55

as we travel from the superior portion, which is completely,

5:59

um, uh, steno, uh, down

6:03

to the mid portion where we can see both

6:05

of the presumed walls right here, we're seeing

6:08

that this is greater than 70, uh, greater than 50%.

6:11

And here we have it extending beyond that.

6:14

So if it's greater than, um, 50%

6:16

and we're left with two other categorizations, right?

6:19

The categorizations that we're leading towards then is, uh,

6:23

50 69 or uh, 70 99.

6:27

Now, those are very, very wide,

6:29

but they are under one combination, which is

6:33

obstructive coronary artery disease.

6:35

Now, the obstruction means then that 50% of the lumen is,

6:41

um, obliterated by some mechanism.

6:44

And so we now have

6:46

where functional meets anatomic at that 50%.

6:49

So I think at this point here,

6:51

the best thing we can do is try to determine

6:55

what we should do next,

6:56

but getting an idea on the, uh, percentage

7:00

of stenosis is our best bet, um,

7:02

because that I can hopefully bin it.

7:04

But if as long as you say greater than 50%,

7:06

we then jump into functional assessment.

7:08

So if you can hit that first base, then you're good to go.

7:11

Now the second base is accurate, um, lumen stenosis as well

7:15

as plaque, um, grading here.

7:18

Additionally with plaque, which is its own biomarker,

7:20

we have mild moderate than severe, um, amounts of plaque.

7:23

And then we have, um, uh, plaque features.

7:26

And those plaque features can be divided into high risk

7:29

black features or, um, um, non-high risk black features.

7:35

All these, again, as I mentioned

7:36

before, are discreetly outlined in the, uh, CADRAD 2.0,

7:41

um, documents.

7:42

So it's pretty easy to, uh, refer back to that if needed.

7:45

But what we're gonna do is we're gonna identify then the

7:49

anatomic location, the percentage of stenosis, the amount

7:53

of plaque deposition, and then any high risk plaque feature.

7:56

So here this is 70, 99%, obviously greater than 50%

8:00

and greater than 70%, um,

8:02

plaque stenosis in the mid LED secondary

8:04

to per calcified plaque.

8:06

Um, there is positive remodeling here.

8:09

How can we really, really tell?

8:12

Well, you, you sort of create then a contrast space

8:16

dependent, um, and independent from, uh, the,

8:21

the fat and then from the lumen here.

8:23

And so you can then see that there is positive remodeling.

8:27

It's, uh, it is, um, convex.

8:30

It's kind of got a little curvature to it right there.

8:32

When we go to the, uh, cprs

8:35

and the NPRs, we'll see this a little bit better,

8:36

but alright, 70, 99% mid LAD.

8:39

Let's just follow the rest of that.

8:40

Have some extensive, um, calcification along over here.

8:44

Let's just see that right there. Calc. All right.

8:48

And then we're gonna just turn this back up here

8:54

and can see then that all looks

8:59

really great, the remainder of it.

9:01

Okay, let's get on over to the, um, LCX

9:06

and if we follow the LCX similar sort of thing, um,

9:08

per calcified plaque, the ostia, um, seen right there.

9:15

L one goes off here a little bit right there on the

9:18

proximal, and then this carries around onto

9:21

to the lateral and it looks fine.

9:22

Okay, we'll pick up PDA and PLA right along in here.

9:26

Follow up here again, distal or CA looks pretty good.

9:30

PLA little bit of disease right there.

9:33

See that positive remodeling.

9:44

All right, so this is called the wink sign

9:46

where you have a normal diameter, you have a sloping

9:50

or thinning of that diameter, and then a reconstitution.

9:54

Oftentimes we will see this, um, in other anatomy, right?

9:58

I mean this is, uh, you know, apco, uh, um,

10:02

this is in the colon.

10:03

This is, um, you know, similarly in the esophagus

10:06

where we have, um, a circumnavigation of mass,

10:11

or in this case stenotic plaque that is limiting the,

10:14

um, the lumen.

10:16

And so when we get that wink, um, it's pretty common then

10:19

to determine that that's somewhere in the 50

10:22

to 69% stenosis area.

10:25

So let's take a quick look at

10:27

that under other circumstances.

10:30

So how about we go to the

10:34

CNPR

10:38

and there are a couple, this are, these are 90 degrees

10:40

to each other,

10:45

and we can see then that there's calcified

10:47

and part calcified plaque

10:49

and it has a significant narrowing.

10:56

And we constrain this. Of course,

11:03

there's a little bit of off, um, off axis here

11:06

that it didn't follow correctly, but obstructive disease.

11:09

Now let's take a quick look at the LAD

11:12

and review that under NPR conditions.

11:27

Alright, so for the sake of, um,

11:29

it didn't look like it went all the way down,

11:31

but for the sake of where our lesion of interest is,

11:34

we can twirl this one around here and we can see that

11:36

after that diagonal branch we have in that area of 70,

11:39

99% stenosis right there.

11:42

So poston dilatation, pre stenotic dilatation, focal area

11:45

of narrow, um, that's just fluid dynamics, right?

11:49

So we have a pretty good, um, evaluation there.

11:51

Alright, so let's, uh, review this case.

12:00

See, oh, that's two. Okay. Okay.

12:05

So again, chest pain, dyspnea.

12:07

Those are very discreet, uh, biomarkers

12:11

to consider in the symptomatology.

12:13

But, uh, as we look at, um, chest pain

12:16

and dyspnea, there is, um, more of a consideration of,

12:21

uh, of disease in its pre pretest probability, um,

12:25

as we look at, uh,

12:26

than the chest pain component in older population.

12:29

But dyspnea seems to be the thing

12:30

that we can oftentimes see being more of an occurrence, um,

12:34

in our younger population.

12:36

Pretest probability based on age, sex

12:38

and symptomatology, again, low pretest as you're, um,

12:42

in relation to coronary calcium scoring here.

12:45

Um, we don't expect then to have this disease,

12:48

but that dyspnea thing is a really concerning issue here.

12:52

Alright, let's jump on over to the, um, the RCA real quick.

12:56

That RCA lesion under ica, as you can see here,

12:59

that's a focal, uh, stenotic, uh, component

13:01

and that could go angioplasty or stent.

13:04

Um, and I don't recall how that, uh, individual ended up,

13:07

when we look at the LAD similar sort of thing there,

13:10

that lesion that you identified there, um, had, um,

13:13

an ICA correlate and looked like it was pretty bad.

13:16

So, um, in this case here, um, this, uh, uh,

13:20

report should have landed somewhere along the, uh, uh,

13:25

four a severe stenosis, 70 99% both in the LAD, um,

13:29

as well as in RCA.

13:32

And then there was areas of mild disease, um, both in,

13:35

in the mid RCA and then lm and then LAD and so forth.

13:40

So this should have been a a pretty good

13:44

and I'm, I'm not gonna say easy,

13:45

but at least a, a pretty useful sort of a, uh, way

13:48

to introduce them to for a component.

13:53

All right, so we're gonna do a little bit more here under

13:55

the same sort of guise, which is

13:57

that we expound upon the four A, which is that SE occlusion,

14:02

but 70 to 99% occlusion.

14:04

And what we're gonna try to do is continue to iterate four A

14:07

and show you some of the different

14:08

ways that it can be presented.

14:10

This is a common, uh, PLAD or MLAD, so proximal

14:15

or mid LAD very common to have a 79 9% lesion there.

14:19

Proximal or mid RCA very rarely a distal,

14:22

but um, proximal

14:24

or mid RCA are oftentimes where I see most of the 79 9%

14:28

that I'm calling to.

14:30

So, um, if we look at our tree of blood flow,

14:32

we're gonna get more on the left side than the right side.

14:35

And on there we're gonna get more on the proximal versus

14:37

the, um, distal aspects of it.

14:39

So we can kind of get a rubric, um, beyond that for us.

14:43

So in the next patient here, case two,

14:55

this is a 65-year-old male history of lipidemia tobacco use,

14:59

family history of early cad, new onset

15:01

of chest pain with exertion.

15:03

So we're in that chest pain 65.

15:05

So we should expect a fair amount

15:07

of calcification on this examination.

15:10

We should expect some remodeling.

15:12

So what we're looking for is not only just a,

15:14

a significant deposition of um, calcified plaque,

15:18

but then there are areas of low attenuation plaque

15:20

that can be useful for us.

15:22

Alright, you guys excited to see this one as much as I am?

15:27

I hope so. All right,

15:29

let's just take a quick look at the VR here

15:31

and just kind of get an idea of what our flow opacification

15:35

and contrast look like.

15:37

So regions of disease, right there, there,

15:39

and there's the calcifications.

15:40

So you can see, uh, dependent, uh, long,

15:46

lemme just move this on over here.

15:48

Alright, take a quick look at the LCX, we can see LCX

15:52

with an OM and significant amount of disease through there.

15:55

So obviously as it's contorting along, um, like a helix in

15:59

that tube, we can see that those are the areas where the,

16:03

uh, shoulder area of where the calcification is even on.

16:05

This is where we're gonna expect to be spending a lot

16:08

of our time doing the adjudication, right?

16:11

And then if we look at the RCA, we have then a pretty brisk

16:14

good looking vessel here with a little bit

16:16

of disease up there, maybe down here.

16:18

Nothing too crazy. All right?

16:21

So, you know, I like the axial, um, look

16:24

and evaluate it the way that you acquired it.

16:27

Uh, what we are seeing from this one here is again,

16:29

another modeled, uh, comp scattered

16:32

where the noise index is a little bit

16:34

higher than we would like.

16:35

A lot of this is again, due to that AP diameter in males.

16:39

Um, so we could have, um, sort of improved that, uh,

16:43

by kicking off the ad admire on Siemens

16:46

or, uh, similarly doing the same thing

16:49

with the GE construct here.

16:51

Okay, so we're just gonna do a quick,

16:54

um, check through here.

16:56

So we've got disease straddling that L-M-P-L-A-D area,

17:00

which we've seen before.

17:01

We got some there in that LCX area, right?

17:04

And then similarly, I,

17:06

I might have brought this up a little bit earlier

17:07

before, um, we've gone to disease in, um,

17:12

in the RCA, but this is called the trifecta, right?

17:15

Where you get to a point where you can see all three ve um,

17:17

coronary arteries in row here.

17:18

And what you're looking for is where's the areas

17:20

of ification, where are the areas

17:22

where the vessels a little bit smaller, um,

17:25

asymmetrically compared to the other ones.

17:26

And what I'm seeing is that the LED is a little bit

17:30

smaller, um, than it should be.

17:32

Remember mo 80% of the coronary blood flow is

17:35

through the left side, which should be the LED obviously

17:37

filling in a majority of the septum and the, um, anterior

17:40

and um, uh, inferior aspects of the left ventricle segments.

17:45

So that bothers me that that's a little bit smaller.

17:48

So, so let's come on back here

17:51

and let's just take a quick look at what we're finding

17:53

and what we're not finding.

17:55

And if we look at this, what are you seeing?

17:58

What is concerning you anyway?

18:06

Well, it's hard to catch it.

18:08

And, um, we threw this in there

18:10

because we wanted to repress, uh, upon the importance

18:13

of reviewing the lm.

18:15

That is honestly one of the best things that we can do, um,

18:18

to ensure that us as imagers are keeping track of our, um,

18:23

fake outs in the areas that are weak in the search pattern.

18:27

But the osteo LLM has a collar of low attenuation,

18:32

and what is hard is finding the LCC,

18:37

the left coronary cusp and where the osteo is.

18:39

And so this is the osteo, right,

18:41

just starting right along here.

18:43

But the problem is that's where the plaque is.

18:46

So it looks like that plaque is nearly starting,

18:49

there's just probably this little channel right here

18:56

and it completely stays with you.

18:57

It is occluding that entire thing.

18:59

Now, in this course, we try to do not best cases,

19:04

ideal cases, we've tried to do normal cases, cases

19:08

that you're gonna see day in, day out.

19:09

And why we're trying to do that is

19:10

because you have an idea, almost not, not a scary component,

19:15

but that you realize that even in the darkest corners of

19:20

of disease, they're uh, they can always be lurking in here.

19:24

So we have a low quality examination due

19:28

to high content scatter noise index, um, and,

19:32

and not really the greatest, um, contrast opacification

19:36

between the right system and the left system.

19:39

But we have anatomy and that's why we're here

19:41

and we're following this

19:42

and we can see that this is a significant amount

19:44

of low attenuation that just stays there.

19:46

This should be our first thing. Now, how did we get there?

19:49

Again, we looked at the size of the coronary arteries at

19:52

that trifecta, right at that 1, 2, 3 size,

19:55

and we noticed that it was a little bit smaller.

19:57

We expected a fair amount of calcified plaque,

20:00

but even on our first glimpse of this here,

20:03

not really seeing a significant amount of plaque

20:05

that is gonna really cause us to be too worried.

20:08

I mean, we will adjudicate this

20:10

and this will be, you know, 25, 49, somewhere around there,

20:13

um, for the proximal and the mid lesion right there.

20:16

But that thing doesn't go away, alright?

20:19

And, uh, unfortunately that's our lesion of concern.

20:22

Similarly here, the proximal LCX, um, calcified plaque, 25,

20:27

maybe 49% if you looked at it, that over there.

20:30

Alright, so, um,

20:32

let's take a quick look at this a little bit more

20:35

so we can evaluate it.

20:36

Now, how would you have been saved if you missed this?

20:39

If you had looked at, um,

20:46

cprs, you, you might have been saved.

20:49

Doubtful, I've never been saved by them.

20:53

So let's just say that, uh, delete this tree here

20:59

and, uh, oops, try this one again.

21:03

Hopefully you guys weren't, um,

21:05

I didn't lose you guys too long here, but this is the LCC

21:09

and uh, this is the LM popping up right here.

21:12

And again, we are super, super zoomed in,

21:14

that's why it looks like garbage.

21:16

Um, but as we are kind of looking long here,

21:19

we are seeing then proximal

21:22

and then here's the distal aspect of it here.

21:23

So this is gonna be our area that we're gonna focus on

21:27

and let's, um, lemme get rid of all these little things

21:32

that are going on here.

21:33

And so this is where our area of concern is right here.

21:41

And you can see there's very little channel here.

21:44

There's calcification, calcification, and then that plaque

21:48

and that stays with us.

21:50

Obviously that's all occluded right there.

21:54

So that's it, that's it in the lm.

21:57

So what were our cutoffs for the lm?

22:00

Anything less than 50%, you're fine.

22:04

Anything 50% or greater, you're not fine. And why?

22:06

Because we have, uh, reason to believe that as the,

22:11

um, LM occludes, then you increase in your ischemia

22:15

and your chest pain and then your symptomatology.

22:18

So here we have something that is greater than 50%, right?

22:21

I'd probably say it's around 60% given just that little,

22:24

that bit of chi tiny channel right there.

22:27

And, um, that's really the concern.

22:29

That's really what we're, um, gonna be focusing on here.

22:32

There's obviously that collar along here too,

22:34

but as we looked along that, um, not as bad

22:37

as we saw in the axial right there.

22:39

That's, uh, that's it.

22:41

So as we're looking at this, I, I, we decided

22:44

to put in a couple another round of that, um, lm, um, to try

22:49

to get you guys to reconsider.

22:50

Then the osteo and the LM are really, really big things.

22:54

They're very, very big areas to clear for, um, for stenosis.

22:58

And in this unfortunate case here, um,

23:00

this one was missed on the original read.

23:03

Um, and then when we came back to it, um,

23:05

it certainly did have some issues.

23:07

Uh, what kind of issues?

23:08

Well, let's go and let me share this in with you.

23:16

So that's, um, the distal LM with that cha uh, channel

23:20

that we had seen there, and that's under ICA.

23:22

So while we might have, uh, discounted a lot of the, uh,

23:26

the bloom artifact there,

23:27

that channel unfortunately looks smaller actually, um,

23:32

under ICA conditions there.

23:34

So, um, that's, that's unfortunate, um,

23:37

that we have an opportunity

23:39

to see these pretty clearly under, um, ICA

23:42

and unfortunately didn't go, um, directly to a cath.

23:45

It sort of bounced around a little bit under functional

23:47

assessment until finally we got there.

23:50

Okay? So in this case here, it's a CAD RADS four B.

23:55

The four B indicates then a designation

23:57

of LM involvement greater than 50% stenosis,

24:00

or that there is, um, three vessels that are 70 to 99%.

24:05

Either way. What we do at this point, the recommendation is,

24:08

is that we are evaluating for viability.

24:10

What that means is if we were to go ahead

24:13

and do a standard, um, cabbage where we're gonna reperfuse

24:17

the left ventricle right ventricle with um, all this blood,

24:20

um, the viability is to determine then the ratio

24:23

of dead tissue to, um, to live tissue.

24:27

And that gives us, first of all an idea then, okay,

24:30

if there's more dead tissue than live tissue,

24:32

then we wouldn't do that.

24:34

But secondary then, um, if we did do a reperfusion strategy,

24:38

adding oxygen and oxygen

24:40

and blood flow to dead tissue actually has a very well

24:44

and understood, um, uh, major adverse cardiac event,

24:49

uh, risk factor, um, and event rate associated with it.

24:53

So we would wanna make that, uh,

24:54

conclusion based on functional assessment.

24:56

Um, cardiac MRI is another good way of doing it.

25:00

If you have more viable tissue, let's say, um,

25:05

a live tissue than dead tissue, then you can determine then

25:08

what is, um, at risk in terms of the tissue.

25:12

And you can do this by doing a stress component behind it.

25:16

So all in all very interesting components here,

25:19

but, um, that's our area of, of weakness and concern.

25:22

So as I'm looking through this, I would be looking for areas

25:25

of prior infarct.

25:26

Um, this is a contrast or a, an, uh, an enhancement exam.

25:30

So looking for areas where there's low attenuation in some

25:33

of that areas of the septum

25:35

and the anterior wall along here comparatively

25:38

to lateral wall

25:40

and inferior wall to see if there's any other issues.

25:42

And thankfully in this case there is not.

25:45

Okay, so any questions on this? Uh, exam number two.

25:52

So case three is going to be a 72-year-old male history

25:55

of hyperlipidemia, hypertension,

25:57

and diabetes, DM two onset of chest pain and exertion.

26:02

So older age male,

26:05

we have quite a few risk factors if you were

26:08

to pretest probability should be a fair amount

26:11

of calcification

26:13

or smaller, um, vessels that is vessels that are unable

26:17

to react to nitric oxide, um, dilatation, uh,

26:23

via in increased blood flow.

26:25

Uh, we should then, uh, see some other concerning, um,

26:29

components behind that.

26:30

Right? Alright, so let's, um,

26:40

let's take a quick look and see what we see.

26:45

So I, again, I always start with the volume renderings.

26:47

I think the volume renderings are just a, a really good way

26:51

of getting a lay of the land.

26:52

So, uh, proximal LADD one LAD

26:56

and there's a little bit of disease right there

26:58

and then there and then some little rat bites along in here.

27:01

We look at the LCX, so there appears

27:04

to be a vessel along the lateral aspect of it.

27:07

Um, you know, not sure what's going on over here, um,

27:11

but that could be, uh, the LCX there.

27:14

We really brisk looking RCA, um,

27:17

very nice, well-defined.

27:20

So what do we see in terms of asymmetry?

27:22

We see the left system not being as large

27:24

as the right system, which is always a concern for me.

27:27

And then similarly we see, um, maybe a,

27:31

a nice looking vessel along here,

27:32

but we're not seeing the LCX as brisk

27:35

and as, uh, well a pacified

27:37

as the RCA not that uncommon.

27:41

Um, but let's just see what else we, uh,

27:43

find out additionally here.

27:46

What do you think about the quality as, um, assurance here?

27:49

We have the majority of contrast yes in the left system.

27:52

Okay, great. But then we have a fair amount

27:54

of contrast in the right as well.

27:56

Um, this is not a good finding.

27:59

Um, the LA is usually very

28:03

dilated is it's got fluid in there,

28:05

it's a passive system, right?

28:07

So this is telling me that we, um, have an um, um,

28:12

an oleic system, right, where there's not a lot

28:14

of blood flow or blood volume in the system

28:16

or at least in reserve.

28:19

And, um, I,

28:20

if you just even start scrolling here on extra coronary sort

28:24

of, um, findings, you'll see here that the MPAs large, it's,

28:28

you know, somewhere around 29 here we got 30

28:31

and then we've got uh, uh,

28:35

essentially an occlusive thrombus in the distal RPA in the

28:39

bronch, um, intermediary, um, PA system as well

28:44

as then into the lobar branches

28:46

that we can see here and here.

28:48

So PEs, pulmonary embolisms that, um,

28:51

that are present can be acute or chronic.

28:54

Um, there is, uh, an entire differentials related to um,

28:58

the amount of, uh, disease that you see there

29:00

and what you should be considering given the history

29:03

that we have here.

29:04

Um, this doesn't, uh, appear

29:06

to be anything exotic other than just a,

29:08

a normal garden variety pulmonary embolisms, uh, um, due

29:12

to static, um, blood flow

29:14

and potentially then, as we can see here, oliguric,

29:16

so low blood volume, um, blood volume that's sticking around

29:21

and then probably, um, de novo formation

29:24

of thrombus within the pulmonary, um, arteries

29:27

here it is dilated.

29:29

So there is significant disease along that aspect of it,

29:32

but um, nothing too crazy.

29:36

Okay, so now let's do the, um, LEDs

29:39

and the LMS here.

29:41

We have then, um, disease.

29:48

Let's take a quick look at the LM LM to LCC

29:51

and then there's a, um, LAD to LCX.

29:57

So good BI bifurcation along there.

30:00

And let's see that LAD then has a D one

30:03

and then a, a mid LAD and an LCX system.

30:07

Not a lot of disease in there, right?

30:09

I mean it's really amazing that there isn't anything

30:11

that's um, that's consequential within the LAD.

30:14

Same thing here. So then what about the LCX?

30:17

Well, let's just follow it along in here.

30:21

Is that the normal sort of presentation of the LCX?

30:26

No, it's not. And I love this case

30:28

because this um, helps us really come back to

30:32

what is important in life

30:33

and that's the atrial ventricular groove.

30:36

The atrial ventricular groove is the um, area

30:40

where LCX is supposed to inhabit.

30:42

If it is marginal

30:43

and it crosses along there, not only should you see um,

30:47

the LCX, but you should potentially see then an om in this

30:50

case here we do not see um, an om, I'm sorry,

30:54

an LCX we see an OM only.

30:59

And then in there, what else did we see?

31:04

We see this little wis of a vessel right in here

31:07

and that comes right off there.

31:08

And then you can see that's a very tiny opacified vessel.

31:12

It's not a vein, but it is the REMI remnant

31:15

of a chronic occluded LCX.

31:18

So this is something that's either 70

31:19

to 99% in the proximal component

31:22

or it's something that has been chronically occluded.

31:26

Now in this case we pop this in here, not to mess

31:30

with anybody, but really

31:31

to remem if you guys would come back to

31:34

what is the entire point

31:35

of the coronary CTA in an anatomic evaluation,

31:38

what is an anatomic evaluation?

31:40

The recall of where the vessels are supposed to be in time

31:44

and place and in a location.

31:46

And so, um, the LCX is supposed

31:49

to always be within the atrial ventricular groove

31:52

unless it's an anomalous origin course or termination.

31:55

And in this case here we do have a very brisk looking obtuse

31:59

marginal, but we have a vessel here that is the LCX,

32:03

but it is extremely atretic.

32:05

Atretic means that it's very narrowed, very small.

32:08

Um, there are a lot of, um, tortuosity associated with it.

32:12

So this is why I suppose that probably is an,

32:15

a chronic occlusion that's going on in this space here.

32:19

Very interesting stuff. Lovely, lovely.

32:23

So let's follow the R-C-A-R-C-A. Looks pretty good.

32:27

No issues there. Really not as, not a lot of disease.

32:31

Maybe a little bit right along in here that we had seen

32:34

before, but nothing too crazy, right?

32:36

Okay, all,

32:41

so in this case here, what we had um, was a really, um,

32:46

interesting opportunity to find, uh, what we call a, um,

32:51

a cutoff sign where we have a branching of the proximal LCX,

32:56

but then all of a sudden what we would assume

32:58

to be the LCX is now just the,

33:01

the actual Optus marginal coming across here,

33:03

whereas the remainder

33:05

of the LCX is this tiny little thing here

33:08

that is continuing on in the atrial ventricular groove.

33:11

So at this point you have the opportunity

33:13

to really look at this, discern that the LCX is a TRA 70

33:17

to 99% stenosis

33:19

or take the bait that the LCX was the obtuse marginal.

33:24

So hopefully, um, you saw that after the fact,

33:28

after the review, it's very uncommon for people

33:31

to ever get this one right?

33:32

Um, we obviously design these things so

33:36

that nobody should ever get all of them right?

33:38

If you are, then you probably shouldn't.

33:41

You should be teaching as well.

33:43

Um, but the nice thing is,

33:44

is is we're looking at the areas of concern, right?

33:47

The areas where there's potential disease.

33:58

Okay? Alright, any questions on that one?

34:03

Alright, so let's go then to case number four.

34:08

Case number four 59-year-old male with history

34:11

of hyper lipedema hypertension, tobacco use in DM two,

34:14

new onset of chest pain with exertion

34:17

and acute coronary citra is ruled out negative cardiac

34:20

biomarkers and no evidence of ischemia and ECG.

34:23

Okay, so guy presented individual presented 59-year-old

34:27

male, um, in acute distress,

34:30

probably a nine one one call rolled up to the ER

34:32

or some sort of urgent care center.

34:34

Um, obviously the first thing is

34:36

to evaluate the symptomatology

34:37

to determine where's the concern.

34:39

So chest pain, okay, chest pain

34:41

that radiates potentially up, uh, up in extremity.

34:45

Okay, well that sounds like it could be an

34:46

acute coronary syndrome.

34:48

Let's get the, uh, troponins

34:49

and an ECG to correspond to either ST elevation, depressions

34:54

and then biomarkers if those were negative,

34:56

which it sounds like then the next thing is, is

34:57

what potentially is also, um, the issue here.

35:00

Okay, so let's take a look at that.

35:02

In this case here we have um, a bo um, a

35:07

um, algorithm that is um, body 49

35:11

and then we have just the regular one.

35:12

So I'm just gonna do the body 4 9 1 here.

35:16

Okay, so let's take a quick look at um, the vr.

35:20

VR is a mess, right? Woo.

35:22

First modeling here

35:23

and then significant amount of disease along in here.

35:26

Significant amount of disease in the LCX, D one, D two,

35:29

D three, those all look pretty awful.

35:31

Similar sort of thing here.

35:33

Um, proximal RCA with significant amount

35:36

of calcify disease, we can see that there.

35:39

Recall how old this patient was?

35:40

This was a 59-year-old male.

35:43

Um, so this is one of those cases

35:45

where this individual did not waste any time, um,

35:48

in the course of his disease.

35:50

Okay? Another, um, exam purposely, well not purposely,

35:55

but where we're gonna have, um,

35:57

difficulties in the interpretation.

35:59

So not only do we have then significant disease,

36:01

but then we have an interpretation component behind it here.

36:04

Okay? So what do you guys think

36:07

when you re reviewing this one?

36:09

Was this one? Um, easy, hard, not so difficult and stuff.

36:13

Again, the idea behind this was to try

36:15

to help everybody understand

36:16

and discern then um, what is disease, what's not disease.

36:20

Um, and then kind of go from there.

36:23

So your guard was hopefully, uh, raised, there was a lot

36:27

of concern that there was disease

36:28

and a lot of potentially a lot of areas.

36:31

Um, you know,

36:33

what are we gonna do here with this one, right?

36:35

Well, um, what I like about this is that um,

36:38

we have the opportunity to add things in your weeks

36:43

that are just um, what we call them setters.

36:46

We built you up in terms of stenosis

36:48

and the amount of plaque.

36:49

But then we're gonna reset it to see how well you do

36:52

with being able to discriminate between the artificial,

36:56

um, increase in the amount of stenosis that we've been doing

37:00

by week to then just reset it.

37:02

So what this means is in your normal practice you might get

37:06

that cataracts four B or that for a

37:08

and the next thing might be a

37:09

cataracts one or cataracts two.

37:11

So being able to reset after each case is really important.

37:14

That's essentially what we're doing with this one here.

37:17

So there's a little bit of plaque here,

37:18

we're gonna get rid of that.

37:20

Um, plaque. We're gonna see then that there's a little bit

37:22

of disease in the LM and in the distal LM here.

37:28

And this is our concern, right?

37:29

The whole significant amount of calcified disease along

37:32

that there

37:37

and then here

37:47

and then along here too.

37:48

But as long as we are kind of moving across here,

37:50

we don't really see some anything significant.

37:52

25 49, right? This is all 1 24 and this is 25 49.

37:56

Get into the distal aspect of the LAD.

37:58

No real issues going on there.

38:04

LCX, not bad, right?

38:06

And you can see then the LCX staying within the atrial

38:09

ventricular groove, not an

38:11

issue here.

38:15

RCA we do have a little, um, some plaque here.

38:20

What would you say that is? Just on

38:21

that picture right there, we're looking at the short axis,

38:23

so we won't need to do a long access short access view here

38:27

we're about 25, 49, maybe 50% if you wanted to get uh, kind

38:30

of froggy, but really nothing too crazy.

38:33

A little bit of plaque disease along in here. Here.

38:37

Not a big problem. Not a big problem.

38:40

Alright, so what did we do here?

38:42

25 40 9% stenosis, um, no cataracts.

38:46

Two, uh, the degree of plaque, um,

38:49

you know is a moderate degree of plaque,

38:51

a partial calcified plaque.

38:53

So I think the idea behind this is that we are trying

38:56

to introduce the normalizing cases.

38:58

The individual had a significant history,

39:01

acute coronary syndrome has a significant amount of disease

39:05

as you can see here with this extensive amount

39:07

of calcified plaque.

39:08

But what you're not seeing here is in the luminal stenosis

39:11

to go along with it.

39:17

Alright, last case.

39:26

Last case is, um, 68-year-old male with a history

39:30

of obesity, hyperlipedemia, hypertension

39:32

and diabetes, coronary artery disease with prior PCA,

39:38

Prior PCI to the LAD

39:40

and LCX request for coronary disease evaluation.

39:45

So now we've gotten to the point

39:47

where we've just got a really difficult

39:49

case to evaluate, right?

39:51

I mean there is just disease everywhere

39:53

they've gone through intervention.

39:55

This is just one of those really difficult ones.

39:57

But even on here we can discern then some degrees

40:00

of opacification and none.

40:02

Alright, so lm, LAD,

40:12

long segment LAD with a stent looks really well pacified.

40:17

What are we looking for here? Low attenuating regions.

40:22

Some of this high attenuation obviously within the lumen

40:25

would be, um, redeveloped calcium within the stent.

40:29

Don't see it. Very clean entry of the stent

40:34

and short segment looks pretty good.

40:35

Not a lot of disease. There's the OM coming across

40:38

and there's the LCX move along in there.

40:41

Very hard to see. Absolutely if you wanted

40:42

to do an N on this, which means that you were unable

40:45

to evaluate it, totally fine.

40:49

But what is the real issue here? Bird beak sign.

40:52

We can absolutely see how this narrows

40:54

and occludes down here.

40:57

And this occlusion then is obviously a very big deal

41:00

because it's continuing on for such a long period of time.

41:04

Now in this course, unfortunately we're not gonna go through

41:06

how do you do a chronic, uh, total occlusion evaluation.

41:11

Um, but there is a scoring system,

41:13

a Richter scoring system for that.

41:14

In this case here, what we're just trying

41:16

to do is identify it

41:17

and you can see that's a significant amount of disease

41:19

and long in there and most of you got this,

41:23

so it wasn't really that difficult, um, to eval.

41:26

But that is absolutely one of the, um, more

41:28

concerning things, um,

41:30

where we have then significant disease within there.

41:34

Um, so I think that's about it.

41:39

There really wasn't too much other than uh,

41:41

CADRAD five, an introduction of it.

41:43

We're gonna do a little bit more in the terms

41:45

of cadrad five in your week, five cases.

41:47

So, um, definitely look into that a little bit later. Okay,

41:51

Dr. Loren, we

41:52

do have a question in the chat.

41:54

Um, how do we identify the various types of graphs?

41:58

Yeah, there are a lot of graphs.

42:00

There are graphs, um, that are, um, saphenous grafts

42:04

or from veins and then arterial grafts.

42:06

And essentially what that has to do with is the size

42:09

of the graft, the lum, the diameter size,

42:12

and then where they're typically done, um, graft off

42:15

of the aorta are typically sino, um,

42:18

saphenous venous grafts, SVGs,

42:21

and um, they could be diameter around six to seven.

42:24

If it's greater than 8, 9, 10, then

42:26

that usually is a dilation of the graft.

42:28

But they usually come off here and then come across

42:31

and then do a distal, um,

42:33

obtuse marginal dis a D one diagonal or an RCA.

42:38

The only time we would do that for a, for an LED

42:43

is if we've already tried to do a lima graft.

42:46

Now Lima, this is an artery.

42:47

This is an artery that does not have the same muscle lining

42:51

as the coronary arteries.

42:52

So you typically do not get any calcified

42:55

component behind it.

42:57

So these are the late stage grafts.

42:59

We usually don't, they're usually not placed, um,

43:02

until late stage or if there's a definitive therapy

43:04

and you just wanna do it once.

43:11

And any pitfalls to be aware of when evaluating graft.

43:14

Absolutely lots of pitfalls. One is motion.

43:17

What is unable to dilate the graft.

43:19

Another one is the anastomosis

43:21

because there's usually a clip right nearby.

43:23

Lots of pitfalls. Essentially what we're looking for is, um,

43:27

as we do with a coronary origin course termination

43:31

and as best as possible luminal evaluation.

43:33

Very commonly because the grafts don't respond as well

43:38

to the native coronary arteries,

43:40

they won't luminary distend.

43:42

And because of that, we're not really on the hook

43:45

for an entire graft evaluation.

43:47

That is, if there is a ification

43:49

and there is plaque, okay, great.

43:51

But in my view, when we have cases that look like this,

43:55

this is not common for us to then nail down the, the

43:59

entirety of stenosis that's involved in there.

44:07

Terrific. Thank you Dr. Lorenz.

44:09

Um, if nobody has any additional questions,

44:12

um, sorry I wasn't on camera.

44:16

If no one has any additional questions.

44:18

Um, thank you for attending.

44:20

Uh, this is being recorded

44:21

and the raw footage will be emailed

44:24

to everybody a little bit later this evening.

44:27

Um, sorry, one more question.

44:29

Do stents have artifacts? Yeah,

44:31

Of course they have metallic artifact

44:33

because they're metal and they're right in that space there.

44:35

Um, they typically what we do is we do, um, as you can see,

44:40

this is not a normal, um, algorithm

44:42

of evaluation or a filter.

44:43

This is one that has a high contrast

44:45

or lung filter where you then you're trying

44:48

to discriminate, contrasting.

44:50

So the edge of the craft to then the contrast in

44:53

between here with the newer systems, we're able then

44:56

to account for the photons

44:58

that are causing artifact and remove them.

45:00

You might be familiar with imar for like, you know, fusion

45:04

and, and metal, um, hip replacements.

45:07

Well that iteration technology is available in coronary

45:11

stents at a great level.

45:13

So that's obviously one of the, it's metal.

45:15

So there's gonna be a metal

45:16

artifact that's associated with it.

45:20

Great. Thank you again Dr. Lorenz.

45:21

Um, if anyone has any additional questions, feel free

45:24

to email me your question

45:25

and I will, um, uh,

45:28

get a response from the faculty at a later time.

45:31

So thank you again and we will see you all the next session.

45:34

Thanks again, Dr. Lorenz.

45:35

Thanks guys. Have a good one.