0:02

Hello and welcome to Case Crunch Rapid Case Review

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for the core exam, hosted by Medality.

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In this rapid-fire format,

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our faculty will show key images along

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with a multiple-choice question,

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and you'll respond with your best answer via

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the live polling feature.

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After a quick answer explanation, it's on to the next case.

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You'll be able to access the recording

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of today's case review

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and previous case reviews

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by creating a free account using the link

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provided in the chat. Today,

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we are honored to welcome

0:30

Dr. Muhammad Umair for a cardiac imaging board prep case review.

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Dr. Umair, whose focus is in cardiac and vascular imaging

0:38

and cardiovascular MRI, earned his medical degree from King

0:42

Edward Medical University.

0:44

He completed a fellowship in interventional radiology

0:47

and general surgery residency at Johns Hopkins.

0:50

He subsequently completed a diagnostic radiology residency

0:54

with early certification in interventional radiology at

0:56

Northwestern University, as well

0:59

as a cardiovascular imaging fellowship at the

1:01

Feinberg School of Medicine.

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Questions will be covered at the end if time allows.

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So please remember to use the

1:07

Q&A feature to submit your questions.

1:09

With that, we are ready to begin

1:11

tonight's board review. Dr. Umair, please take it from here.

1:15

Hello everyone. I'm very excited

1:17

to present this board review

1:19

um, for the cardiac imaging.

1:22

I have about 20, uh, cases, uh, put together.

1:25

Um, I think these are commonly tested pathologies.

1:28

Uh, we're gonna touch on imaging physics a little bit.

1:31

So let's, uh, without any delays, let's get started.

1:36

Here's my disclosures.

1:39

Um, I did obtain some of the explanation, uh, some

1:44

of the images I included in my,

1:45

in my explanation from this open-source, um,

1:48

pocket guidebook.

1:50

Um, here's a QR code if you guys are interested,

1:53

you guys can scan it, um,

1:55

and can have access to that, uh, particular resource.

2:00

And here's the poll question, just to understand

2:04

a little bit better, um, what kind

2:07

of group we have here today.

2:18

Alright, we're gonna get started.

2:20

51 00:02:25,645 --> 00:02:27,445 So here's the case 1.

2:29

A 56-year-old female,

2:31

cardiomyopathy with regional wall motion abnormalities,

2:34

new-onset heart failure with a reduced ejection fraction (EF),

2:38

new diagnosis of breast cancer, normal CT coronary, and normal stress test.

2:42

And here is their, um, four-chamber,

2:47

three-chamber, and two-chamber short-axis cine's.

2:52

Uh, sorry, uh, cine imaging.

2:58

So, which of the following cardiomyopathies

3:01

is most likely in this case? Ischemic cardiomyopathy,

3:09

restrictive cardiomyopathy, stress-induced cardiomyopathy,

3:13

or constrictive cardiomyopathy?

3:16

And we're gonna play these cines

3:20

one more time.

3:34

Okay. So, majority of the group thinks

3:39

that this is stress-induced

3:41

cardiomyopathy, which is correct.

3:43

Um, you can see that there is apical hypokinesis, um,

3:48

more so than the, uh, than the basal segments.

3:51

Now, one of the clues here is obviously in the question stem,

3:52

72 00:03:55,765 --> 00:03:58,065 recent diagnosis of the—of, um,

3:58

breast cancer, which is the stressor.

4:00

Um, another cue here is

4:02

that I'm not including any LGE imaging.

4:05

I'm not giving any scar-related imaging here.

4:09

So, I'm not asking a question that is gonna go

4:12

for a scar-pattern kind of question.

4:15

Typically, there is no scar, uh,

4:17

in stress-induced cardiomyopathy,

4:18

which is also called Takotsubo cardiomyopathy.

4:21

So, recent stressor demographics is important.

4:24

More common in females,

4:26

typical hypokinesis in a nonvascular distribution.

4:29

So, this is a non-ischemic process.

4:32

Now, there could be atypical presentations.

4:35

In some cases, there could just be one segment

4:37

that is hypokinetic.

4:39

Now, sometimes you can have a reverse Takotsubo

4:42

where you have just basal akinesis.

4:45

Um, a finding that can actually, uh, help you

4:49

make the diagnosis is isolated T2 abnormality,

4:53

isolated edema in—

4:54

in respective segments which are hypokinetic.

4:57

For example, if there is akinesis in the, uh,

5:00

apical segments, you will also see edema in those segments.

5:06

We're gonna move on to the next case.

5:11

Case two.

5:16

LGE imaging provided here.

5:19

61 years old male, palpitations, history of smoking

5:23

and type 2 diabetes.

5:24

Now presenting with shortness of breath, PVCs,

5:27

and EKG abnormalities.

5:32

CTA coronary demonstrates obstructive

5:34

narrowing in which vessel?

5:46

Okay, excellent.

5:47

So, most of you think that this is a circumflex

5:51

infarct, uh, which is correct.

5:53

In most anatomies, you're gonna have basal lateral

5:59

inferolateral wall infarct.

6:01

Now, this is more so a transmural infarct, um,

6:06

and typically, the thickness

6:08

of the infarct also predicts outcomes.

6:11

Um, generally, if it's less than 50% transmural extent

6:16

of infarct or myocardial scar, then you think

6:19

that the likelihood of functional recovery

6:21

after revascularization, a.k.a. PCI or CABG, is high.

6:26

If it's more than 50% involvement of the wall thickness,

6:30

then your chances of successful revascularization,

6:33

in functional recovery sense, is small.

6:37

And, uh, the question stem did include, uh, cardiac, uh,

6:42

CAD-related risk factors like diabetes and all.

6:46

Now, this is a subendocardial pattern,

6:48

vascular distribution, transmural extent.

6:50

Um, this distribution is common in most patients.

6:54

Uh, these segments are being supplied by the circumflex, uh,

6:57

artery. Case three.

7:01

In the image on the right, the arrow represents which

7:05

of the following artifacts? Bending,

7:09

wraparound artifact,

7:12

signal loss from respiratory navigator,

7:16

or signal loss from EKG gating?

7:29

All right, so most of us think

7:31

that this is banding artifact, which is, uh, not correct.

7:35

Now, banding artifacts typically are curvilinear

7:39

lines at the periphery of the images, which happen

7:42

because of the magnetic field inhomogeneity

7:45

at the periphery of the images.

7:47

When you put, um, a person into the magnetic field,

7:52

the body itself perturbs the magnetic field.

7:55

And that's why banding happens more so at the periphery,

7:57

but it can happen in other parts of the body too.

7:59

So I think, um, the takeaway here is that we all need

8:03

to look at what banding artifacts on balanced,

8:06

steady-state free precession

8:07

or TrueFISP imaging looks like.

8:09

Now, this is a common artifact—signal loss from respiratory

8:13

navigator pulses.

8:15

And you see it on cardiac imaging.

8:18

You see it in vascular MRIs.

8:20

You will see these findings on body MRI.

8:23

So it's a very common finding, um, common imaging artifact.

8:28

And what's happening here is that, um, essentially, you are

8:34

selecting a vertical

8:37

plane selection.

8:40

And if you can see my laser pointer here, vertically,

8:43

that cuts through the diaphragm.

8:45

And you are doing some lower-resolution, low CNR,

8:49

low SNR kind of imaging very rapidly through this region,

8:53

in parallel to your actual image acquisition.

8:56

And that imaging is basically plotting the

8:59

movement of the diaphragm.

9:00

So, the contrast here is so low

9:03

that you only see air up.

9:08

You only see air high up,

9:10

and you only see liver here and the diaphragm.

9:13

And here is a more digital version of that, uh, image

9:18

where you can actually— the illustration shows

9:21

that you can actually select a gating window,

9:24

and you can just tell that, "I wanna fill the k-spaces for

9:28

whenever diaphragmatic position is here,

9:31

and I wanna discard everything else."

9:33

All data you acquire during NMR experiments is discarded.

9:37

I'm only filling k-spaces in this particular, uh,

9:41

diaphragmatic position consistently.

9:43

And that's how you are freezing diaphragmatic motion,

9:47

'cause you're only filling k-spaces at that time.

9:49

That's how respiratory navigation works.

9:52

Case

9:53

435

10:02

A 35-year-old male with exercise-induced arrhythmias,

10:06

single episode of fainting during exercise.

10:10

Echocardiography was performed,

10:12

which demonstrated right ventricular dilatation.

10:15

This led to the performance of a cardiac MRI.

10:23

Which of the following is the most likely diagnosis here?

10:38

Excellent. Most of you got it correctly.

10:42

So this is a genetic cardiomyopathy.

10:45

So this is a case of ARVC.

10:49

And the pertinent findings here are basal

10:55

dyskinesis, hypokinesis in this region— basal

10:58

to mid— when everything else is contracting.

11:01

That basal free wall is kind of bulging out a little bit.

11:05

Or not, or—

11:06

Or at least not contracting as the rest

11:08

of the segments are contracting.

11:10

And typically, in ARVC, you're gonna have segmental

11:13

or global RV systolic dysfunction.

11:16

Um, now, previously, it was thought that there is

11:22

fat deposition, which is not

11:24

as commonly associated as previously thought.

11:26

However, scar—either in the right ventricle

11:30

or left ventricle—um, is something that is commonly seen.

11:33

So in this case, you can actually see

11:35

that there is scar at the acute, um, margin

11:38

of the RV. The scar kind of extends into the inferior wall here

11:42

and into the free wall of the RV.

11:44

Now, there is a variant of ARVC

11:48

where you have more left-sided involvement, um,

11:51

called ALVC.

11:53

Um, I doubt they're gonna test that in, in, um, the board.

11:56

But, um, it's good to know—

11:58

like, you can have genetic cardiomyopathy, a variant

12:02

of ARVC where you can have RV dysfunction

12:05

with left-sided scar.

12:08

And here's a companion case.

12:10

You can see that there is marked

12:13

enhancement throughout the free wall of the RV.

12:17

You can see it in here on the short axis.

12:20

You can see it on the four-chamber.

12:26

Alright, we're gonna move on to case five.

12:34

What does the arrow demonstrate on this phase

12:38

contrast image?

12:49

Okay, so almost half of you got it right,

12:54

which is imaging artifact based on the phase shift.

12:57

So this is aliasing here, and an easy way to understand—

13:02

sometimes, you can argue that what if it's the dark

13:07

signal here, which is opposite flow—flow

13:09

in the opposite direction.

13:11

The thing is that anytime you have phase shift

13:16

based imaging artifact—AKA aliasing—

13:19

you're gonna have a pixelated appearance.

13:22

'Cause this is basically a pixel-based phenomenon.

13:25

Um, at the, um, when, when image reconstruction happens,

13:28

and you are plotting the, uh, intensities,

13:31

the whole region is gonna be the same

13:36

color darkness, like it's gonna be pitch black uniformly.

13:40

Well, when you have a reverse flow,

13:42

you're gonna have a gradation of the reverse flow.

13:45

'Cause the flow, natural flow, um, is, is more,

13:48

um, in, in layers.

13:50

So you have more central flow and less peripheral flow.

13:53

So you're gonna have different, uh,

13:55

gradation to, to the color.

13:57

So that's one clue you can actually find on the imaging, uh,

14:02

to, to tell these two apart.

14:04

Now, this is aliasing, which is, uh,

14:06

basically if you did not set, set up your rank settings, um,

14:10

to the, to the Nyquist limit.

14:13

Um, if you are falling short, then everything above, in terms

14:17

of velocity, is gonna wrap back in the opposite dimension.

14:21

And just to understand the, uh, imaging physics

14:24

behind velocity encoding, essentially, you are applying two

14:28

opposite but equal intensity gradients.

14:31

And when,

14:33

whenever, uh, protons move into a magnetic field along a

14:36

gradient, they're gonna pick

14:38

up or lose phase depending upon if they're precessing towards

14:42

the direction or against the direction of the gradient.

14:45

So the phase picked by the stationary tissue is the same

14:50

as the phase, um, lost

14:52

after the application of the opposite polarity, um, gradient.

14:57

So all the tissue in that single selected slice

15:02

is gonna suppress after this NMR experiment when you try

15:06

giving a positive gradient,

15:08

and then you reversed it

15:09

with the same intensity negative gradient.

15:12

However, if there is a flow in the direction

15:16

or against the direction of one of these gradients,

15:19

depending upon which direction the flow is, it's gonna

15:22

pick more phase and lose less phase,

15:24

or pick less phase and lose more phase.

15:27

And eventually you're gonna have a flow towards

15:30

or flow away from you, kind of encoding from the,

15:34

from the phase shift into those images.

15:37

And that's how you utilize this imaging physics into, into,

15:41

um, calculating velocities.

15:43

Essentially, the phase shift is proportionate to your

15:47

velocity changes in that region.

15:50

We're gonna move on to the next case. K six.

15:54

The graphic on the right demonstrates which

15:57

cardiac CT gating method.

15:59

Now tube current here is plotted along the Y axis. The

16:13

gray shaded area represents the tube current.

16:25

Okay, so in this particular case,

16:28

this is actually retrospective gating with the pulsing on.

16:32

Now, I guess I wasn't very clear on

16:36

what exactly we are looking at.

16:37

So this gray box is, is the tube current here?

16:42

Now this line, sorry, apologies.

16:46

This line is the baseline here.

16:48

This gray box is the tube current,

16:53

um, plotted on your Y axis here.

16:57

So essentially

16:58

during diastole you are having your tube current maxed out.

17:02

And during the rest of the cycle, you have dropped it to,

17:06

to a minimal value.

17:08

Now this is a type of, uh, gating technique

17:12

where you are essentially trying to get maximal information

17:16

during the diastole.

17:18

And you are also trying to achieve very low

17:23

SNR/CNR kind of images of, uh, the rest of the cardiac cycle

17:27

'cause you're trying to do some volumetric quantification.

17:30

So you wanna see the whole cardiac cycle.

17:33

And, um, pulsing is on here, which means

17:36

that you are pulsing during.

17:41

So this is a tube current modulation kind of technique,

17:44

and it's a variant of, um, of, uh, your, um, retro, uh,

17:49

retrospective, um, gating.

17:52

Now you have to understand the point of this question is

17:54

that you have to understand that, um,

17:57

although historically we talk about the retrospective

18:01

and prospective gating,

18:02

however, um, there are some, um,

18:06

there are some alterations that you can tweak around things

18:09

to make them look like a different,

18:12

um, one or the other.

18:16

We're gonna move on to the next case.

18:18

This was also a review of understanding

18:20

between the retrospective

18:22

and prospective gating case seven.

18:26

Which of the following

18:31

incidental finding is presented in the provided images?

18:43

So this is basically an incidental finding.

18:45

The patient was scanned for another reason.

18:59

Okay? So there is a tie between the cause,

19:03

mitral annular calcification and coronary artery aneurysm.

19:07

I can see that, um, this being thought of as

19:12

coronary, like a circumflex aneurysm or something.

19:16

Um, anyhow, you can see that this is the level

19:19

of the mitral annulus

19:20

and there are chunky, chunky calcifications,

19:22

but there is a low-intensity region in between.

19:25

And this is a commonly described variant

19:28

of mitral annular calcification.

19:30

Uh, the clinical significance of this finding

19:33

is not very well known.

19:35

Typically, the patients don't present with, uh, something

19:38

unless they are having, let's say, mitral stenosis

19:42

or regurgitation secondary to that,

19:43

or sometimes these cases, uh, gelatinous kinds

19:47

of material can embolize into different, uh, parts in

19:50

through the arterial systemic arterial, um, route.

19:54

And only those cases are gonna be symptomatic.

19:56

Otherwise, typically indistinct

19:59

symptoms have been associated with chest pain

20:02

or palpitations, discomfort in the chest, dyspnea, syncope.

20:06

But most of the time you'll be scanning these patients

20:09

for some other cardiac or chest pathology reasons.

20:12

And you find this finding, it's good to identify this.

20:16

Almost all these cases are gonna have extensive mitral

20:19

annular calcifications with low-density, uh, central areas.

20:25

And typically these areas can enhance on LGE imaging if

20:28

you're doing a cardiac MRI.

20:30

Um, case eight,

20:34

which spatial frequencies are represented at the

20:37

edges of case space?

20:39

Um, low spatial frequencies, high spatial frequencies,

20:43

intermediate frequencies.

20:55

Okay, so a little over 50% think

20:58

that this is high spatial frequencies, which is correct.

21:01

Um, boards love to test the case-based properties.

21:06

So, um, if the bare minimum you wanna remember is that

21:11

center has the contrast information and edges

21:15

or boundaries, edges, boundaries

21:18

and interface information is at the edges.

21:21

So high spatial frequencies are encoding at the periphery

21:26

peripheral part

21:27

of your case space while the central portion is a low

21:31

spatial frequencies, AKA high-contrast region.

21:35

And that's why many of the techniques, modern techniques

21:38

of faster image reconstruction kind

21:40

of utilize just filling these central case spaces.

21:43

And you can still get decent enough contrast into the image.

21:46

Now you can alter, you can, you can use AI

21:49

or other, uh, image reconstruction techniques

21:52

to essentially, um, augment the edge

21:56

or boundary kind of, uh,

21:59

information into those imaging techniques.

22:02

Uh, but the center is where the most, um,

22:05

information in terms of contrast lies; edges is

22:07

where the most information in terms of, um,

22:10

spatial resolution, in-plane resolution, um, interfaces

22:14

and boundary definitions exist.

22:18

We're gonna move on to case nine.

22:23

I have a cine four-chamber here to play.

22:28

And the question, uh, the

22:31

clinical history here is 45 years old female presenting

22:34

with shortness of breath and tachycardia with heart failure

22:37

with reduced EF on echocardiography; cardiac MR ordered

22:42

for assessment of heart failure

22:44

and their cardiomyopathy of non-ischemic origin.

22:51

Top is four-chamber cine, oh sorry,

22:55

four-chamber cine and bottom is your short-axis LGE image.

23:09

Alright, excellent. Almost all of you got it right.

23:15

Um, you almost all

23:17

of you think this is DCM, which is correct.

23:19

The chamber here is dilated, the function here

23:24

is declined, is decreased.

23:26

You can see that the contractility is not as much

23:29

as you would expect and on your

23:33

LGE images in the short axis, you can kind of

23:37

make out this thin mid-myocardial stripe-like

23:43

enhancement right here.

23:46

And that has been associated with the DCM.

23:49

Um, for boards purposes.

23:50

Um, if they show you this

23:52

and if they show you this, they want you

23:54

to pick DCM basically.

23:56

So it's a non-ischemic cardiomyopathy.

23:58

Um, there's not gonna be any ischemic, uh, process,

24:01

there's not gonna be any vascular distribution

24:04

to the scar if there is any scar.

24:06

Um, your CTA coronary

24:08

and stress testing typically is gonna be negative

24:10

unless this person has superimposed CAD

24:13

and associated stenosis, which is not uncommon, um, just

24:16

for the fact that demographics

24:17

are kind, kind of overlapping.

24:19

People who have DCM

24:20

are also, um, age-wise, the same age range,

24:24

which can have CAD and all that stuff.

24:27

Um, and DCM also increases the chances

24:30

of someone having a CAD-related event.

24:33

So, uh, there is common association,

24:34

you're gonna see them commonly in the same patient.

24:37

Um, but for all practical purposes,

24:39

it's the non-ischemic cardiomyopathy.

24:41

Uh, you have dilated left ventricle

24:44

globally reduced ejection fraction, mid-myocardial,

24:48

delayed gadolinium enhancement in septum as been described.

24:51

Now you can sometimes have RV insertion site LGE associated

24:55

with, um, with DCM as well.

24:57

You can have ECV and native T1 abnormalities,

25:01

but I doubt that this will be tested on boards case.

25:05

10 35

25:12

years old male with syncope

25:14

and exercise intolerance, inverted T waves

25:19

in the leads V4

25:20

and V5, which

25:24

of the following is the most likely diagnosis here?

25:29

Ischemic cardiomyopathy, hypertrophic cardiomyopathy,

25:32

restrictive cardiomyopathy, or constrictive cardiomyopathy.

25:45

Okay, excellent. So the majority of you got it right.

25:49

This is a hypertrophic cardiomyopathy case.

25:56

So hypertrophic cardiomyopathy with apical variant.

26:00

You can see that the most thickening here is in the apex.

26:03

Arguably, there may be mild thinning at the true apex,

26:06

which might be early and regional formation in this case.

26:09

And if that happens, then you look for clot, uh, thrombus in

26:14

that, uh, aneurysm because of the hypokinesis.

26:17

Um, and, uh, scar burden in HCM cases,

26:22

irrespective of whether this is apical variant

26:24

or basal septal variant.

26:27

Um, any scar in this could be associated, um,

26:30

or could be a source of, uh, ventricular tachycardia.

26:33

And there are studies that show that if you quantify scar,

26:37

um, it could help you lead, uh, towards, um,

26:41

therapeutic interventions.

26:43

For example, using, uh, an ICD in those cases

26:46

who have ventricular tachycardia secondary

26:48

to scar from hypertrophic cardiomyopathy.

26:50

So know your HCM, they love this stuff.

26:52

They love to ask for different variants of HCM.

26:56

On boards case

26:57

11, 24 years old

27:02

male athlete with syncope

27:04

and wide complex ventricular tachycardia

27:07

and EKG in ICU on echocardiogram, subaortic pressure

27:12

gradient was increased.

27:19

And we have a three-chamber view here.

27:27

Which of the following types of HCM

27:31

best describes this patient's imaging?

27:34

Apical HCM, asymmetric HCM, non-obstructive subtype,

27:41

septal HCM, obstructive subtype, basal HCM.

27:56

Okay, so

28:01

all of, uh, most of you, um, got it, right?

28:05

It's the septal HCM obstructive subtype.

28:08

So you can see that there is basal septal hypertrophy out

28:13

of proportion to most of the, um, myocardium.

28:16

You can also see that there is kind of low intensity

28:20

mid-myocardial predominant scar in the septum.

28:26

Now most scar burden also goes with the most, um,

28:29

hypertrophied, uh, parts.

28:31

Now if you, um,

28:33

if you think about the pathology in these cases, it’s the, uh,

28:36

myofibrillar disarray, the basically the cardiomyocytes are,

28:41

are not, um, are not organized in,

28:45

in the most efficient ways

28:46

and is a simple way of thinking of this,

28:49

which gives you a hypertrophy of the myocardium.

28:54

Now we can also see that there is some

29:00

subaortic flow acceleration

29:06

because of the narrowing from the basal septal hypertrophy.

29:10

So this was an obstructive subtype

29:12

because of the narrowing and flow acceleration.

29:15

So we talk about the HCM morphological subtypes,

29:19

so symmetric HCM, which means

29:22

that you have concentric hypertrophy of the myocardium.

29:25

Asymmetric HCM, one or more segments could be thickened

29:29

or hypertrophied.

29:30

Hypertrophied is the preferred term. Apical HCM,

29:33

we saw the case where there is predominant apical, uh,

29:36

hypertrophy. Septal.

29:37

HCM was this particular case we talked about.

29:39

You have the basal septal hypertrophy here.

29:43

And then you can have basal HCM variant

29:45

where there is more predominant basal

29:47

circumferential hypertrophy.

29:50

Now you can also talk about the HCM subtypes by hemodynamics.

29:54

And, um, this is more pertinent from a clinical standpoint.

29:58

'Cause if you have obstructive, um, HCM,

30:01

then you might need, uh, intervention, um,

30:04

given certain thresholds for, um, for, um,

30:09

subaortic flow gradients.

30:11

Um, so obstructive is the one

30:13

where basal septal hypertrophy kind of narrows down the

30:16

LVOT tract.

30:18

Um, and it leads to flow exploration, which means

30:21

that you may or may not have associated

30:23

with systolic intrusion.

30:25

A non-obstructive subtype is where there's no significant,

30:28

uh, subaortic flow gradient.

30:32

Case 12.

30:32

30:32

24-years old male athlete with cardiac arrest

30:43

during a basketball game. On echocardiographic

30:47

subaortic pressure gradient was increased.

30:55

What kind of HCM is seen in this case?

31:09

Excellent. All of you got it right, which is amazing.

31:12

Um, so this is concentric, symmetric HCM.

31:16

With systolic anterior motion.

31:18

Now, I did not very, um, convincingly show you

31:23

systolic anterior motion here.

31:25

I have given you a secondary sign though; you can see

31:28

that there is huge posteriorly directed

31:31

mitral regurgitation.

31:32

So even that, even though you have not seen

31:36

anterior leaflet being pulled into the, uh,

31:40

LVOT from Venturi effect, you still know

31:43

that this is happening

31:44

because of your, uh, secondary sign that there is a big,

31:47

big, um, regurgitation.

31:49

Now this doesn't have to be a big or moderate

31:53

or severe regurgitation.

31:54

Many, many cases with systolic, uh, systolic anterior motion

31:58

are gonna be cases with very mild

32:01

or even minimal, uh, regurgitation

32:03

or sometime no regurgitation associated.

32:06

Um, when you, we talk about the systolic anterior motion,

32:11

essentially it's not just that the anterior leaflet

32:14

of, uh, mitral valve is being pulled into the LVOT,

32:18

but it could be the, what's called the anterior mitral

32:22

apparatus, um, which constitutes the anterior leaflet,

32:27

the edge of the leaflet

32:28

and the chordae tendineae attached with the anterior leaflet.

32:31

So even if you, even if you see just the chordae tendineae,

32:36

um, inserted into the anterior leaflet being pulled into the

32:41

LVOT, that counts as, uh, SAM.

32:44

Now subaortic flow ex acceleration equals pressure,

32:47

increased pressure gradient.

32:48

We talked about this. There are thresholds, uh,

32:51

that cardiologists, um,

32:52

or interventional cardiologists do interventions based on,

32:54

or cardiac surgeons might have to do, let's say, um,

32:58

a myomectomy or something.

33:00

And this is, um, increased pressure basically drops, um, um,

33:05

increased pressure gradient basically drops pressure in the

33:09

region, which leads into the, um, pulling

33:12

of the anterior mitral valve into the LVOT, which may

33:17

or may not cause regurgitation.

33:21

All right, we're gonna move on to case 13.

33:30

Identify the abnormality shown here, pericardial mass,

33:35

essence of pericardium, cardiac malrotation

33:39

or abnormality.

33:53

Excellent job. Most of you know that this is agenesis

33:57

of pericardium.

33:59

So first off, you barely see any

34:04

pericardial tissue

34:09

surrounding the heart.

34:12

Secondly, the heart is kind of levo-positioned.

34:17

Uh, it's more tilted to the left side of the chest cavity.

34:22

And third, typically when they're trying to show you this,

34:25

um, particular finding, they're gonna probably show you one

34:29

of this image at the level of aortic window

34:32

where they're trying to show you a little bit of a tongue

34:36

of pulmonary parenchyma going in

34:40

between the ascending aorta and main pulmonary artery.

34:43

So technically there should be a bridge of pericardium here

34:47

and fat in between.

34:48

But once you don't have pericardium

34:52

or pericardial sinuses in complete agenesis,

34:55

you're not gonna have that pericardium here

34:58

to interpose or intervene.

35:00

And then you have the pulmonary parenchyma kind of wedge

35:03

between these two um, structures.

35:06

So it's a good, um, place to look for

35:08

whenever you suspect, um, pericardial agenesis.

35:13

Um, this could be associated with A-S-D, B-A-V, and TOF.

35:17

Most of these patients are asymptomatic.

35:19

This is found incidentally, they don't even know they got,

35:22

um, pericardial agenesis.

35:25

Now very uncommonly in case reports has been described,

35:29

that patients can have torsion

35:31

or twisting of the heart onto, onto the vascular pedicle,

35:36

which is very uncommon

35:37

'cause the pressures in pulmonary artery

35:39

and, uh, ascending aorta at least are very, very high too.

35:42

So twisting that great vessels, um,

35:46

sounds impossible,

35:48

but there's been, uh, case reports of, uh,

35:50

cardiac torsion associated with complete agenesis

35:55

and here is a companion case.

35:58

Um, you can see that the part of the right atrium is kind

36:02

of pooching out from this defect, just a small defect

36:06

into the, into the pericardium.

36:11

And this is the, what's called the partial disease

36:15

of pericardium.

36:17

Um, it can happen in any part of, uh,

36:19

pericardium essentially, uh, typically no hemodynamic, uh,

36:23

significance in most cases with this finding, case 14

36:27

36:36

56-year-old male with a history

36:37

of coronary artery disease on statin, presenting

36:40

with exertional chest pain.

36:43

CCTA was performed, and the images are shown.

36:53

What is the most likely etiology

36:55

of multiple aneurysms shown in this case?

37:09

All right, so most of you think that this is

37:14

Kawasaki disease, and so 50% think

37:19

that this is Kawasaki

37:20

and 41% think that this is coronary artery disease.

37:24

Um, so this happens to be coronary artery disease.

37:28

The point of this case is that you have

37:30

to know your demographics.

37:33

Multiple coronary aneurysms.

37:37

The most common etiology in, let's say, a 40-50 male

37:41

with risk factors and established coronary artery disease is

37:44

gonna be coronary, is gonna be coronary artery disease.

37:48

Now, if I show you this case in a pediatric population,

37:51

then you're gonna select Kawasaki.

37:53

Of course, most of Kawasaki patients, you're not gonna see

37:58

calcific plaques in them, uh, vasculitis cases,

38:01

completely different demographics.

38:03

It's gonna be someone who already has

38:05

or probably has an established, um,

38:09

large vascular disease

38:10

or some sort of other autoimmune condition.

38:13

Um, female predominance.

38:16

So demographics, that's the, uh, that's the take-home point.

38:20

Most common reason

38:21

to have multiple coronary aneurysms in an adult population

38:25

is gonna be coronary artery disease.

38:30

So basically, the question stem will give you the specifics

38:33

and the clinical information needed.

38:37

Case 15,

38:43

what associated condition is seen in this case

38:46

with P-A-P-V-R con?

38:48

So P-A-P-V-R here is shown in the lower image,

38:54

sorry, the condition is, sorry,

38:57

the associated condition is shown in the lower image.

39:00

And top images are the P-A-P-V-R.

39:03

So A-V-S-D, P, PDAC, primum,

39:07

A-S-D, D-S kingdom, a, S-D,

39:10

and E sinus, osis A-S-D, which association

39:15

of P-A-P-V-R is shown here.

39:18

Excellent, all of you got it.

39:19

Boards tend to love this question.

39:24

They want you to know that PBRs are associated with ASDs.

39:33

Alright, case 16.

39:41

Alright, 22 years old male with exertional shortness

39:44

of breath, EKG, nonspecific abnormalities.

39:48

So basically, ST changes noticed in all leads,

39:52

mildly elevated troponin

39:54

and negative CCTA cardiac amor done top image

39:59

is a T two map

40:01

and bottom image is an LGE image.

40:06

What is the abnormality shown in these images?

40:20

All right, excellent.

40:22

Most of you, um, got it right.

40:29

So this is myocarditis

40:31

and you don't for this kind of questions, tam, most

40:36

of the time you don't even have to look at the images.

40:39

The pretest probability here is high.

40:42

I'm giving you a young person.

40:44

I'm telling you that they are having

40:45

non-specific EKG changes.

40:48

So, which is obviously not gonna be STEMI.

40:51

Now non and STEMI could have some overlap,

40:55

but you hear non-specific EKG changes, EKG changes in ST

41:00

or U wave abnormalities throughout all, all EKG leads.

41:07

Troponin is elevated but not elevated to the, uh,

41:10

to the MI level, right?

41:12

And then there is a clean coronary CTA.

41:16

This text is telling you that this is myocarditis,

41:20

under proven otherwise.

41:22

Now here on the T2 image, you do see that there is

41:26

mild bright signal, which tells you

41:28

that this is elevated T2.

41:30

So there is edema here,

41:32

in LGE images in the basal segments, um,

41:36

give you the typical distribution of basal lateral

41:40

and infralateral subepicardial midmyocardial distribution.

41:44

So typically, most commonly it's gonna be subepicardial

41:47

basal lateral basal in lateral segment involvement when it

41:50

comes to the scar.

41:52

Um, but it could also be midmyocardial.

41:55

Now here in these LGE images, the,

41:59

the late gadolinium enhancement you see here could be a mix

42:02

of edema and scar

42:04

or could just be all edema depending upon

42:06

what's the timeline here.

42:07

Now in acute myocarditis,

42:10

and same applies for acute myocardial infarction,

42:13

you have predominant edema

42:15

and necrosis going on in the cardiomyocytes

42:17

and interstitial spaces between the cardiomyocytes.

42:20

And as those changes, um, acutely inflammatory kind

42:23

of changes subside, then you have deposition of, um,

42:29

collagen and extracellular matrix in the form

42:32

of a scar deposition.

42:34

So it's impossible without having information about T2 abnormality, whether this is scar or edema.

42:39

abnormality, whether this is scar or edema.

42:42

And that's what, um,

42:43

parametric mapping adds value in these cases.

42:46

So essentially the clinical, um,

42:49

presentation here had high pretest probability

42:52

of myocarditis T2 elevation in these segments

42:55

with associated scar corresponding.

42:59

So that basically meets one of the, that meets the criteria,

43:05

uh, as per modified Lakeview criteria for, um, high,

43:09

high likelihood of having, uh, myocarditis.

43:12

Now modified Lakeview criteria,

43:14

which came out in 2018, basically uses, um,

43:17

a T2 abnormality

43:19

and corresponding T1 abnormality to make the diagnosis.

43:22

If you have both in the same segments,

43:25

then you have high likelihood of having myocarditis.

43:27

So T2 abnormality is either gonna be bright signal on T

43:30

two dark blood imaging

43:31

or it's gonna be bright, uh, high quantifiable,

43:35

high numbers on T2 mapping, which tell you

43:38

that there is edema in these segments.

43:39

Uh, T1 abnormality could be a native T1

43:43

mapping abnormality.

43:44

It could be an LGE abnormality

43:46

or could be an ECV abnormality case.

43:51

1746

43:57

years old male with angina undergoing coronary CTA

44:02

what abnormality is shown here.

44:10

So attention to the coronary arteries here in this case.

44:26

Excellent, most of you got it right.

44:30

Myocardial bridging.

44:34

So you can see that this

44:37

part in this part.

44:39

So right after the takeoff of this diagonal branch, LAD

44:44

is severely narrowed to nearly,

44:48

nearly collapsed into a myocardial bridge.

44:52

You can see that the LAD kind of dives down here

44:55

and peters out and then comes back up.

44:57

So that is the myocardial bridging.

45:01

Now in this particular case,

45:02

there was a deep myocardial bridging about 24 millimeters in

45:06

length and six millimeters in depth.

45:08

And it had high-grade external compression,

45:11

which you can see here that it nearly, nearly compresses

45:14

to complete, um, narrowing from external compression.

45:18

Um, here's, um, a good paper on myocardial bridging

45:22

and it goes over what is a superficial bridging.

45:24

What is a deep bridging?

45:26

Essentially two millimeters

45:27

or so deeper than

45:29

that is gonna be your deep myocardial bridging.

45:32

And then the length is this, as per this article,

45:35

it's about 2.5 centimeters in length.

45:37

If more than that, you call it a long segmental.

45:40

Now you have to understand the longer the myocardial bridge

45:43

is or the deeper the coronary goes into the myocardium, the

45:47

higher the likelihood of functional association. Many,

45:50

many myocardial bridging are not gonna have

45:52

any functional significance to them.

45:54

Um, there's not gonna be any significant associated, um,

45:58

narrowing of the coronary arteries.

46:00

However, if you have a deeper bridge

46:03

or if you have a longer bridge, then, um,

46:07

those could be, um, significant.

46:09

Uh, from a hemodynamics standpoint, there is a QR code here,

46:12

you can scan it and actually have access to this paper.

46:16

Um, treatment options, obviously medical therapy,

46:19

if it could be managed medically, if it's a mild one,

46:24

if it's, um, if it's, uh, really symptomatic

46:27

and it affects their functional status.

46:30

Um, exercise tolerance, all that, then you can go for a PCI

46:34

or a bypass of that segment

46:36

or unroof, uh, slash myotomy of, of the bridge

46:40

above the coronary, to coronary, to release it.

46:46

Moving on to case 18.

46:52

All right, 33 years old male with chest pain,

46:56

non-specific EKG changes,

46:58

no coronary abnormality seen on CCTA.

47:04

So, um, Tru FISP here, kind of four chamber.

47:09

There is a four chamber LGE and then three chamber LGE.

47:16

What is the etiology of the patient's

47:21

chest pain here?

47:23

Pericardial effusion, pericardial tamponade,

47:28

pericarditis or pleural effusion.

47:43

Okay, excellent.

47:46

Most of you got it right, it's pericarditis.

47:51

Now agree that there is some pericardial,

47:55

um, effusion here.

47:57

However, their bigger problem is that their

48:00

pericardium is inflamed, so that's what's gonna give most

48:04

of their symptoms out of having pericardial fluid

48:08

or pleural fluid here.

48:10

So, you can, excuse me, you can see that the

48:14

pericardium is thickened and you can see it splits here.

48:18

There's fluid in between here,

48:20

which is the same fluid here seen on the fast sensitive inco

48:23

inversion recovery images.

48:25

PSIR fluid typically is dark on PSIR images,

48:29

which is one of the types of LGE images.

48:32

I don't think you need to know that

48:34

for the board's purposes, just

48:36

for explanation purposes here.

48:38

And you can see that there is this enhancement

48:42

of the visceral pericardium as well

48:45

as the parietal pericardium.

48:48

And it goes all along the pericardium.

48:50

You can also see that there is all this bright signal.

48:54

And then here is the enhancement of the visceral

48:58

and parietal pericardium.

49:00

So, this is a pericarditis case, um,

49:06

thickening, enhancement, fluid.

49:09

Now, obviously if they want you, if they want you

49:12

to pick tamponade, they're gonna give you some sort

49:15

of imaging where they're trying to show you

49:17

that there is effect on the RV side of the chamber.

49:21

There is some ventricular interdependence,

49:23

there is some flattening of the septum.

49:25

So, since I have not included any NIAs here,

49:28

it should give you some clue that if they want you

49:30

to pick up, um, tamponade case, they're probably gonna try

49:34

to show you, um, show you at least flattening on a,

49:39

uh, static image or preferably on a theta image.

49:43

Um, PLU obviously is here,

49:45

but there are bigger problems you can see.

49:49

Alright, case 19

49:51

49:51

42 years old, African American male with shortness of breath

50:00

on lab testing, they had elevated ACE enzyme levels,

50:05

uh, ventricular tachycardia is associated, you have

50:10

LGE imaging in short axis

50:14

three-chamber, four-chamber short axes again, which

50:19

of the following infiltrative cardiomyopathy is shown here?

50:35

Excellent. Most of you got it right.

50:37

If you, if you go back to the clinical presentation,

50:40

we have all the buzzwords that go with the, um,

50:43

systemic sarcoidosis, um, demographics here,

50:47

then elevated ACE enzymes, tachycardias

50:50

and arrhythmias are typically associated

50:52

with cardiac involvement with sarcoidosis.

50:55

And then on your images here, you see

50:57

that there is nonvascular distribution of scar.

51:00

You have subepicardial scar in parts,

51:03

you have midmyocardial scar.

51:06

It just involves myocardium in a patchy kind of

51:11

in a nonvascular, uh, pattern.

51:14

But there is, there's just no pattern here.

51:16

It's just involving a bunch of different areas

51:18

of myocardium in either subepi or,

51:21

or, um, midmyocardial distribution.

51:24

And that's pretty typical for sarcoidosis. For amyloidosis.

51:27

Typically, it's either circumferential subepi, uh,

51:31

epi-subendocardial preferential distribution,

51:34

or it could be more patchy,

51:36

but more circumferential involvement.

51:39

Um, how so? There is a pattern typically,

51:41

but when you don't see a pattern, think sarcoidosis.

51:44

Um, other things to think about when you don't see a pattern

51:47

are genetic cardiomyopathies.

51:50

Uh, prior myocarditis, inflammatory myocarditis, giant cell

51:54

myocarditis, typically can have similar, uh,

51:56

appearances sometimes.

51:59

So, this was a case of sarcoidosis.

52:02

So, if sarcoidosis involves the heart,

52:05

then it's, then obviously you have cardiac sarcoidosis.

52:08

Now, you can have chronic phases of cardiac sarcoidosis

52:11

where you're gonna have scar, which is shown here

52:14

with the different areas of LGE.

52:16

Now, if there is a T2 abnormality associated

52:19

with these areas, then it's hard to tell if this is

52:22

previous scar from prior involvement, uh, with the, um,

52:26

let's say non-caseating granulomas,

52:29

or if this is an active inflammation, like a new site

52:31

of sarcoid involvement.

52:33

So that obviously you need the T2 information

52:36

or perhaps you need a PET-CT scan to correlate.

52:39

If there is hypermetabolic activity on, uh, on cardiac PET,

52:43

then you know that those areas are active involvement.

52:46

Um, the rest of the areas where you don't have

52:49

elevated T2 or you don't have, um, evidence

52:52

of myocardial edema based off either T2, uh, mapping

52:56

or other T2 imaging

52:57

or PET scan, then, uh, those are areas of previous, uh,

53:01

cardiac involvement, AKA scar from prior, uh, involvements.

53:06

So, no definitive recognizable LGE pattern,

53:09

patchy multifocal involvement, mainly subepicardial

53:12

and midmyocardial distribution.

53:15

Now, quantification of the scar in these cases could be

53:18

of value to under,

53:21

if you know scar burden, you can understand, um, how to,

53:26

well, how to best treat their, um, arrhythmias.

53:29

For example. Now, case 20, 49 years old male

53:34

with exertional chest pain, known history

53:36

of coronary artery disease, EKG changes, uh,

53:39

support a diagnosis of STEMI.

53:42

So there were ST elevation in precordial,

53:47

uh, uh, leads, for example, elevated troponin,

53:50

and you have four-chamber, um,

53:54

four-chamber true-fist image.

53:56

Here you have a short-axis LGE

53:58

and you have four-chamber LGE images, which

54:02

territory infarct is shown in this case.

54:15

Okay, so most of you got LED infarct

54:20

and, um, we can go over why this is LED infarct.

54:27

So, you see that there is involvement of the anterior and

54:32

septal segments,

54:33

which is pretty typical within LED infarct.

54:35

You have the apical involvement

54:37

and you have the septal involvement.

54:38

So these distributions are pretty typical of an LAD infarct.

54:43

Now you can also see

54:44

that there is something sitting in the chamber here,

54:47

which is pretty dark on your LGE imaging

54:50

and that was an associated thrombus, intracavitary thrombus.

54:54

So in acute MI

54:56

or subacute MI cardiac cases, it's very important

54:59

to actually pay attention to, um, to, uh, thrombus

55:04

or microvascular obstruction.

55:06

Um, so yeah, here it's a vascular distribution.

55:09

The distribution kind of matches with the LAD territory.

55:16

Now I think we've talked about this already, the thickness

55:18

of myocardial, um, involvement in infarct cases

55:23

in MI cases predicts the outcome

55:25

after revascularization A-K-A PCI

55:29

stenting, CABG, all that.

55:31

If you have less than 50%, uh, thickness of LGE involvement,

55:35

uh, in vascular distribution, um, if you go

55:38

for revascularization,

55:39

the patient is probably gonna have high chances of

55:43

functional recovery after intervention.

55:46

And with that, um, we are done here.

55:50

Um, I see that there are a few questions posted

55:54

into, uh, the chat.

55:58

All right, so I'm gonna use the laser pointer now if they

56:02

want you to, if they're going to show you one of these

56:05

schematics, um, to, to basically, um,

56:12

decide between if it's prospective

56:17

and retrospective gating,

56:19

they're gonna show you something like this

56:20

that's gonna give, they're gonna give you a Cartesian plane

56:24

and in X on X-axis is gonna be your time.

56:27

And on the y-axis is gonna be the MES your tube current output.

56:32

Now, if they are giving you something like this,

56:44

what is this gonna be like versus

56:49

they're giving you this

56:59

right and here

57:02

and they're obviously gonna give you EKG, um, tracing.

57:07

Here's your

57:11

EKG tracing.

57:13

Uh, well I messed up anyhow. You get the point, right? Now.

57:18

Here's another EKG tracing here.

57:30

Did you guys lose me again? No, we can hear you. Oh, okay.

57:35

Sorry. Okay, so they're gonna give you this or that.

57:40

Does, does anyone wanna shout out like

57:44

what is this showing?

57:46

Which kind of key is?

57:51

So this is gonna be prospective,

57:53

you're basically scanning in just a part of the cardiac cycle.

57:57

Tube current max scan.

58:01

Tube output zero. Oh, I see, okay.

58:05

You guys cannot talk, I see.

58:07

Um, then it's gonna start again in the next cardiac cycle.

58:11

Irrespective, you can scan DLI if you like,

58:15

you can scan in Sicily, you can scan any part

58:18

of DLI you wanna scan in early DLI versus late DLI.

58:21

You, you can just plan that on the scanner.

58:23

So that's the prospective scanning tube current max.

58:27

And drops to zero very quickly in just part

58:30

of the cardiac cycle you wanna scan compared

58:33

to tube current is consistently on no matter what part of,

58:38

um, consistently on, no matter what part

58:41

of the cardiac cycle you are at,

58:43

what in anatomy you are scanning,

58:44

it's just gonna keep scanning and the,

58:47

and the table is constantly just slowly gonna keep feeding

58:51

into, and that's how you do your retrospective,

58:55

uh, gating here.

58:56

Retrospective, like two current on

58:59

constantly prospective, two current on, off, on,

59:04

off, on, off in the exact same part of the cardiac cycle.

59:08

So the, if they want you to pick between these two graphics,

59:11

that's what you, they're gonna show.

59:13

Now in this case, you can see that the tube current comes up

59:16

and then does not drop to here's your zero line.

59:19

So essentially, this is your, your plane here.

59:27

Um, and basically you're not

59:32

dropping all the way, you're just maximizing your tube

59:35

current in part of the cardiac cycle you're most interested in.

59:38

And that's what the pulsing on means.

59:40

You are pulsing to get the most information

59:43

in the part you are most interested in.

59:46

So if you're interested in the diastole,

59:47

you're gonna give the maximum tube current output there.

59:52

Um, is that clear?

59:58

The person in the chat who asked

60:00

the question said yes. That's clear.

60:01

Okay, excellent. Next one.

60:03

On the previous question, can you explain how

60:05

to orient yourself?

60:06

Um, I have no idea which, so

60:08

That's for, that's for case seven.

60:11

I see that question. How do you

60:13

orient yourself? I, I see. Yep,

60:14

There you go. Okay,

60:15

excellent.

60:16

So this is more of a, a two, a short axial cine kind

60:20

of image on a CT examination, on a CT scan, right?

60:22

So you see that this is your

60:26

mitral annulus here

60:30

and that's your aortic sinuses

60:32

and ascending aorta.

60:37

You can actually see sinuses here,

60:39

you can see the leaflet open.

60:41

So this part of the cycle,

60:44

the ventricle is already contracting.

60:46

Leaflets are open,

60:47

and blood is rushing through the LVOT into the,

60:50

through the aortic valve.

60:52

So that is the anatomy here.

60:54

Um, pulmonic up here,

60:55

and then, um, your right

61:00

atrium sitting here.

61:01

And then all this is basically partless,

61:06

part basal myocardium,

61:08

'cause it's not a perfect cut through the,

61:10

through the mitral valve.

61:11

If you may. Also, my mitral valve annulus is not a completely,

61:17

um, it's not a structure

61:19

that sits into one plane if you may, it kind

61:23

of sits a little bit like this.

61:26

Uh, right, so it's like a little off.

61:29

The whole annulus cannot sit into the single,

61:32

um, plane if you may.

61:34

Now that's why you have like some my basal myocardium

61:37

showing and then you have part of mitral annulus showing,

61:41

and that's where the mitral annular, um, calcifications are.

61:48

Alright, makes sense. I'm gonna move on.

61:53

Does that answer your question for the orientation?

62:01

Hopefully it does. I'll monitor the chat.

62:03

Alright, I'm gonna move on to, uh, case

62:08

17, and if there are any more questions, you guys can

62:13

put it in the chat.

62:14

I'm happy to take them.

62:16

Sorry, I, I, I have, have a very painful way of

62:21

moving along cases here.

62:23

Um, case 17.

62:24

Do patients need treatment

62:26

for superficial coronary artery bridging?

62:27

Typically not. Now.

62:29

It doesn't, the, the treatment does not go, um,

62:34

mostly does not go with how deep the myocardial bridging is

62:37

or how long the myocardial bridging is.

62:39

Completely, completely.

62:42

What is the hemodynamic significance in

62:44

that particular patient from that myocardial bridging?

62:47

Is it, uh, number one, is the patient symptomatic?

62:49

Number two, do they have hemodynamic significance?

62:52

Number three, have they done stress testing

62:55

and is there evidence of ischemia

62:58

or have they had infarct related to that?

63:00

All those factors. So that is,

63:03

I mean, obviously they're not gonna test you with complex

63:06

questions about treatment, quite honestly.

63:08

Um, if they're gonna test you with a question about, uh, treatment,

63:12

they might give you a deep, long segmental

63:15

myocardial bridging where they actually are showing you

63:18

critical, critical narrowing or complete compression at the,

63:21

in systole,

63:23

and they want you to pick, um, one

63:24

of the options of treatment.

63:26

It doesn't, probably wouldn't matter which one.

63:28

Um, could you explain

63:33

findings with Fabry disease?

63:36

Okay, so for Fabry disease, if they are gonna

63:40

show you a case of Fabry disease, they're basically gonna

63:45

try, um, they're gonna give you some sort of information

63:48

that there is some, um, decrease in the T1 values

63:53

or decrease in native T1 in the myocardium.

63:56

Um, 'cause this is basically a deposition disease

63:58

and myocardium has deposition.

64:01

Um, and, and, uh, more like a lipid deposition, right?

64:06

So there's your, uh,

64:07

T1 values are gonna drop in those segments

64:09

and they're also gonna give you some basal lateral,

64:13

infra lateral kind of subepi

64:16

or mid myocardial kind of scar pattern.

64:18

So scar in those regions, um,

64:20

they're probably gonna give you some, um,

64:24

pertinent history too.

64:25

'Cause, uh, RY sometimes can be very hard

64:28

to differentiate from other, uh, genetic cardiomyopathies

64:31

for example, or, um, even myocarditis sometimes.

64:35

Um, so yeah, they're probably gonna give you like the

64:38

buzzwords, uh, either in the question stem

64:41

or they're gonna tell you that the native T1s are low.

64:43

All that stuff. Alright,

64:48

any more questions

64:50

guys? If not,

64:55

I guess I think I got 'em all. Yeah.

64:57

Alright, well I am, um, super excited for you guys.

65:01

Uh, hopefully, uh, we prepared you guys well.

65:04

And good luck with your exam.

65:07

Thank you, Dr. Omar, for this awesome case review

65:09

and for everyone else for participating.

65:11

We appreciate you being here.

65:13

Thank you all and good luck.

65:16

Be sure to join us on Monday, April 29th.

65:19

We're doing another case review with Dr. Robin Roth.

65:22

She'll lead us in a rapid review of breast imaging cases.

65:26

You can register for that at the link provided in the chat.

65:29

Or follow us on social media

65:30

for updates on future case reviews.

65:32

Thanks again for learning with us and we will see you soon.