0:00

Okay, section two, viability imaging.

0:02

This is really one of the workhorses that caused cardiac MR

0:06

to really mature a lot over the last 20 years.

0:09

One of the first main applications of cardiac MR

0:12

that really had a clinical indication.

0:14

So it's really important to understand

0:17

what viability imaging is, uh, when we can use it, how

0:20

to do it well to perform cardiac mr.

0:23

So the goal of viability imaging is to identify

0:26

myocardial territories that are likely to recover

0:30

function following revascularization.

0:32

Usually that means after something like a coronary artery

0:36

bypass grafting.

0:37

In some instances it may be considering stunting the patient

0:40

or taking them to invasive

0:42

angiography for further evaluation.

0:44

But the goal is really to try to give the clinician an idea,

0:47

if I do a revascularization, it's gonna have an impact.

0:51

And here's just some examples

0:52

of late GA limb enhanced imaging.

0:55

Notice that these, again are short axis images.

0:59

The myocardium in this case is really dark black.

1:02

That's what we want. And then the hyper enhanced areas

1:06

of myocardium kind of seen in this region here on this image

1:11

and in this region here on this image,

1:13

that's late gadolinium enhancement.

1:15

And that's what it looks like when it's in

1:16

a vascular distribution.

1:17

So these are very classic images of LGE

1:21

that are used to assess viability.

1:24

So before we get too much further into the technique, uh,

1:28

I just want to provide a

1:30

background of the evidence for this.

1:31

Where does it even come from

1:32

that cardiac R can be used for this?

1:34

And uh, again, all the way back in the year 2000, Dr. Kim

1:39

and colleagues uh,

1:41

published a paper in the New England Journal

1:43

of Medicine showing that the extent of myocardial thickness

1:47

of LGE correlated with functional recovery in patients

1:51

that had infarct.

1:53

And you can see this bullet point list

1:56

that I have here is directly from the Society

1:58

of Cardiovascular Magnetic Resonance.

1:59

And I would highly recommend exploring that website

2:02

for further details on this if you're

2:04

interested in these topics.

2:06

But again, patients who had less hyper enhancement

2:10

of their myocardium had a higher likelihood

2:13

of functional improvement.

2:15

And they particularly found this threshold of 50%

2:18

of the myocardium.

2:20

And this can be very qualitative in, in many instances,

2:23

but about 50% of myocardial thickness, if you have more than

2:26

that showing hyper enhancement than your likelihood of

2:31

functional recovery of that segment is quite a bit lower.

2:34

And this is displayed again in this table

2:36

or in this graph in the top right this bar graph

2:38

where you can see after about 50% the height of the bars

2:42

represent the improved contractility with revascularization.

2:45

And you can see that in all these subgroups.

2:48

Once you kind of get to that, beyond that 50% threshold,

2:52

very low percent improved contractility

2:54

of each of these segments.

2:56

So this has kind of led to this idea that cardiac m mr

2:59

and percent kind of transmural

3:01

or extent of thickness of the myocardium is important

3:04

for understanding viability.

3:06

In another study by Gerber

3:07

and colleagues where they were looking at patients treated

3:10

with revascularization

3:11

or optimal medical therapy, actually the amount

3:14

of LGE seen on cardiac MR was an independent predictor

3:17

of mortality in patients with optimal medical therapy.

3:21

And the highest extent of LGE did actually the worst

3:24

of all groups in that study.

3:26

And one thing that's come up in maybe the last five years

3:30

as a result of something called the stitch trial is there's

3:32

a question of the actual value of viability where, uh,

3:36

stitch showed that doing revascularizations based off

3:39

of viability imaging did not have an impact

3:42

on functional recovery.

3:44

The issue with that is they only use spec

3:46

to determine viability.

3:47

There's been no prospectively randomized trials showing

3:51

what happens when you use cardiac MR

3:54

to do viability assessment

3:55

and revascularization based off of that.

3:57

So we're still a believer, uh, in viability imaging

4:00

and uh, most of our clinicians are as well, I would say,

4:03

and, and we still get plenty of referrals for this,

4:06

here's a basic viability imaging protocol.

4:09

So notice in the bottom in the kind of purple outline,

4:12

these are things that are optional sequences, things

4:14

that we do at my institution at least,

4:17

but aren't necessarily crucial

4:20

for actually doing viability imaging.

4:22

You can have a very, very brief protocol

4:25

and still do really good viability imaging.

4:27

So you can see that in this protocol. We start with scouts.

4:31

If we're just focusing on the kind

4:33

of non-optional sequences, then we do a set

4:35

of long axis syn images in the two, three,

4:38

and four chamber orientation.

4:39

Then you follow that up with short axi syn a acquisition

4:43

and then lake GA lay enhanced images.

4:45

And so really you should inject contrast.

4:47

Some people would inject contrast in this time point right

4:51

here after the short axis syn nase.

4:53

And then you have to wait 10 minutes

4:54

to do late gadolinium enhanced images.

4:56

We'll talk about why that's

4:57

important here in a couple minutes.

4:59

The way we do it is we actually inject contrast

5:02

before we do short axis syn nase

5:04

because then you're kind of got less dead time on the

5:06

scanner since you have to wait about 10 minutes to get

5:08

to LG imaging.

5:09

Anyways, so the first step as as I mentioned, CNA imaging,

5:14

uh, where we're looking for regional wall

5:15

motion abnormality is important.

5:17

And so kind of the things

5:18

to look at on CNA imaging is you should always assess

5:22

overall wall thickness.

5:23

This should be a done at end diastole.

5:26

And so if you're gonna call something thin,

5:28

it should be kind of relative to other normal segments

5:31

and how that looks at in diastole.

5:34

Okay, while motion abnormalities are actually based off

5:38

of the amount of thickening

5:40

that occurs in a myocardial segment,

5:42

not the overall squeeze,

5:43

sometimes it can be a little deceptive if somebody has a

5:47

poorly functioning segment or two

5:49

and the rest of the heart is moving okay,

5:51

and you're like, oh, the heart looks like it's beating

5:53

pretty well, the function's not that down,

5:56

but those segments themselves can be hypokinetic or worse

6:00

and can have a little deception.

6:01

So the terms that I'm using here,

6:03

and just for definition hypokinesis means reduced thickening

6:07

relative to other segments in the myocardium are relative

6:09

to sort of a normal amount of thickening.

6:11

A kinetic means there's no thickening,

6:13

so really no function occurring at all

6:15

within those segments.

6:17

And then dyskinetic is actually reversal

6:19

of the normal pattern of thickening.

6:21

So when the rest of the segments are kind

6:23

of contracting in this segment would be ballooning out,

6:26

a dyskinetic segment would be ballooning out.

6:28

And that's kind of, if you're calling something dyskinetic,

6:30

you're basically saying that there's an aneurysm

6:32

within the myocardium.

6:33

And so if we look here on the cynic lip to the right,

6:37

an example of this is we start to look kind

6:40

of here in the mid region of the myocardium here,

6:43

the anterior and anterior septal segments

6:46

are actually thinned out.

6:47

We watch that clip play through.

6:50

You can see in those few slices there in the middle row,

6:52

kind of anterior and interseptal segments are

6:55

relatively hypokinetic.

6:56

And we then we get some more thinning

6:58

and hypokinesis as we move more apically in that middle row

7:01

and bottom row as well, that starts

7:03

to become more circumferential.

7:05

And then probably the most important part

7:07

of this is understanding LGE imaging.

7:09

I'm gonna take a little quick detour of some physics here.

7:13

So this is really the only physics

7:15

that we'll have in the course today,

7:16

but I just think it's important to understand this.

7:18

So of course when we do LG imaging,

7:22

you know it's contrast enhanced imaging

7:23

and galene based contrast shortens T one.

7:26

So all of our imaging approaches for LGE are gonna be more

7:28

of AT one weighted approach to imaging.

7:31

And so just as a reminder, when we do T one weighted imaging

7:34

and all of MRI, we tip the kind

7:36

of main magnetic field there labeled

7:37

as MZ into the transverse plane.

7:40

And then we watch that recover along that Z axis over time.

7:44

And it's the degree of recovery

7:46

of the recovery time there along that Z axis

7:49

that determines T one.

7:51

And so this is just an example of

7:53

what T one recovery looks like in two different tissues.

7:56

You can see tissue A has a shorter T one tissue B has a

7:59

longer T one and T one is defined as 67%

8:02

of the total recovery along that MZ direction.

8:06

And so these two tissues would

8:07

have slightly different T ones.

8:09

And so in T one weighted imaging tissue A would be brighter

8:13

than tissue B, moving along to inversion recovery,

8:17

T one weighted inversion recovery imaging.

8:19

So now instead of just the standard spin echo technique,

8:21

which we see in the left

8:22

where we tip everything in the transverse plane,

8:25

which means we get to kind of MZ equals zero there

8:29

and then watch it recover

8:31

and inversion recover,

8:32

you actually tip everything 180 degrees.

8:34

So now it's kind of anti-parallel to the Z axis.

8:37

And then as it recovers there on the right

8:39

as we're recovering here, we actually now cross zero.

8:44

That's something that is gonna be very important in late

8:46

gado line and enhanced imaging here.

8:48

So inversion recovery, we tip down

8:51

and then we watch it recover and it recover as it recovers.

8:53

It crosses this axis where there's no magnetization.

8:57

And so that is exactly the principle

8:59

that we use in lake gadolinium enhancements.

9:01

So when we give contrast, we wait 10 minutes

9:05

and I'll tell you why that's important in just a second,

9:07

but we wait 10 minutes and then we perform our imaging.

9:09

But our goal again is to get normal myocardium,

9:12

really jet black here and then enhanced myocardium.

9:16

We want it to be bright. And so when we,

9:19

when we do our inversion recovery,

9:21

we tip everything down into the anti-parallel direction,

9:24

we watch it recover because infarcted tissue here in the

9:28

dark black line has taken up contrast.

9:31

It's T one is gonna be shorter than normal myocardium.

9:34

So as we watch these recover over time,

9:37

you should find a point where the normal myocardium crosses

9:41

that zero point and it's black and then enhanced myocardium

9:45

or myocardium that has gadolinium in it is gonna be bright.

9:49

And so we do something called a ti scout image

9:52

when we do LGE.

9:53

And it's exactly watching multiple frames over time of

9:57

of sort of AT one weighted inversion

9:58

and recovery image where you can say, okay, at that point

10:01

that's where the myocardium is black,

10:03

the normal myocardium is black.

10:04

And so that's where I wanna perform my LG imaging.

10:07

That gives you what's called an inversion time.

10:09

And you pick the inversion time then

10:11

and you actually run your full imaging

10:12

after you know what the inversion time is.

10:15

So why does this actually work?

10:17

Why does scar tissue take up gadolinium?

10:19

Well, if we look here at an arterial bed and,

10:23

and this can be a representative of a coronary arterial bed,

10:27

a normal look would be here on the left

10:30

where we have arterials,

10:31

they flow into arterial capillaries, venous capillaries,

10:33

then out through veins right in the middle

10:35

during an acute infarct, all the tissues

10:38

and things around this capillary bed are injured

10:42

or dying, you know, and there's inflammatory markers

10:45

and clot coming in.

10:46

And so this gets really damaged.

10:49

And so what happens then is in an acute injury,

10:54

you actually get, if you give contrast,

10:56

if you ga give gadolinium, it gets into the tissues,

11:00

it leaks out of these capillaries which are damaged

11:02

and then it can't get back out.

11:03

And so it sort of can show you where there's damage

11:07

because it can't, you know,

11:08

gadolinium gets in but it can't get back out.

11:11

So that's kind of an acute injury

11:13

and more chronic injury like we're talking about here in

11:17

viability imaging.

11:19

It actually, there is scar tissue that forms

11:21

and it's kind of the,

11:23

a similar concept except there's really no functioning

11:26

capillary or capillary beds in that scar tissue.

11:29

And so gadolinium again, will sort

11:31

of like seep in slowly into these areas of scar.

11:34

And then because there's really nothing

11:36

that can help it get out, it kind of gets trapped in there.

11:38

And over time people have figured out that about 10 minutes,

11:41

10 to 15 minutes

11:43

after you've give an injection, that's when you kind

11:45

of get optimal sort of leakage

11:47

and retention of gadolinium into these areas of scar.

11:50

And that's why we do LGE imaging

11:53

About 10 minutes after we inject contrast.

11:56

And here's just another example of how,

11:58

what this looks like, where you can see kind

12:00

of fibrotic myocardium here exemplified by sort

12:03

of all this fibrous tissue around

12:06

in the interstem of a myocardium here.

12:08

Once you give gadolinium that actually leaks in

12:11

through these capillary or or arterial beds

12:14

and then it sort of just gets retained in those areas

12:17

because it doesn't have a lot of vascularity to get it out.

12:21

Couple other notes here when you're thinking about LGE,

12:24

location absolutely matters.

12:26

So the chart on the left is a really good example of

12:30

a good way to think about LG imaging just in general,

12:33

whether you're thinking about ischemic heart disease

12:34

or non ischemic and really an ischemic heart disease,

12:39

you know, vascular related scarring.

12:41

What we want to see here is up in this upper left part

12:44

of the figure, part A here,

12:45

there's sub endocardial enhancement.

12:47

It's sub endocardial because that's part

12:50

of the myocardium that's most at risk.

12:52

It's the most distal part of vascular bed,

12:55

so it's most at risk.

12:56

And so scarring tends

12:57

to work its way from a sub endocardial space outward.

13:00

And so we can go all the way from very little enhancement

13:03

all the way to a transmural,

13:04

what's called a transmural infarct tear.

13:06

And then there's other forms of late gadolinium enhancement

13:10

for non-ischemic etiologies,

13:11

which I won't get into in this talk,

13:13

but can actually work quite well to sort

13:14

of distinguish various pathologies.

13:17

The other thing to note is kind

13:19

of coronary artery territories are important here.

13:21

So if we're gonna look for coronary artery disease

13:23

or coronary artery related injury to the myocardial,

13:26

we actually want the damage to follow a coronary territory.

13:30

And so it's important to know the,

13:31

this is the a ha 16 segment model where we,

13:34

if we go from base mid to apex,

13:36

certain segments here are supplied

13:38

by different vascular territories.

13:40

So you know, we have a reference one

13:41

of these up in our reading room.

13:43

Something that we're always thinking about when we're

13:45

thinking about vascular entry is,

13:47

does it follow a typical coronary artery distribution?

13:50

And here's just an example of mural extent.

13:53

So this is kind of in viability imaging, again,

13:55

the extent across the myocardium matters

13:58

and nice examples here, going from left to light, left

14:00

to right of, you know,

14:02

very little mural extent there in the septal region

14:06

and kind of working its way around

14:08

to something like about 26 to 50%.

14:11

So sort of still a viable tissue there in column two.

14:14

And then as we start getting more and more

14:16

and more, 51 to 75%

14:19

and then 76 to a hundred percent, these are

14:21

where you would start to describe things

14:23

as low likelihood of viability.

14:26

So last couple of points here.

14:28

What do we actually describe in viability imaging?

14:31

So the first thing is what regions

14:33

of the heart are involved functionally?

14:34

So is there wall thinning

14:36

and are there regional wall motion abnormalities by segment?

14:39

This is the same syn a I showed you

14:40

before where we saw some

14:42

of those regional wall motion abnormalities starting kind

14:44

of in the mid short axis views here involving the anterior

14:48

interseptal segments

14:49

and then getting more circumferential all the

14:51

way down towards the apex.

14:53

And then we wanna describe the segmental distribution of LGE

14:57

and then also give an indication of percent wall thickness.

15:00

So this is the same patient

15:01

and you can see highlighted by the arrows here,

15:04

starting really towards the base

15:05

and extending into the mid kind

15:07

of anterior septal anter, inferral septal.

15:10

And then working its way almost down to the kind of inferior

15:14

and septal segments of the apex.

15:16

We have lake ala enhancement.

15:19

And on this one it looks like if you compare it to sort

15:22

of normal parts of the LGE,

15:23

I would definitely say this is less than 50%

15:25

of the myocardium qualitatively.

15:27

And so this would be one where you would say,

15:29

this is probably high likelihood of functional recovery.

15:32

The only caveat to that,

15:34

and you can see on this two chamber short axis,

15:36

really the distal apex.

15:38

So probably the most distal part of what's being supplied

15:41

by LAD here in the inferior segment seems

15:43

to be almost transmural.

15:45

And you can nicely see that on that two chamber.

15:47

So that would be the one caveat in this case

15:49

where you'd say this is possibly a, a non-viable segment.