Upcoming Events
Log In
Pricing
Free Trial

CMR Stress Perfusion 1 (Background, Data on use)

HIDE
PrevNext

0:00

Okay, so for the next part

0:01

of the course we're gonna move into more

0:03

of an ischemia evaluation.

0:05

So we have looked at, you know, myocardial infarctions

0:08

with chronic and viability assessment and,

0:10

and then acute myocardial injury.

0:12

We spend a lot of time thinking about this,

0:13

but how about sort of upstream from that?

0:16

Can we use cardiac MR to determine the extent

0:19

of coronary artery disease

0:21

and risk stratify prior to somebody having an event?

0:23

That's, that's obviously what we would like

0:25

to do is prevent people from having myocardial infarctions.

0:28

So in this section, this is gonna be a a two-part,

0:31

kind of didactic section.

0:32

In this one I want wanna talk just a little bit about the

0:34

background and evidence related to cardiac MR

0:37

for ischemic evaluation.

0:38

And then in a second section we'll talk more about the

0:41

techniques and the details of interpretation. So,

0:45

Stress testing is very common in coronary artery disease,

0:49

as most of us I'm sure are familiar with.

0:51

And the goal of stress testing is

0:53

to unmask inducible myocardial ischemia.

0:56

So what does that actually mean?

0:57

If you, if you look at the chart here on the left

0:59

and you look kind of at the sort of yellow line

1:02

that's your resting blood flows, what you can see is

1:06

that at various diameter narrowing percentages.

1:10

So as you increase the narrowing of your,

1:12

of your coronary arteries, you have to get

1:15

to a pretty significant percentage above 80% out towards 80

1:19

or 90% narrowing

1:20

before you have a drop off of flow of your resting flows.

1:25

But if we stress the heart

1:27

and try to induce maximal flows to the coronary arteries,

1:30

which is what the more purple color line is doing there,

1:33

you can see that the flows

1:36

actually drop off at stress much earlier, more around 50%

1:40

or 60% narrowing.

1:41

And so when we actually stress the heart, what we're trying

1:43

to determine is, you know, is there sort

1:46

of a more significant stenosis here, you know,

1:48

around this 50% stenosis

1:49

or something that is gonna be functionally significant

1:52

to somebody you know, when they actually are exercising

1:55

or doing something under stress.

1:58

And does that mean that they need

1:59

to be watched more carefully

2:00

or have an intervention, have a look

2:02

to see if we can actually treat this

2:05

before it goes on to develop that ischemic cascade

2:07

and ultimately infarc that we looked at earlier

2:10

In the day. And

2:11

why does this happen?

2:12

Well, the graph on the right show you why coronary

2:15

flow responds this way.

2:17

So in someone

2:18

who has significant epicardial coronary stenosis, which is

2:22

what you see in the bottom half of that figure,

2:24

what actually happens is at rest sort

2:27

of the distal arterial beds are maximally dilated

2:31

'cause they're trying to allow as much flow to come

2:34

through those vessels as possible.

2:36

And then unfortunately when we stress the heart at

2:39

that point, if you have stenosis,

2:41

there's not much reserve left.

2:42

They can't dilate anymore.

2:44

And so you kind of are already maximally dilated.

2:46

They can't pull any more blood into those tissues.

2:49

And so that's why you end up getting ischemia at

2:52

rest in these patients.

2:53

And that's what we're trying to unmask

2:54

with stress testing. And there's

2:57

Multiple ways to perform stress testing.

2:59

There's physiologic versus pharmacologic stress test.

3:03

Those are kind of the, the two major approaches.

3:05

Physiologic of course is exercise induced.

3:08

And you know, what we most commonly think

3:09

of is this is your treadmill stress test usually done

3:13

most commonly with echo.

3:15

Now where you get somebody in a treadmill,

3:16

you follow something like the Bruce protocol,

3:18

get their heart rate up and then you get them laying down

3:22

really quickly and actually image their heart to look

3:24

for things like wall motion abnormalities to see if the, if

3:27

that was induced by stress.

3:29

While we would love to do something like that

3:31

with cardiac mr, there's some challenges due

3:33

to just the nature of mr.

3:34

You know, it's a very, very strong magnetic field.

3:37

So getting machines that can actually are compatible

3:40

with MR scanners and getting 'em in there into the room

3:43

or doing physiologic stress outside of the room

3:45

and getting patients on an MR scanner and then imaging them.

3:48

It's just that the time doesn't really

3:49

work out very well for that.

3:51

There's some work going on to try to, you know, remedy this.

3:54

There's sort of MR compatible stationary bikes

3:57

and things like that that may at some point allow us to do

4:00

that, but that's not really what we do now, you know,

4:03

we'll talk more about pharmacologic stress testing in the

4:05

next half of the talk, uh, which is what we do with mr.

4:08

But that's kind of what we're into with MRIs.

4:10

We've gotta go pharmacologic again,

4:13

we've seen this slide before today.

4:14

There are a, a huge variety of tools

4:17

for diagnosing coronary artery disease.

4:19

There's a huge variety.

4:20

So why would we choose cardiac MR in this circumstance?

4:24

I'm just gonna give you the rundown of the evidence

4:27

specifically for stress perfusion cardiac MRI.

4:29

We've seen the performance

4:31

and some of the data to support the use in infarction

4:34

and acute infarction.

4:35

But how about, you know, ischemic evaluation?

4:37

So a couple slides on some studies

4:40

that have come out over the last 10 or 15 years.

4:42

First of all, cardiac MR stress perfusion studies have

4:46

really high sensitivity and specificity

4:48

for diagnosing coronary artery disease.

4:50

So you can see the sensitivity bar graph on the left

4:54

specificity on the right here in a meta-analysis

4:56

that included 7,000 patients.

4:58

The comparator here was invasive fractional flow reserve,

5:02

which you see had about a 90% sensitivity

5:04

and 85% specificity for diagnosing significant

5:08

obstructive coronary artery disease.

5:09

And you can see across the bottom here

5:11

how cardiac MR performed relative

5:14

to those numbers at both in terms

5:15

of sensitivity and specificity.

5:17

And notice there's a little difference between whether

5:19

or not you call 50% or 70% stenosis.

5:23

That's what the 50 and 70 is.

5:24

And then whether the test was performed at

5:26

1.5 Tesla or three Tesla.

5:28

So there's still some variability across different types

5:30

of cardiac mr, but it generally performs quite well

5:33

for a non-invasive test.

5:35

And how has it performed to other perfusion techniques?

5:38

So the ones that we're always comparing to are PET perfusion

5:42

and spect and just if you focus down on

5:47

part D of this figure, you can kind of see the

5:50

ROC curve comparisons of SPECT cardiac MR

5:54

and PET using a meta-analysis of 166 studies.

5:57

And really what they found in this particular meta-analysis

6:00

is that CMR

6:02

and PET were very similar

6:03

for accuracy while both outperformed SPECT in terms

6:07

of accuracy.

6:09

Here's some direct comparisons of cardiac MR versus spect.

6:12

This when cardiac MR Stress

6:14

for fusion was first really being explored, everything had

6:18

to be compared to SPECT

6:19

'cause that was kind of considered the

6:21

industry standard at that point.

6:22

And so many studies have looked at this over the years

6:25

and these are two of the larger ones

6:26

that are more well known.

6:28

This is MR Impact two and then the other study is CE mark.

6:32

And what both of these studies showed is that in terms

6:35

of sensitivity, cardiac MR is at least

6:38

as good if not better than SPECT

6:40

for diagnosing significant coronary artery disease.

6:43

And then generally MR Impact two showed a little bit lower

6:47

specificity while CE mark, uh,

6:49

which was a little bit larger study, showed uh, equivalent

6:53

specificity for diagnosing

6:54

significant coronary artery disease.

6:56

So the general thought is that cardiac MR is at least

6:59

as good if not better than spec for this diagnosis.

7:04

And here's, you know, a couple

7:05

of examples from the literature of why this may be the case.

7:08

Now, you know, full disclosure, I don't read spec

7:11

so I'm not maybe the best person

7:13

to talk about the weaknesses of spec,

7:15

but this is kind of what has been published in the

7:17

literature as to why some of this is the case.

7:20

So if we look here at some differences

7:23

between spec cardiac m mr,

7:24

and then the corresponding angiogram findings.

7:26

So at rest we see kind

7:30

of an artifact from spec, probably something from

7:32

below the diaphragm that, you know,

7:34

makes it a little confusing if this area is

7:38

got less uptake or if that's artifact.

7:41

Whereas on cardiac mr, we can sort of see nicely

7:44

that there's no stress perfusion defect Here we'll get into

7:47

kind of understanding what the defects are.

7:49

In the next part of the talk stress, you can kind

7:52

of see there's probably decreased

7:54

uptake in this inferior segment.

7:55

Cardiac mr, you can really see

7:56

that there's hypoperfusion there.

7:58

So in this case cardiac MR just seems a lot more clear

8:02

that there truly is ischemia in the RCA territory

8:05

that was later confirmed by this angiogram

8:07

where you have significant stenosis in the RCA.

8:11

Similarly in terms of balanced ischemia.

8:14

So this is three vessel coronary artery disease most

8:16

frequently, sometimes microvascular disease

8:19

can also present this way.

8:21

spect, if you look at all the SPECT images now stress is at

8:23

the top, rest is at the bottom.

8:25

The stress and rest images look essentially

8:27

identical for spect.

8:29

Whereas I think, uh, you can obviously see

8:32

that there's sub endocardial hypo intensity corresponding

8:35

to, you know, perfusion defects circumferentially in the

8:39

basement and apical slices

8:40

that is not really present at rest.

8:42

So we would call this balance ischemia

8:44

or microvascular disease and cardiac MR

8:46

and probably would've been called normal on spect.

8:49

A couple other notes here in terms

8:51

of performance negative cardiac MR stress perfusions

8:55

associated with low events rates.

8:56

This is a huge meta-analysis, 11,600 patients

9:00

with common cardiovascular endpoints

9:02

and you can see that positive stress CMR negative stress CMR

9:06

were good at delineating all these outcomes.

9:09

So good tests for risk stratification

9:12

and LGE alone, in fact was good,

9:14

but maybe not quite as good

9:16

as the combined stress profusion study itself.

9:20

A large registry sort

9:22

of prospectively following patients now for up

9:25

to four years in patients with stable chest pain.

9:27

This is about 2300 2400 patients.

9:30

This study, uh, was published a couple years ago

9:33

and showed that the presence of ischemia

9:36

and LGE in these patients was associated

9:39

with a four time higher event rate

9:41

and 10 times higher revascularization rate at one year

9:44

following imaging.

9:45

So quite a good tool for sort of identifying patients

9:48

who are probably gonna need intervention.

9:51

Finally, the MR Informed trial,

9:53

which is a randomized control trial,

9:55

which was published in the New England

9:56

Journal a few years ago.

9:58

This was in a little more than 900 patients

10:01

who had stable chest pain

10:02

and some cardiovascular risk factors

10:04

or positive stress tests.

10:06

And they were randomized to receive optical medical therapy

10:09

and then either get CMR directed revascularization,

10:12

so do a stress reason CMR

10:14

and REVASCULARIZE based on the results of that test

10:17

or invasive FFR revascularization.

10:19

So you're taking a non-invasive test and an invasive test

10:22

and trying to use those to

10:24

determine your treatment strategy.

10:26

And what they found in the CMR group.

10:28

There were fewer overall revascularizations,

10:30

which probably isn't surprising.

10:32

You're not already in there

10:34

and so you're, you're not gonna be as inclined to go

10:37

for it if the CMR is telling you

10:39

it looks like things are okay.

10:40

And then it was also non-inferior to the FFR strategy

10:43

for major adverse cardiovascular events.

10:45

So certainly looks like we can use stress perfusion Mr.

10:49

To guide management of these patients based off the results

10:52

of.

Report

Faculty

Bradley D. Allen, MD, MS

Assistant Professor; Chief, Cardiovascular and Thoracic Imaging

Northwestern University Feinberg School of Medicine

Tags

Vascular

Myocardium

MRI

Coronary arteries

Cardiac Chambers

Cardiac