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This is a case of a 55 year old man who has a

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History of SC segment elevation, myocardial infarction,

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And he had a prior

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PCI to his LAD

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and this study was done for viability assessment.

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So to see if he could benefit from

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further revascularization.

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And so starting in our usual pattern, we're gonna start

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with the syn images two chamber.

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And we can already see on this two chamber view

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that there is some abnormal wall motion

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of the anterior segments kind of in here, sort of mid

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to apical anterior wall seems to be actually probably

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at least a kinetic

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and thin, if not a little bit dyskinetic there kind

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of in the mid segment there.

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Moving on to our four chamber view,

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not really detecting

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as much wall motion abnormality perhaps here at the apical

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septal region on the four chamber, three chamber,

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I would say probably in this case the three chamber is

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demonstrating there is kinesis

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and thinning kind of of these apical segments as well.

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So we kind of are getting the sense

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That there's definitely problems in the apex

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and kind of the anterior aspect from our long axis view.

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And then as we work our way down the short axis here,

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again moving from base to apex doesn't look too bad there.

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Okay, here and here is when we're starting to get into

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some abnormal wall motion.

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Again in more of the mid segment here, kind

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of in near end diastole, not as thin

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as we can see in some of these,

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but you can appreciate there's kind of a little bit

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of thinning and then there's gonna be definitely some

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hypokinesis of these segments here in the kind of anterior

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and anterior septal region.

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As I move down we're gonna see more of the same

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and here we really start to get more thinned out

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and again almost are getting a bit of that diskinetic look.

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If you can draw your eyes kind of to this region,

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which is I think exactly where we saw in the two chamber,

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kind of the mid anterior segment is very thin

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and probably moving kind of in a diskinetic fashion relative

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to the rest of the segments here in the anterior septum were

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thin and at least hypokinetic if not a

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kinetic in those regions.

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And now moving more

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and more apically here, kind

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of same story really impacting the anterior

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and anterior septal segments.

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And then as we get into the true apex itself,

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here we're starting to see I think a little bit

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of a difference between the lateral aspect here

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of the segment of the apex and the septal

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and anterior segments where now we're kind

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of seeing more involvement of the septum

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and maybe even inferior aspect of the

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Apex here with a little bit of thinning

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and certainly some hypokinesis relative to others.

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Okay, so moving on to the late

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Glan enhanced images.

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Here you can see as we're moving down

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From base to apex, we'll just kind of take it slice

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by slice very early on

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here at the base you can kind of appreciate, you know,

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here's normal jet black myocardium.

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Here is gonna be our area of sub endocardial,

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late gadolinium enhancement kind of right in this region.

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Now keep in mind this is not an acute mi

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but throughout these we have some of these islands of

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hypo intensity.

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So low intensity mixed in within the areas

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of lake gata limb enhancement.

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This can be a phenomenon if it's acute,

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you think about something called microvascular obstruction,

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which we will talk about specifically later in the day.

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But in more chronic

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infarct sometimes you have what's called no reflow,

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where there's just so much damage to the tissue there.

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There's no blood supply to bring gadolinium

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to those regions.

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And so you can just get these islands

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of abnormal hypo intensity even in chronic disease.

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So really here we're starting to see sub endocardial,

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late gadolinium enhancement involving the anterior

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and anterior septal regions.

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Some of this, you know, again,

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looks like it's probably about 50%

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of the myocardium here back towards the base

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moving more apically here, getting into the mid portions

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of this appear to involve, you know, more transmural

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or you know, greater than 50% while others are kind

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of probably still hanging below that 50% border.

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This site moving more.

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Aply again has some LGE in here that looks like

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less than 50%.

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And if we keep moving down kind of the same story kind

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of right where we saw the thinning and regional wall mesh

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and abnormalities as we have a lot

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of sub cardio late gadolinium enhancement.

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In this case though it seems

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to be involving about less than 50% as we get to this slice

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and on on towards the apex though more

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and more mural extent of the myocardium is involved.

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So for example, here you have some LGE that seems

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to be involving almost transmural myocardium.

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And then as we keep clicking down towards the apex,

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it looks like it's probably going to be transmural in most

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of these segments of the at least septum

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and inferior aspect of the apex.

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This is probably normal here in the lateral aspect

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of the apex, which is a different coronary artery territory.

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So this is looking based off

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of our distribution looking like an LAD

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territory infarction.

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We know he has LAD disease from his history

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of PCI in that area.

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And let's look at a couple of other long axis views.

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I think, you know, these can be really useful to, especially

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as you're starting to try to understand transmural extent,

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I think the three chamber view on this one

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really shows nicely.

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So here is some of those findings in the anterior septum

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where we see probably better than we appreciated on the

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short axis use that you have.

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This is sort of a three chamber orientation.

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You have LGE in the septum here,

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this is gonna be anterior septum.

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That definitely does not involve 50%

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of the myocardial thickness.

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So you know, if I draw your attention here,

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this would be the whole myocardial thickness

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and then we have definitely not 50% of that that's enhanced,

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you know, sort of this hyperintense area.

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So this would be consistent with a viable segment.

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Contrast that now with some of the areas in the apex,

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which again are often seen much better on long axis views

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than they are on short axis

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where we see no real normal myocardium

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kind of at the true apex.

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Uh, I think we can see this nicely on some

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of these other long axis views as well.

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And so, you know, non-viable myocardium here at the apex.

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So when you describe these, you oftentimes have

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to describe multiple segments

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Being viable or non-viable and that can certainly inform

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Their strategy. I

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think the other key finding in this is

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that we really don't see LGE in vascular LGE in

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any other territory.

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So this seems to be really LAD disease exclusively,

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which is important for them to know.