Interactive Transcript
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All right, so the first case we're gonna look at in this
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course is a 73 year old man who had a TAVR performed
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and also had coronary artery bypass grafting.
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It's got a history of myocardial infarction
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and I want to use this case as, as an example
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to illustrate the difference between transmural
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and Nont transmural infarction.
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And then we'll actually look at some
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coronary artery territories.
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So as you'll see, uh, is a theme
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whenever we look at any of these cases, I,
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I at least always start with the functional imaging
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and start here with the long axis view.
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So this is a two chamber view.
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A couple of points while we're going through,
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again related to two chamber.
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The two chambers we see are the left ventricle here,
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the left atrium here.
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I always like to point out the left atrial appendage,
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which is a good place to just keep an eye out for thrombus.
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And then as I scroll through this on my syn a clip,
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you can see actually in this case this is the mitral valve
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here and we can see that as I scroll through,
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there is actually some mitral regurgitation.
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So just a couple of basic cardiac MR points,
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not really related to ischemic cardiomyopathy.
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And then what we can see as I get
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to end diastole here, something about here we can see
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that there's actually wall thinning of this sort
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of apical anterior segment, true apex
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and then down into the inferior aspect of the apex
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and probably some wall thinning here
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and what ends up being the basal inferior segment.
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So we'll investigate those further on
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the short axis imaging.
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Moving on to our next long axis view,
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this is the three chamber view.
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So just again for anatomy, basic anatomy orientation,
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left ventricle, left atrium,
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this is the aorta in this patient.
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This is his TAVR valve
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and this is the right ventricle right here.
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We do see some susceptibility artifact in the sternum
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related to sternal wire sutures from his prior cabbage.
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But uh, again, we're seeing kind of a very similar look here
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where we have mitral regurgitation
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and a lot
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of regional wall motion abnormalities and thinning.
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In this case, just kind of based off of the orientation
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of the three chamber, we again see that they're thinning
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an kinesis at the true apex and then a little bit here
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and sort of the apical aspects of the eth intercept.
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Moving on to our last long axis view,
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this is a a four chamber again as an anatomy overview.
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Left ventricle here, left atrium here, right atrium,
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right ventricle mitral valve, tricuspid valve here.
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This is the aorta descending aorta back here.
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And as we're watching again,
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we see some regional wall motion abnormalities,
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probably seen better on some of the other views.
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This is a nice overview to take a look at mitral
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and tricuspid valve disease
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and it's really the, the view
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that we get the best look at the long axis function
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of the right ventricle.
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So a couple of kind of key points on cardiac Mr
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Next I'm gonna start in on our short axis view.
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So as we, we move through the short axis,
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at least the way these cases will be set up,
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we're gonna move from base to apex.
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And so for example, on this view, we start to see the aortic
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valve prosthesis.
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So you kind of know we're at the distal base here
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and as we work, this is the mitral valve
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that we're kind of seeing the leaflets on.
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And as we start to work through, I think you'll start
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to appreciate
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that there's some wall thinning here in the basal infra
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septum and also probably kinesis
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what I would term kinesis there.
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And we really start to see it nicely in this view now
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involving not only the inferior wall
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but also the infra septal aspect
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here at the left ventricle thinning and,
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and probably kinesis at least of this and
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and severe hypokinesis or kinesis of the infra septum there.
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Keep working our way down.
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Kind of see continued kinesis of the infra septal wall.
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Notice up here we, we see kind of hypokinesis of all
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of these segments and particularly this interseptal segment
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but not a lot of wall thinning there, right?
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So more of the same.
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Now we're starting to get a little bit more apically and,
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and you kind of get the sense
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that all segments almost circumferentially are starting
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to be quite thin and,
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and we have more involvement of the anterior segment here
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and some of the anterior septal aspects here with thinning
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and kinesis and then some sort of hypokinesis of the septal
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and lateral segments here, kind of global hypokinesis
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and thinning as we move more, more
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and more towards the apex.
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And then on down.
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So now we have a pretty good overview of the
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wall motion of this patient.
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So let's look at the LG images.
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This is kind of, you know,
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when we're thinking about infarcts
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and viability imaging, obviously the LG imaging
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is gonna be really crucial.
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So here's our LG imaging
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and I'm gonna start up here at the base
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and walk kind of slice by slice.
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And so first thing we note is as we start to get into kind
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of the basal inferior segments here we see sub endocardial,
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late gadolinium enhancement involving the basal
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inferior segment and infra septal segments here.
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And I would describe this particularly,
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I think this is a nice example as transmural,
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you can really see that, we know this was thin
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on the semi imaging,
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but you can really see there's like a pretty dramatic sharp
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cutoff here between these two sites.
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And you know, if this didn't have LGE,
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you would really see myocardium all through there.
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So that's a transmural infarct.
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I don't see anything left over
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probably still definitely greater than 50% near transmural
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here in this segment starting to be a little
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Less than 50% here as we get more
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apical here in that inferior segment.
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And then we kind of pick up a little few spots of LGE
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that are a little bit more focal kind of RV insertion point.
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But really this is an example of a transmural infarct
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and based off of what we know from our 16 segment model,
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this is in the RCA territory,
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it fits really nicely in the RCA territory.
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So this is an example of a non-viable trans bural RCA
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infarct on this patient.
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But that's not all that we see in this patient.
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And this is important, you know, kind of satisfaction
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of search idea to keep in mind.
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So the other thing, if we move back here towards the base
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and start to look at a few other regions, you start to see
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as we get here towards the basal to mid kind
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of anter septal segment, we start
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to see some sub endocardial lake GA lame enhancement.
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Not quite as dense as this.
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Our intense as the RCA infarct is in terms
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of just overall signal
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and we maybe see a little dot
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of what's called hypo intensity.
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And this may be microvascular obstruction, which we'll go
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to later in the course,
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but this is still sub endocardial,
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late gaden lay enhancement.
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So kind of is following more of an ischemic, more
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of a vascular kind of infarct type pattern.
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But notice in this case, first of all, there wasn't
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as much wall thinning on the CNA images that I showed you.
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And here we can kind of make out like, you know,
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there's still some normal myocardial kind of hypo intensity
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that isn't totally taken up by LGE.
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You know, for example, this image it looks like, you know,
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maybe this is kind of the extent of LGE right here.
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So this would be an example of a non transmural infarct.
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And so kind of you see on the same slide here, an example
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of a transmural infarct in probably what we would at least
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estimate to be roughly 50% maybe.
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And perhaps this is more of an acute process.
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So this would be a one that we would say is,
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has a higher likelihood of functional recovery
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with revascularization in this patient.
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The last thing that I want to show you
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in this particular case,
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'cause it can be tricky if you're just looking at the short
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axis images, the long axis images can actually be quite
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helpful as well.
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So here's a two chamber LGE image
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and one thing that is helpful is you can kind of see like,
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okay, here is actually the extent of that inferior LGE.
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It really truly is kind of truly transmural here.
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So you get a different view, a long axis view kind of
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of the LGE, but you also get the sense down in some
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of those areas of the apex that were totally thinned out,
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that there is really no myocardium here.
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That's normal. So this is also gonna end up being a
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transmural infarction in the true apex,
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which is usually supplied by the LAD.
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So you kind of got LAD disease here, some
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of which is viable in the basal anter septum.
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And then this more distal LAD disease
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that you probably only see well on these long access views
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as non-viable.