Interactive Transcript
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Our next case is a 49 year old man with a history of uh,
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coronary artery disease who presented
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to the emergency department with an upper GI bleed
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and then was found during his workup
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to have evidence of a stemi.
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So he went to the cath lab
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and then we get an MRA few days later to assess
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for complications or viability.
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So starting in our usual fashion two chamber
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would be a little bit of apical
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and inferior wall motion abnormality here.
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But overall, not too bad here though, I think you can start
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to appreciate on this four chamber view,
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the septum is actually moving and contract
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and thickening pretty normally.
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But the lateral wall out here,
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while not really thin, is not really thickening,
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at least not to the same extent that the septum is.
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And here's our three chamber view showing some similar
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findings, particularly down towards the mid
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and apical region here.
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So then moving into our short axis stack,
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moving from base to apex.
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So we can already start to see that here.
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Even at the base, there's sort of
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what I would term global hypokinesis.
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It's not like these segments and the anterior septal
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and inferior segments are contracting great,
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but compared to they are moving better compared to sort
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of these antola inferolateral segments in this case,
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you can see here and it'll be even more apparent
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as we move down
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and even more so here as we get more apical really Now
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inferior segments involved
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and the anterolateral infra lateral segments are
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basically a kinetic.
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And the only thing that's thickening is the septal
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and anterior segments.
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So next in our algorithm is the LGE images
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get a good window and level for you here.
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And as I start back towards the base,
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it's gonna be pretty apparent very
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quickly that there's a problem.
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So normal myocardium here
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and in the areas where we saw hypokinesis,
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it's actually kind of difficult to tell.
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If we look at this slice,
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we definitely see late GTA limb enhancement.
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It's transmural, but there is so much of that, those islands
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of hypo intensity here.
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So the areas of microvascular obstruction here
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that sometimes it totally almost takes up the whole
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thickness of the myocardium.
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The other thing that's interesting about this case,
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as I scroll back and forth here to to notice
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is the papillary muscles themselves
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actually don't show any enhancements.
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So this is, you know, suggested that, you know,
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this infarct is involving vasculature
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that actually supplies these papillary muscles,
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which can be a risky risks, you know, potential fla,
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mitral valve leaflets and those sorts of things.
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So it's relevant to mention that.
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But the descriptor here would be basically transmural,
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late Gaden Liam enhancement,
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which involves the basal two apical,
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anterior lateral, and infra lateral segments with
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extensive microvascular obstruction
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and non enhancement of papillary muscles is kind of the way
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that you would wanna describe this finding.
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Let me go to, I think a four chamber view.
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We'll show it nicely as well. I get a good window and level.
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Again, there's so much MVO here, microvascular disease
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that it's really, so this is, you know,
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transmural enhancement, but all of this hypo intensity
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is microvascular obstruction.
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And then, you know, this is an acute case.
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So we've, we've got the T two maps to look at as well.
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Here are these sort of like more purpley regions are areas
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of elevated T twos here qualitatively.
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And then if we look at the T two map, you can see that in
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that territory where there's LGE
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and WAMO abnormality, there's certainly areas
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of elevated T two involving those regions.
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A couple of remote regions are actually involved as well,
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which is kind of relevant to mention, um,
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because that may imply some area at risk,
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even though it's in a different vascular territory.
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But all this together is consistent
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with an acute myocardial infarction
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and the circ territory with microvascular obstruction.