Interactive Transcript
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This case is a 78 year old woman with a history
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of non-ischemic cardiomyopathy and heart failure.
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And it actually looks like she's a kind
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of dilated cardiomyopathy phenotype.
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And so they wanted to do an evaluation to look both
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for signs of ischemia in case there is an ischemic component
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to her underlying cardiomyopathy.
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And also look for other signs related
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to her cardiomyopathy enhancement, any patterns of disease
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that may be diagnostic.
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So, uh, again, showing you the profusion images first,
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stress across the top, rest across the bottom,
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and then base mid and apex here.
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And so what I want you
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to notice about these exams is the stress
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and rest images look almost identical
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in this particular case.
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And particularly pay attention to some areas here, like
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as I kind of go through time, you notice
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that maybe there's a little bit of hypoperfusion here
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in the septum and maybe even lateral,
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almost circumferentially here,
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but it kind of does the exact same thing at rest.
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And that's true for all of our slices.
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You know what looks like hypoperfusion here in the septum
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Also, we see it at rest.
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Same thing in the septum here in the apex. Same here.
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And so one thing that you have to sort
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of do first is you do a quality check.
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And so we talked about the splenic switch off sign.
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So here's actually the spleen right here, spleen right here.
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And you can notice it's stress.
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The spleen is dark at rest, the spleen is bright.
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So you know, we feel like the adenosine
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had an appropriate response.
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The patient had a response
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to the adenosine, her heart rate went up.
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So we don't think that this is a sort
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of a image acquisition issue.
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This wasn't a quality issue.
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So we're kind of left, you know, mass profusion defects.
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So we're thinking either this is a big infarct,
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which we'll look on LGE or this is an artifact.
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And so let's look at LGE next.
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And by artifact I mean dark rim artifact.
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This is kind of classic dark rim artifact.
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And just to tell you, that's what we kind
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of thought it was initially.
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So here we're looking now at our LGE images, again,
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you notice that the myocardium is really thin
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and an LV is dilated.
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So kind of classic dilated cardiomyopathy.
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Look, no LGE here.
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Certainly nothing that looks like infarct
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or something that would cause circumferential fusion defect.
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So we were pretty comfortable with the idea qualitatively
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that this was gonna be dark grim artifact.
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But as I'd mentioned, we do more quantitative profusion now.
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And I'm just gonna pull up, uh, side by side here the
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results of the quantitative profusion evaluation to show you
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how this can perhaps be helpful.
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So from left to right,
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I have the flow at stress, the flows at rest,
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and then the myocardial perfusion reserve.
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And what we thought was quite interesting here, this,
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the flows at stress were pretty low
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while the flows at rest were pretty normal overall.
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So when you do that division, which you can appreciate,
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you know, myocardial perfusion reserve is
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stress flow divided by rest flow.
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And you can see almost all of these are less than two.
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And the global overall perfusion reserve
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is quite a bit less than two.
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And so given the fact
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that we had a good physiologic response,
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we ended up calling this likely microvascular disease
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or three vessel disease and this person
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because the quantitative perfusion was so abnormal
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and we had no other reason to believe this is the case.
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So I think this is just a nice example of
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where quantitative profusion can help you work through some
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of those artifacts or or questions that may come up.
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And it sort of makes us wonder, you know,
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we've been doing qualitative for years.
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How many of these cases have we actually may be under called
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where quantitative mabo now will get us to the right answer.