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All right case number nine.

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We have a 52 year old female who presents with Progressive dyspnea

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on exertion for one month.

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She has CHF on chest x-ray.

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and low voltage on ECG

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as well her Echo reveals an objection fraction

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with approximately 45%

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I'm showing two cardiac MRI series on

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the left. We have mid ventricular

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short axis in a

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and on the right we have post contrast.

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LGE Imaging as

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I described earlier

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take a look.

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See if you can identify the Imaging abnormalities

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and the cause.

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of these findings

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All right on the left the Sinai is showing.

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Global mild hypokinesis, and

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it would be consistent with what Echo saw of an

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ejection fraction 45% There are also appears to

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be circumferential healthy thickening a bit

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worse and accepted.

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the

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the differential at this point would still be pretty broad. But then

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when we look at the post contrast study

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we see.

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An image that is basically diagnostic

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for the pathology.

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And this is a case of cardiac amyloidosis.

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And let me go back to that image for a

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second. This is not like the

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LGE images. So I've shown in the

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prior cases.

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This is a horrible looking image. And sometimes it's the

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best that the technologists can achieve and sometimes

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they'll call us and give us our first clue

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that the patient has cardiac amyloid by saying we

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can't find a satisfactory null point.

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And that's the first clue because amyloid is

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is really the only thing that I

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know as far as cardiac pathology is concerned where the myocardial

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T1 is shortened.

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To a degree that

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is even shorter than the LV cavity blood.

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And that happens because amyloid protein

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is deposited in the interstitium.

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The contrast that we administer is extracellular

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and it goes into the interstition and in an

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expanded extracellular space the gadolinium

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really accumulates quite substantially.

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And at CMR it makes it really difficult to

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find a good null point to make normal.

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Myocardium black.

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And that's the clue that will often be

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revealed first. This is a restrictive cardiomyopathy with

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thickened myocardium. But usually you have low or normal

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ECG voltage because in contrast

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to hypertrophic cardiomyopathy, which

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is also too thick and which is also a restrictive cardiomyopathy.

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There's not too much muscle

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here. It's that there's too much extracellular space

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and amyloid deposition.

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And so the voltages which result from muscle are

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normal to low.

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In contrast in HCM, the voltages

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will be elevated.

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And cardiac MRI turns out to be very good for identifying

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diagnosing cardiac

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amyloid.

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Um a this is an example of a series

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of images from what we call TI Scout

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Imaging where you look to see using different inversion

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times what the appropriate TI

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to null normal. Myocardium is and what you

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see in cardiac amyloid. Is that very early

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on using short TI's you

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already see some black myocardium, but

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we haven't gone through

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the null point of the blood pool yet that occurs later.

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And at the no point of the

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blood pool you you start to see already, right? Myocardium and

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that's not something that you expect to see with I think

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virtually any other pathology. Here's another example of a

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horrible looking LG image that's virtually

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pathognemonic for cardiacamole.