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Applied Clinical Procedures > MPI > Flashcards

MPI Flashcards

1
Q

coronary artery disease

A
  • decrease in blood flow to heart due to atherosclerotic plaque, or occlusive thrombus/embolism
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2
Q

where is plaque likely to form?

A

in a bend or bifurcation in the coronary artery
- where there are more blood turbulence occurring

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3
Q

what contributes to CAD?

A
  • HTN, hyperlipidemia, diabetes, smoking, obesity, diabetes, sedentary lifestyle, family hx, gender
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4
Q

how does plaque formation occur?

A
  1. injury - damage to inner lining of blood vessels
  2. healing
  3. localization of macrophages and smooth muscles
  4. plaque progresses
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5
Q

how does plaque progression occur?

A
  1. fibrous tissue deposition (fibrous cap)
  2. calcium deposition
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6
Q

how do drugs reduce the size of plaque?

A
  1. by reducing lipids in plaque
  2. increasing lipids out of the plaque
  3. limit number of macrophages present
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7
Q

what drugs are used for plaque reduction?

A

statins
Lipitor, Crestor, Zocor

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8
Q

which wall will be seen to have more uptake?

A

lateral > ant or inf

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9
Q

normal LHR when using 201Tl

A

<0.5:1

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10
Q

normal TID

A

stress:rest
~1

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11
Q

normal summed stress score (SSS)
normal summed rest score (SRS)

A

<4
<4

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12
Q

normal LVEF

A

> 50%

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13
Q

stress/rest matched with NO defects

A

normal
but watch out for triple vessel disease

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14
Q

stress/rest mismatched defects

A

stressed induced reversible myocardial ischemia

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15
Q

stress/rest matched defects

A

chronic hibernating myocardium
/ myocardial infarction

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16
Q

what is triple vessel disease?

A

stenosis in all major coronary arteries = overall decreased perfusion making it look normal

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17
Q

what pathological conditions will make it easier to see the ischemic myocardium?

A

when one vessel is affected significantly more than the others

18
Q

when does sensitivity increase for ischemic myocardium?

A

when two obstructed vessels “watersheds” affect the same portion of myocardium

19
Q

TID >1.4

A

multi-vessel disease

20
Q

polar plots

A

semi-quantitative method of analyzing regional perfusion
- data obtained is compared to a large database of normal

21
Q

increase Rt:Lt ventricular uptake ratio to indicate CAD

A

> 0.42

22
Q

summed stress score indicating mild risk

A

4-8

23
Q

summed stress score indicating moderate risk

A

9-13

24
Q

summed stress score indicating severe risk

A

> 13

25
Q

low SDS is due to…

A

matched SSS and SRS

26
Q

what does low SDS indicate?

A

irreversible

27
Q

large SDS =?

A

mismatched SSS and SRS

28
Q

SSS scoring is created by…

A

infarcts or stress induced ischemia

29
Q

SDS scoring is created by…

A

fixed perfusion defects or hibernating myocardium caused by chronic ischemia

30
Q

stunned myocardium

A

acute + temporary
- after acute ischemic event
tissue viable but function and contractility is diminished

31
Q

what does a stunned myocardium look like on a NM scan?

A

normal perfusion but poor ventricular contraction

32
Q

how do you treat stunned myocardium?

A

it should spontaneously resolve after a few weeks!

33
Q

hibernating myocardium

A

chronic ischemia caused by severe coronary artery stenosis
no perf on rest, fill in on redistribution images

34
Q

201Tl perf
stress: normal
redistribution: normal
24hr delay: n/a
interpretation?

A

neg for cad

35
Q

201Tl perf
stress: abnormal
redistribution: normal
24hr delay: n/a
interpretation?

A

ischemia

36
Q

201Tl perf
stress: abnormal
redistribution: abnormal
24hr delay: normal
interpretation?

A

chronic ischemia/hibernating myocardium

37
Q

201Tl perf
stress: abnormal
redistribution: abnormal
24hr delay: abnormal
interpretation?

A

non-viable/infarct/scar

38
Q

201Tl viability
rest: normal
redistribution: n/a
interpretation?

A

viable myocardium

39
Q

201Tl viability
rest: abnormal
redistribution: normal
interpretation?

A

viable/hibernating myocardium

40
Q

201Tl viability
rest: abnormal
redistribution: abnormal
interpretation?

A

non-viable myocardium

41
Q
A

Applied Clinical Procedures (6 decks)

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