1. Cardiac p29-31 (Ischaemic)

Question 1

Progression of ischaemic necrosis in MI

Answer 1

Starts subendocardial, progresses to subepicardium

Question 2

Microvascular obstruction - definition/imaging

Answer 2

Dark islands where destroyed capillaries don’t let contrast through

Question 3

Significance of microvascular obstruction

Answer 3

Independent predictor of death and adverse LV remodelling

Question 4

Stunned Myocardium - definition (2)

Answer 4

Days to weeks after acute injury (ischaemia or reperfusion injury)
Dysfunction of myocardium persists

Question 5

Stunned Myocardium - Imaging (2)

Answer 5

Abnormal wall motion (reduced contractibility)
Normal perfusion (Sestamibi or Thallium)

Question 6

Hibernating myocardium - Definition (2)

Answer 6

Due to chronic hypoperfusion from chronic artery disease.
Areas of decreased perfusion and contractility.

Question 7

Hibernating myocardium - Imaging (4)

Answer 7

Wall motion abnormality
Abnormal fixed perfusion
Will take up FDG more intensely than normal myocardium.
Will demonstrate redistribution of thallium.

Question 8

Scar - Definition (2)

Answer 8

Dead myocardium
Associated with prior, chronic MI

Question 9

Scar - Imaging (4)

Answer 9

Abnormal wall motion.
Abnormal fixed perfusion.
No FDG uptake.
No redistribution of thallium.

Question 10

Delayed imaging - uses (2)

Answer 10

Increased contrast in acute MI and inflammation.
Scarred myocardium washes out more slowly.

Question 11

Delayed imaging - technique

Answer 11

Inversion recovery to dull normal myocardium, followed by gradient echo

Question 12

Delayed imaging - findings

Answer 12

T1 shortening from gadolinium looks bright (bright = dead)

Question 13

Why stress imaging? (2)

Answer 13

Cornaries can autoregulate. 85% stenosis at rest can be asymptomatic. Under stress, 45% stenosis is significant.

Question 14

Stress imaging - how (2)

Answer 14

Inotropic agent (dobutamine) for wall motion.
Vasodilator (adenosine) used for perfusion analysis.

Question 15

MRI in acute MI - when

Answer 15

Can be done in first 24hrs

Question 16

MRI in acute MI (findings) (2)

Answer 16

Late gadolinium enhancement will reflect size and distribution of necrosis (vascular distribution).
Characteristically - zone of enhancement extending from subendocardium towards epicardium in vascular distribution.

Question 17

Microvascular obstruction - findings (2)

Answer 17

Islands of dark signal in delayed gadolinium enhancement
Best seen in first pass imaging (25 seconds)

Question 18

Microvascular obstruction - cause (2)

Answer 18

Acute and subacute finding
NOT seen in chronic infarct, this turns to scar

Question 19

Microvascular obstruction - clinical

Answer 19

Poor prognostic finding, associated with lack of functional recovery.

Question 20

Acutely injured myocardium (1 week) findings

Answer 20

T2 bright - bright = salvagable tissue

Question 21

Acute vs chronic MI (4)

Answer 21

Both delayed enhancement
Acute will always have normal thickness, chronic can be thinned (if infarct was transmural)
Acute may have microvascular obstruction
Acute is T2 bright (oedema), Chronic is T2 dark (scar)

Question 22

Ventricular aneurysm - association

Answer 22

Can occur as result of MI (5%)

Question 23

True ventricular aneurysm - anatomy (3)

Answer 23

Mouth is wider than body.
Myocardium is intact.
Usually antero-lateral wall.

Question 24

False ventricular aneurysm - anatomy (4)

Answer 24

Mouth is narrower than body.
Myocardium is NOT intact (pericardial adhesions contain the rupture).
Higher risk of rupture.
Usually postero-lateral wall.

Question 25

Viability predictor post MI (3)

Answer 25

Depends on thickness involved:
<25%: likely to improve with PCI
25-50%: may improve
>50%: unlikely to improve function