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2. CARDIAC > CARDIAC Section 6: Ischemic Heart > Flashcards

CARDIAC Section 6: Ischemic Heart Flashcards

1
Q

How is myocardial infarction typically initiated?

A

Rupture of an unstable coronary atherosclerotic plaque, leading to abrupt arterial occusion.

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2
Q

Where does necrosis start?

A

From subendocardium to subepicardium

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3
Q

Ischemic necrosis affects what structures?

A

Not just the myocardium but the blood vessels.

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4
Q

This manifestation of islands of dark signal in anocean of delayed enhancement

A

“Microvascular obstruction”W

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5
Q

What is an indipendent predictor of death and LV remodeling?

A

Presence of microvascular obstruction.

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6
Q

After an Acute Injury (ischemia or reperfusion injury), dysfunction of myocardium persists even after restoration of blood flow (can last days to weeks).
A perfusion study will be normal, but the contractility is crap.

A

Stunned myocardium

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7
Q

This is the result of severe CAD causing chronic hypoperfusion

A

Hibernating myocardium

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8
Q

What will you see in a hibernating myocardium?

A

decreased perfusion and decreased contractility even when resting

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9
Q

Is hibernating myocardium an infarct? why? What do you see on FDG PET (A fluorodeoxyglucose (FDG)-positron emission tomography)?

A

this is not an infarct.

On an FDG PET, this tissue will take up tracer more intensely than normal myocardium, and will also demonstrate redistribution of thallium.

This is reversible with revascularization.

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10
Q

IS hibernating myocadium reversible?

A

It is reversible with vascularization

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11
Q

When you see scarring in the myocardium, what does it mean?

Describe.

A

This is a dead myocardium.

It will not squeeze normally, so you’ll have abnormal wall motion. It’s not a zombie.
It will NOT come back to life with revascularization.

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12
Q

Wall Motion Abnormal
Normal Perfusion (Thallium or Sestamibi)
Associated with acute M

A

Stunned myocardium

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13
Q

Wall Motion Abnormal
Abnormal Fixed Perfusion
Will Redistribute with Delayed Thallium and will take up FDG
Associated with chronic high grade CAD

A

HIbernating Myocardium

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14
Q

Wall Motion Abnormal Abnormal Fixed Perfusion
Will NOT Redistribute with Delayed Thallium, will NOT take up FDG
Associated with chronic prior MI

A

Infarct/Scar

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15
Q

What is the appropriate procedure for DIastolic Dysfunction?

A

Echochardiography.

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16
Q

What is the appropriate procedure for Systolic Dysfunction?

A

CArdiac MRI

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17
Q

Cardiac MRI Probable Contraindications:

A

ICDs / Pacemakers
Cochlear Implants
Intracranial Shrapnel
**Cardiac Stents are usually safe

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18
Q

Delayed Imaging works for these two (2) reasons:

A

(1) Increased volume of contrast material distribution in acute myocardial infarction (and inflammatory conditions)
(2) Scarred myocardium washes out more slowly.

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19
Q

How is Delayed Imaging done? and why?

A

It is done using an inversion recovery technique to null normal myocardium, followed by a gradient echo.

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20
Q

What does T1 shortening from the Gd in Delayed Imaging looks like?

A

Bright (“Bright is Dead”)

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21
Q

Why is stress imaging done?

A

Because coronary arteries can auto-regulate, a stenosis of 85% can be asymptomatic in a resting state.

22
Q

How is stress imaging done?

A

Demand is increased (Excercise or drugs) making a 45% stenosis significant.

23
Q

In stress imaging, what is used for wall motion?

A

An inotropic stress agent (dobutamine)

24
Q

In stress imaging, what is used for perfusion analysis?

A

A vasodilator (adenosisn)

25
Q

Describe the Typical Sequence Pattern / Technique - with appropriate time in minutes

A
26
Q

When can Cardiac MRI be done in Acute MI?

A

Can be done in the first 24 hours post MI (if stable)

27
Q

What MRI sequence can reflect size and distribution of necrosis?

A

Late Gd enhancement

28
Q

What is the characteristic pattern of Acute MI?

A

zone of enhancement that extends from the subendocardium toward the epicardium in a vascular distribution.

29
Q

What does microvascular obstruction look like in MRI in Acute/subacute MI?

A

islands of dark signal in the enhanced tissue (as described above)

30
Q

Why does micrpvascular obstrucion NOT seen in chronic disease?

A

These areas will retrun to scar evenatually

31
Q

In Acute MI (1 week), injured myocardium will be ____ on T2, which can be used to estimate area of risk.

A

T2 Bright - Enhanced = Salvageable Tissue

32
Q

Acute vs Chronic MI enhancement pattern?

A

Both have delayed enhancement.

33
Q

What happens to the myocardium if the infarct was transmural and chronic?

A

If the infarct was transmural and chronic you may have thinned myocardium

34
Q

What MI will have normal myocardial thickness?

A

Acute will have normal thickness (chronic can too but shouldn’t for the purposes of MC tests.

35
Q

T2 signal irom edema may be ____ in the acute setting. Chronic is T2 _____ (scar)

A

T2 signal irom edema may be INCREASED in the acute setting. Chronic is T2 DARK (scar)

36
Q

What type of MI will you see Microvascular Obstruction?

A

Acute only.

You won’t see Microvascular Obstruction in Chronic

37
Q

How do you diagnose Myocardial Infarction with Contrast Enhanced MR?

A

(1) Delayed Enhancement follows a vascular distribution,

(2) The enhancement extends from the
endocardium to the epicardium

38
Q

These are islands of dark tissue in an ocean of late Gd enhancement?

A

Microvascular Obstruction

39
Q

What do these microvascular obstruction indicate?

A

These indicate microvascular obliteration in the setting of an acute infarct.

40
Q

Can Gd get to the microvascular obstruction after restoration of epicardlal blood flow?

A

No.

The Gd is unable to get to these regions even after the restoration of epicardial blood flow.

41
Q

Prognosis and recovery of Microvascular obstruction

A

Microvascular obstruction is a poor prognostic finding, associated with lack of functional recovery.

42
Q

When is Microvascular Obstruction best seen?

A

First pass imaging (25 seconds)

43
Q

What is the difference between True and False Ventricular Aneurysm?

A

True:
Mouth is wider than body.
Myocardium is INTACT.
ANTERO-lateral wall.

False:
Mouth - Narrow vs body
Myocardium - NOT Intact (pericardial adhesions contain the rupture)
POSTERO-lateral wall
HIGH RISK of Rupture

44
Q

What % of transmural thickness involved in MI is likely to improve on PCI?

A

<25%

45
Q

DEscribe the VIability Imaging

A

Segmental imaging (imaging over multiple heart beats)
T1 post contrast (10-15 min delay) inversion recovery gradient echo

46
Q

Timing of bad Sequelae of an MI:

Dressler Syndrome

A

4-6 weeks

47
Q

Timing of bad Sequelae of an MI:

Papillary Muscle Rupture

A

2-7 days

48
Q

Timing of bad Sequelae of an MI:

Ventricular pseudoaneurysm

A

3-7 days

49
Q

Timing of bad Sequelae of an MI:

Ventricular Aneurysm

A

Months - Requires remodelling and thinning

50
Q

Myocardial rupture

A

Within 3 days (50% of the time)

2. CARDIAC (13 decks)

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