Robbins 9th ed - Chapter 12 - The Heart - Myocardial Infarction (1)

Question 1

Name three pathologic processes that can constitute “acute plaque change” and lead to AMI.

Answer 1

1) Rupture or fissuring, exposing thrombogenic constituents
2) Haemorrhage into the plaque, expanding its volume
3) Erosion or ulceration, exposing the thrombogenic basement membrane

Question 2

What is the natural progression of the coronary artery thrombosis after an MI?

Answer 2

In 90% of cases, the thrombosis is still there after 4 hours. In only 60% of cases is the thrombosis still there after 24 hours, suggesting resolution due to fibrinolysis and/or relaxation of spasm.

Question 3

What are some statistics about age of patients with AMI?

Answer 3

45% occur before the age of 65.

Question 4

What is the length of time between occlusion and irreversible cell injury?

Answer 4

20-40 minutes.

Question 5

Which part of the myocardium becomes ischaemic first?

Answer 5

The subendocardium. As time passes with coronary artery occlusion, ischaemia progresses from the subendocardium to the epicardium.

Question 6

What is meant by the “dominant” coronary artery? Which one is it in most cases?

Answer 6

This is the coronary artery that supplies the posterior third of the interventricular septum. In 80% of individuals, it is the RCA. In others, it is the LCX.

Question 7

Describe the nature of collateral supply in coronary vessels.

Answer 7

Although most hearts have numerous intercoronary anastomoses, little blood usually passes through these. In times of slowly progressive ischaemia, these collateral circulations become progressively more perfused.

Question 8

What is the definition of transmural infarction? What is the cause?

Answer 8

This occurs when a coronary artery becomes occluded and is not treated. Ischaemia and necrosis progress from the subendocardium through to the epicardium until there is full-thickness infarction of approximately 2.5cm wall thickness.

Question 9

What is another name for non-transmural infarction? What is the cause?

Answer 9

Subendocardial infarctions occur when there is coronary artery occlusion that is quickly reperfused, after thrombolysis / stenting / spontaneous resolution. Global subendocardial infarction can occur when there is a period of systemic shock.

Question 10

Describe the gross morphologic features of an infarct at these times after AMI:
Less than 4 hrs
4-24 hrs
1-3 days
7-14 days
6 weeks

Answer 10

Less than 4 hrs : None
4-24 hrs : Dark mottling
1-3 days : Progressively yellow-tan softened centre
7-14 days : Rim of hyperaemic granulation tissue
6 weeks : Fibrous scar replaces the infarct

Question 11

Describe the microscopic features of an infarct at these times after AMI:
Less than 4hrs
4-12 hrs
12-24 hrs
1-3 days
7-14 days
6 weeks

Answer 11

Less than 4 hrs		: None
4-12 hrs	: Oedema
12-24 hrs	: Neutrophilic infiltrate
1-3 days	: Coagulative necrosis
7-14 days	: Phagocytosed dead cells, granulation tissue
6 weeks	: Dense collagenous scar

Question 12

Which cardiac myocytes are involved in reperfusion injury?

Answer 12

The cardiac myocytes that are not already irreversibly injured, but are ischaemic and “vulnerable”.

Question 13

What is thought to mediate reperfusion injury?

Answer 13

Oxidative stress, calcium overload, and inflammatory cells recruited after reperfusion

Question 14

CK and cTnI : At what time after AMI do they

1) rise?
2) peak?
3) stay raised for?

Answer 14

They both start to rise at 2-4 hours, then peak at about 24hours. CK has fallen by 72 hours, whereas troponin takes a week to fall.

Question 15

Name the potential complications of AMI.

Answer 15

1) Pump failure –> progresses to cardiogenic shock in 10%
2) Arrhythmia
3) Myocardial Rupture
4) Ventricular aneurysm
5) Papillary muscle dysfunction –> valvulopathy
6) Pericarditis
7) Infarct extension