Lecture 2- Acute myocardial infarction

Question 1

What is acute myocardial infarction?

Answer 1

It is the death of cardiac myocytes in the heart, due to vascular insufficiency of the coronary arteries.

Question 2

what is the vascular insufficiency that causes acute myocardial infarction?

Answer 2

myocardial ischaemia, meaning oxygen deficiency to the cardiac myocytes.

Question 3

what is the major underlying cause of acute myocardial infarction?

Answer 3

Atheroscerosis- the formation of fatty plaques in the blood vessels.

Question 4

How does artherosclerosis cause coronary arterial occlusion, which leads to acute myocardial infarction if unresolved?

Answer 4

1. Artherosclorotic plaque within the coronary arteries ruptures.
2. The necrotic plaque contents are exposed to the blood and cause platelet adhesion and activation and a microthrombus forms.
3. The microthrombus formation from the platelets causes vasospasm of the coronary artery.
4. The coagulation pathway is activated and so other clotting factors now increase the size of the microthrombus into a thrombus.
5. The thrombus keeps growing until it completely occludes the coronary artery and now blood can flow to the heart.

Question 5

What is the first step in the formation of atherosclerotic plaque?

Answer 5

1 Endothelial injury which causes (among other things):
increased vascular permeability, leukocyte adhesion, and
thrombosis

Question 6

what is the second step in atherosclerosis?

Answer 6

2. Accumulation of lipoproteins (mainly LDL and its oxidized
   forms) in the vessel wall

Question 7

what is the third step in the atherosclerosis?

Answer 7

3. Monocyte adhesion to the endothelium, followed by
   migration into the intima and transformation into macrophages
   and foam cells

Question 8

what is the fourth step in artherosclerosis?

Answer 8

4. Platelet adhesion

Question 9

what is the fifth step of atherosclerosis?

Answer 9

5. Factor release from activated platelets, macrophages, and
   vascular wall cells, inducing smooth muscle cell recruitment,
   either from the media or from circulating precursors

Question 10

what is the sixth step of atherosclerosis?

Answer 10

6. Smooth muscle cell proliferation and ECM production

Question 11

what is the seventh step of atherosclerosis?

Answer 11

7. Lipid accumulation, both extracellular and within cells (macrophages and smooth muscle cells).

Question 12

The site of the coronary arterial occlusion due to atherosclerosis is causes infarction in which part of the heart?

Answer 12

It will cause infarction in the myocardial tissue within the immediate vicinity or closest to the occluded blood vessel.

Question 13

The size of the coronary arterial occlusion due to atherosclerosis will result in what size of myocardial infarction?

Answer 13

The larger size of the myocardial infarction will be proportional to the relative amount of coronary artery occlusion.

Question 14

How does atherosclerotic plaque stability contribute to acute myocardial infarction?

Answer 14

A stable plaque within the coronary arteries is less likely to rupture. Inflammation around the plaque or general plaque weakness makes a plaque unstable.

Question 15

Where does necrosis of cardiac myocytes occur at first after coronary arterial occlusion?

Answer 15

Myocardial cell death occurs in the region furthest away from the occluded blood vessel surface, called the sub endothelial zone. These cells depend most on perfusion from blood vessels. Then the necrosis kills all other cells gradually.

Question 16

what are the three possible scenarios for the myocardial cells during coronary arterial occlusion?

Answer 16

1.Apoptosis – occursrapidly post‐ischaemia
‐ apoptosisinhibitorsreduceinfarctsize.
2.Reperfusion – inunder 20 minutes, the myocytes surviveinfarctevent.
3.NoReperfusion– necrosiscompletein6– 12hr

Question 17

A patient survives myocardial infarction and is able to reperfuse their heart. What happens to the ischaemic, damaged myocardial cells one day after the event?

Answer 17

Nothing- the infarct will remain, next to the healthy myocardial tissue.

Question 18

A patient survives myocardial infarction and is able to reperfuse their heart. What happens to the ischaemic, damaged myocardial cells 3-4 days after the event?

Answer 18

Monocyte infiltration- the immune system will detect the damaged cells and send neutrophils first to clean up.

Question 19

A patient survives myocardial infarction and is able to reperfuse their heart. What happens to the ischaemic, damaged myocardial cells 7-10 days after the event?

Answer 19

Phagocytosis- phagocytotic immune cells now infiltrate the necrotic area of the myocardium and phagocytose it to physically remove it from the heart.

Question 20

A patient survives myocardial infarction and is able to reperfuse their heart. What happens to the ischaemic, damaged myocardial cells 21 days after the event?

Answer 20

Collagen- collagen is laid down by fibroblasts to replace the cardiac myocytes that died. This forms fibrosis or scarring of the heart and may affect heart functioning.

Question 21

A patient survives myocardial infarction and is able to reperfuse their heart. What happens to the ischaemic, damaged myocardial cells 60 days after the event?

Answer 21

Scarring- the fibrosis is complete, and the necrotic tissue has been completely replaced with scarred tissue.

Question 22

what can be done medically to prevent acute myocardial infarction when the patient has coronary arterial occlusion?

Answer 22

• Thrombolysis: streptokinaseortissueplasminogen activator, activatesfibrinolytic enzymesystems systems and dissolvesthrombus.
• Balloonangioplasty: (percutaneous transluminal coronaryangioplastyPTCA)
• Coronaryarterialbypassgraft(CABG)

Question 23

How can acute myocardial infarction be detected by in the blood?

Answer 23

During the early stages of necrosis, the damaged cardiac myocytes start to leak out their functional proteins into the blood. These myocyte proteins like , Troponin I, C or T and creatine phosphokinase and MB fraction are used as diagnostic biomarkers.

Question 24

Normally, the prevention for acute myocardial infarction is reperfusion (unblocking the coronary occlusion). Reperfusion however, can also be lethal if too much occurs at once. Why is this so?

Answer 24

Mitochondrial damage- damaged mitochondria produce ROS’s, which further injure the tissue.
ROS damage- ROS enter from the blood into the damaged tissue and injure the mitochondria.
Polymorphs- cytoplasmic xanthine oxidase is activated by reperfusion and causes production of ROS’s.

Question 25

How does acute myocardial infarction change the functioning of surviving myocardial cells?

Answer 25

Damaged myocardial cells have abnormalities in their functioning. This can lead to ventricular dysfunction (stunned myocardial cells with abnormal biochemistry).
Myocardial cells that are repeatedly stunned will eventually go into hibernation, as a protective adaptation.

Question 26

what are the complications of acute myocardial infarction?

Answer 26

cardiac dysfunction, arrythmias, rupture of myocardial tissue, pericarditis and infarct expansion.