Lecture 2- Acute myocardial infarction Flashcards Preview

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Flashcards in Lecture 2- Acute myocardial infarction Deck (26):
1

What is acute myocardial infarction?

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

2

what is the vascular insufficiency that causes acute myocardial infarction?

myocardial ischaemia, meaning oxygen deficiency to the cardiac myocytes.

3

what is the major underlying cause of acute myocardial infarction?

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

4

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

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.

5

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

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

6

what is the second step in atherosclerosis?

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

7

what is the third step in the atherosclerosis?

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

8

what is the fourth step in artherosclerosis?

4. Platelet adhesion

9

what is the fifth step of atherosclerosis?

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

10

what is the sixth step of atherosclerosis?

6. Smooth muscle cell proliferation and ECM production

11

what is the seventh step of atherosclerosis?

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

12

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

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

13

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

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

14

How does atherosclerotic plaque stability contribute to acute myocardial infarction?

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

15

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

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.

16

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

1.Apoptosis – occurs rapidly post‐ischaemia
‐ apoptosis inhibitors reduce infarct size.
2. Reperfusion – in under 20 minutes, the myocytes survive infarct event.
3. No Reperfusion – necrosis complete in 6 – 12 hr

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?

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

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?

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

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?

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

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?

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.

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?

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

22

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

• Thrombolysis: streptokinase or tissue plasminogen activator, activates fibrinolytic enzyme systems systems and dissolves thrombus.
• Balloon angioplasty: (percutaneous transluminal coronary angioplasty PTCA)
• Coronary arterial bypass graft (CABG)

23

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

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.

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?

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.

25

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

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.

26

what are the complications of acute myocardial infarction?

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