L48 – Myocardial Ischaemia

Question 1

Anatomy of the myocardium.

Describe cardiac muscle cells? (B,A,S)

Answer 1

Branching
Anastamosing
Striated

Question 2

Compare the amount of mitochondria in cardiac muscle cell vs skeletal muscle. Why?

Answer 2

Contain 10x more mitochondria per muscle cell than skeletal muscles

extremely dependent on aerobic metabolism > need
constant supply of a lot of energy

Question 3

How do coronary arteries penetrate myocardium?

Answer 3

arise from aorta > runs
epicardially > branches penetrate myocardium as
intramural arteries

Question 4

During which phase of the cardiac cycle does blood flow to myocardium?

Answer 4

Blood flow to myocardium occurs only during ventricular diastole:

When microcirculation in myocardium not compressed by cardiac contraction

Question 5

How does elevated HR protect the heart from overworking?

Answer 5

Faster heart rate > shorter diastolic time (needs more

blood supply for oxygen, energy; but actually getting less) > stops heart from overworking

Question 6

Which part of endocardium has limited supply?

Answer 6

endocardium in direct contact with oxygenated blood in left ventricle

Question 7

Branches of Left coronary artery?

Answer 7

Left marginal, Left circumflex, Left anterior descending (LAD)

Question 8

Branches of Right coronary artery?

Answer 8

Right marginal, Posterior interventricular Artery, Sinoatrial nodal artery

Question 9

What structures do Left anterior descending artery supply?

Answer 9

 Most of heart apex
 Anterior wall of left ventricle
 Anterior 2/3 of ventricular septum

Question 10

What structure does Left circumflex supply?

Answer 10

Lateral wall of LV

Question 11

What structures does right coronary artery (dominant) supply?

Answer 11

 Right ventricle
 Posterior 1/3 of ventricular septum
 Posterior-basal wall of left ventricle

Question 12

What method is used to detect which CA is blocked in heart?

Answer 12

Angiogram

Question 13

Define Ischaemic heart disease (IHD)?

Answer 13

a group of closely-related syndromes that result from myocardial ischaemia

Question 14

What is the most likely cause of IHD?

Answer 14

Due to Coronary obstruction > reduction in coronary blood supply

Question 15

What classifies as coronary obstruction?

Answer 15

One or more leasions that causes at least 75% reduction of cross sectional area of at least one of the major epicardial arteries

Question 16

What is the effect of ischaemia on myocytes within seconds of MI?

Answer 16

Onset of ATP depletion

Question 17

What is the effect of ischaemia on myocytes within minutes of MI?

Answer 17

<2 mins = loss of contractility

continuous reduction of ATP

Irreversible damage within 20-40 mins

Question 18

What is the effect of ischaemia on myocytes after one hour of MI?

Answer 18

Microvascular injury (capillary network in heart is damaged)

Question 19

How does MI change the rhythm of heart beat within minutes?

Answer 19

1) Cardiac arrhythmias

2) Asystole (heart ceases to beat)/ ventricular fibrillation

Question 20

How does MI cause contractile dysfunction in heart?

Answer 20

myocytes cannot successfully compensate lack of O2 > dead myocytes cannot conduct electrical impulses / lead to short-circuiting > contractile dysfunction

Question 21

What is angina pectoris caused by?

Answer 21

symptom complex caused by transient myocardial ischaemia

Question 22

Does Angina pectoris classify as MI?

Answer 22

Angina pectoris does not induce cellular necrosis > not defined as MI

Question 23

What is stable angina?

Answer 23

Chronic stenosing coronary atherosclerosis (Fixed coronary obstruction) becoming critical > leave heart vulnerable to increased demand

Question 24

What is stable angina typically relieved by>?

Answer 24

Rest

Vasodilator

Question 25

What is unstable angina?

Answer 25

Pain occurs with progressively increasing frequency Tends to be more prolonged

Question 26

What is unstable angina associated with?

Answer 26

Disruption of previously stenosing atherosclerotic plaque Superimposed thrombosis, Embolism or Spasm Predictor of MI

Question 27

What 3 processes can lead to disruption of atherosclerotic plaque?

Answer 27

Hemorrhage into atheroma > expand plaque volume Rupture / Fissure or Erosion / Ulceration > Expose thrombogenic plaque constituents

Question 28

What is the difference in coronary obstruction between stable angina and chronic IHD?

Answer 28

Stable angina = fixed coronary obstruction Chronic IHD = SEVERE fixed coronary obstruction

Question 29

What is the difference in coronary obstruction between unstable angina and acute transmural MI?

Answer 29

Unstable angina: Mural thrombus with variable obstruction Acute transmural MI: Occlusive thrombus

Question 30

How does vasoconstriction contribute to plaque fracture?

Answer 30

Increase local mechanical forces > contribute to plaque fracture

Question 31

What is vasoconstriction stimulated by?

Answer 31

1) Circulating adrenal agonist 2) Locally-released platelet contents 3) Impaired secretion of endothelial cells relaxing factors 4) Mediators released from pervascular inflammatory cells

Question 32

What is the clinical manifestation of angina pectoris progressing to sudden cardiac death?

Answer 32

Angina pectoris (stable or stable > unstable) > MI > either Chronic myocardial ischaemia or sudden death

Question 33

What are the biomarkers of MI?

Answer 33

Lactate dehydrogenase (LDH) Creatine kinase + isoenzymes (CK, CK-MB) Troponin I & T Myoglobin Aspartate aminotransferase (AST)

Question 34

What ECG changes can be observed in MI?

Answer 34

ST elevation (in STEMI ) T wave inversion Enlarged Q wave

Question 35

Apart from angiogram, ECG, what other diagnostic tools are there for MI?

Answer 35

MRI, Radioistope studies Cardiac catheterisation Echocardiogram

Question 36

What does Echocardiogram visualise?

Answer 36

Non-contracting part of ventricular wall + Ejection fraction in ventricle

Question 37

Which 2 diagnostic tools are not used in acute MI?

Answer 37

MRI | Radioisotope studies

Question 38

What is the extent of ischaemic necrosis in Transmural infarction?

Answer 38

Involves (nearly) full thickness of ventricular wall

Question 39

What is the extent of ischaemic necrosis in Subendocardial infarction?

Answer 39

Limited to inner 1/3 - 1/2 of ventricular wall (most distant from blood supply) ``` Recall: dominant artery gives rise to posterior descending branch (i.e. supplies the posterior 1/3 of interventricular septum) ```

Question 40

Compare the perfusion territory affected by transmural vs subendocardial infarction?

Answer 40

Transmural = perfusion territory in distribution of single coronary artery Subendocardial = May extend laterally beyond perfusion territory of single coronary artery

Question 41

What is transmural infarction caused by?

Answer 41

Chronic coronary atherosclerosis > Acute plaque change > Superimposed completely obstructive thrombosis

Question 42

What is subendocardial infarction caused by?

Answer 42

Diffuse stenosing coronary atherosclerosis

Question 43

How is MI caused in patients with normal coronary arterial supply? (uncommon)

Answer 43

Increased HR or increased heart size > increased demand of energy from heart

Question 44

What causes increased HR?

Answer 44

 Thyrotoxicosis > increased metabolic state |  Stress, anxiety states (shock)

Question 45

How does chronic hypertension lead to change in heart size?

Answer 45

chronic hypertension (heart needs to work against higher pressure) > cardiomegaly, cardiomyopathies > hypertrophy

Question 46

How does myocardial rupture arise from MI?

Answer 46

Infarct > zone of necrosis extends > replaced by dense collagenous/ fibrous scar > weakened myocardial wall bulges out > rupture

Question 47

What are 3 distinctive microscopic changes oberved in MI 4-12 hours after?

Answer 47

 Early coagulative necrosis  Oedema  Haemorrhage

Question 48

What are 3 distinctive microscopic changes oberved in MI 12-24 hours after?

Answer 48

 Pyknosis of nuclei (dense haematoxylinophilic mass of chromatin)  Hypereosinophilia (different staining property: opaque “tombstone”)  Early neutrophilic infiltrate

Question 49

What are 2 distinctive microscopic changes oberved in MI 1-3 days after?

Answer 49

Coagulative necrosis Dead tissue is yellow, firm, dull (fibrin, denatured cellular protein (structural, enzymatic) block proteolysis of cell) Interstitial infiltration of neutrophils (react to cellular death)