CVS 20 - CHD

Question 1

What is the job of the epicardial coronary arteries?

Answer 1

They are conductive vessels that depend on arterial BP

Question 2

What is the job of the coronary circulation?

Answer 2

Ensure that, over a wide range of perfusion pressures, flow remains constant (auto regulation). Also ensure that coronary blood flow matches myocardial demand.

Question 3

How do the intramyocardial vessels compensate if the epicardial compartment is stenosed?

Answer 3

They intramyocardial resistance vessels increase (vasodilation) in order to maintain flow.

They can only compensate unto 70% stenosis, at which point coronary blood flow decreases.

Question 4

What is the Coronary Flow Reserve?

Answer 4

Ratio of resting blood flow: blood flow achieved under MAXIMAL STRESS

Question 5

What does the coronary flow reserve indicate?

Answer 5

They ability of coronary circulation to adapt to increased demand, in the face of increasing epicardial coronary stenosis.

Impairment to meet demands begins to occur at about 50% stenosis

Question 6

What can be used as a vasodilator to treat angina pectoris?

Answer 6

Glyceryl trinitrate

Question 7

What are the 2 types of tests for coronary artery disease?

Answer 7

Functional - supply and demand imbalance

Anatomical - look at anatomical severity of narrowing artery, and judge how it is compromising flow.

Question 8

What is the basis for non-invasive CHD diagnostic tests?

Answer 8

Giving stressing agents - create situations of increased oxygen demand.

e.g. exercise, beta agonists, vasodilators

Alternatively, imaging (e.g. echocardiography, MRI/Nuclear perfusion imaging can be used)

Question 9

Which 3 principles are treatment strategies centred around for CHD?

Answer 9

1. Preventing atherosclerosis progression
2. Reduce myocardial oxygen demand
3. Improve blood supply

Question 10

What are the 3 main categories of medication given to CHD patients?

Answer 10

1. Aspirin
2. Statins
3. ACE inhibitors

Question 11

How can giving beta blockers be beneficial for patients with CHD?

Answer 11

They increase the time in diastole which means coronary perfusion is improved.

Question 12

In which ways can myocardial cell death be caused?

Answer 12

1. Coronary plaque rupture
2. Coronary plaque erosion
3. Coronary dissection
4. Calcific nodule

Question 13

What are the differences between white and red thrombus?

Answer 13

White thrombus - platelet rich, common in ARTERIAL thrombosis, benefit from anti-platelet therapy.

Red thrombus - fibrin rich with trapped erythrocytes. Common in veins and low pressure areas. Benefits from anti-coagulant of anti-fibrinolytic therapy.

Question 14

How may Tissue factor contribute to coronary thrombosis?

Answer 14

Tissue factor can be made from cellular constituents of atherosclerotic plaque, or through ischaemic heart muscle, or circulating inflammatory cells.

Tissue factor promotes the atherosclerotic process, which could lead to coronary thrombosis.

Question 15

Which 2 factors are important molecular targets?

Answer 15

2a and 10a.

Question 16

What is the universal definition of acute MI?

Answer 16

Detection of a rise or fall in a biomarker (Troponin) and at least one value >99th percentile reference limit, and at least one symptom indicating heart damage (or ECG/imaging)

Question 17

Troponin is the principle biomarker for MI. Why?

Answer 17

Cardiac Troponin consists of isoform I and T, which are specific to cardiac muscle.

When MI occurs, cardiac troponin levels rise and fall (detectable for unto 2 weeks after MI)

Question 18

What are the 2 types of acute coronary syndrome?

Answer 18

1. ST ELEVATION - Complete blockage of coronary artery - these people have ST elevation.
2. NO ST ELEVATION - Partial occlusion of coronary artery - ST depression/T wave inversion/normal ECG.

Question 19

What is PPCI for STEACS?

Answer 19

Guide wire passed through coronary thrombus and a balloon is passed - stent deployed. This recanalises the vessel.

Question 20

When MI happens, which is the area first to die?

Answer 20

Subendocardium is the first and worst hit when there is an occlusion.

If the zone of necrosis then spreads, it will become a transmural MI.

Question 21

What is reperfusion injury?

Answer 21

Reperfusing an occluded artery will bring down damage to 30% heart muscle death.

But the act of reperfusion can cause some heart muscle death itself - so if we can attenuate this reperfusion injury process, we can minimalise the extent of the heart attack even further.

Question 22

Why should we try to limit adverse LV remodelling?

Answer 22

It is accompanied with increased risk of heart failure and arrhythmias.

Question 23

What are the adverse mechanisms which cause LV remodelling?

Answer 23

1. Infarct thinning, elongation, expansion.
2. LV dilates to maintain CO - but this increases wall tension.
   Non-infarcted myocardium also affected
3. LV hypertrophy and myofilament dysfunction.
4. Altered electromechanical coupling
5. Myocardial fibrosis.
6. Apoptosis.
7. Inflammation

Question 24

What are some consequences of adverse LV remodelling?

Answer 24

1. Increased systolic and diastolic wall tension/stress
2. Reduced myocyte shortening
3. Reduced subendocardial perfusion
4. Mitral regurgitaion
5. Ventricular arrhythmias/fibrillation.

Question 25

How is thrombotic risk managed?

Answer 25

Reduce the occurrence of clots (by giving anti platelets/anticoagulants)

Question 26

How can plaque stabilisation be achieved?

Answer 26

Mechanically - stents

Drugs - statins / ACE inhibitors

Question 27

LV remodelling is also managed. How?

Answer 27

Non drug - pacemakers/defibrillators, progenitor cells

Drug - Beta blockers, ACE inhibitors, Angiotensin receptor blockers, aldosterone receptor agonists

Question 28

TIA and stroke can be subdivided. How?

Answer 28

Embolic and haemorrhagic.

Most TIA/stroke are embolic.

Question 29

Name 3 determinants of Myocardial oxygen demand

Answer 29

1. Heart Rate
2. Blood pressure
3. Myocardial wall tension