Ischaemic heart disease

Question 1

So, heart disease is bad yeah?

Answer 1

Yeah, leading cause of death bro

Question 2

What are some causes of atherosclerotic coronary diseases?

Answer 2

Chronic coronary insufficiency
Angina

Unstable coronary disease

Myocardial infarction

Sudden ischaemic coronary death

Heart Failure

Arrhythmia
Acute ischaemic
Scar related

Question 3

Describe the layers used when discussing the anatomy of the coronary artery

Answer 3

• Epicardial–outer surface of heart
• Endocardial–inner surface of heart
• Subendocardialregion is water-shed area of perfusion and first to become ischaemic

Question 4

Name the epicardial coronary arteries

Answer 4

Circumflex coronary

Left anterior descending

Posterior descending artery

Right ventricular branch

Question 5

What can be used to image coronary arteries

Answer 5

Coronary angiography

CT

MRI

Question 6

Discuss what factors increase risk for atherosclerotic coronary artery disease

Answer 6

Age
Hypertension Hypercholesterolaemia Smoking
Diabetes
Obesity
Physical inactivity

Question 7

Discuss the pathology found in atherosclerotic coronary artery disease

Answer 7

 Fatty streak

 Fibro-fatty palque

 Plaque disruption Plaque rupture Plaque erosion

Question 8

What will occur in the coronary arteries in response to total occlusion of the left anterior descending artery?

Answer 8

The supply will be filled by collaterals from the RCA

Question 9

Discuss the symptoms, cause and ECG indications of angina

Answer 9

• SYMPTOMS
– Gripping central chest pain
– Radiation to arm and jaw
– Clear and precise relationship to exercise
– Goes off in 2-10 mins after discontinuation of exercise 
– Worse after food. Worse in cold
– No autonomic features
– Flat of hand/fist to describe pain

• CAUSE
– Sub-Endocardial ischaemia

• ECG
– ST depression

Question 10

What mechanisms are at play in angina in relation to basic physiology?

Answer 10

MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS

Question 11

Discuss the cause of angina pectoris

Answer 11

Mismatch of supply and demand

Supply = Coronary Blood Flow

Demand = Myocardial Oxygen Consumption
(MVO2 )

Question 12

What are the two regulatory systems of the normal control of the coronary circulation?

Answer 12

– Autoregulation (myogenic control) – Metabolic regulation

Question 13

Discuss exercise and myocardial blood flow

Answer 13

 CBF can rise up to five fold (400 ml/min/100g) to accommodate a 20 fold increase in total body O2 consumption.

 Little change in a near maximal O2 extraction.

 A rise in heart rate where per beat CBF is constant can account for 1/3 of the increase seen.

Question 14

What are the determinants of myocardial oxygen consumption

Answer 14

Variable per unit mass of tissue
Tension development – LV pressure and LV volume Contractility
Heart rate
Fixed per unit mass of tissue
Basal activity (10-20%)
Mass of tissue

Question 15

Discuss investigation of chest pain to identify CAD as the cause

Answer 15

• Anatomical assessment
– CT coronary angiography
– Invasive angiography

• Test of Inducible ischaemia
– Exercise stress test
– Dobutamine stress echo
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)

• Anatomic and functional
– Invasive angiography and fractional flow reserve (FFR)
– cMR
– Novel CT

Question 16

Discuss angina treatment

Answer 16

• Reduce Myocardial Oxygen consumption. – Drugs

• Improve coronary flow reserve.
– Percutaneous Coronary Intervention (stents and balloons)
– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators

Question 17

CABG bitches

Answer 17

Coronary artery bypass graft is bae, great saphenous vein grafted to RCA and left internal mammary artery grafted to LAD

Question 18

What are the principles of drug treatment and angina

Answer 18

1. Reduction in myocardial oxygen consumption

2. Reduction in the variability of coronary flow reserve

Question 19

Discuss the action of drugs in angina

Answer 19

• Beta Adrenoceptor Blockers
– Reduce Heart Rate, Reduce Blood Pressure
– i.e. Reduce work of heart

• Nitrates (GTN)
– Venodilation → Reduced LV size → Wall tension. (reduces work) Small effect on epicardial stenosis dilation (improved supply)

• Calcium Channel blockers
– Reduce HR, some reduce Heart rate, small effect on from epicardial dilatation (mixed)

• Ikf Channel Inhibitors
– Selective heart rate reduction by inhibiting channels in SA node - Ivabridine

Question 20

What are the stats on myocardial infarction (heart attack)

Answer 20

• 15-20 % do not make it to hospital • In hospital Mortality ~ 6 -15%

Question 21

What is the clinical presentation of a myocardial infarction

Answer 21

• Chest Pain – severe – crushing radiating to jaw and arm
• Associated “Autonomic􏰀 symptoms (nausea, sweating, terror)
• Breathlessness

Question 22

What are the causes of a myocardial infarction

Answer 22

1. Plaque rupture – 70 – 75%
2. Plaque erosion – 25 – 30%
3. Coronary embolism
4. Coronary artery spasm / drugs
5. Coronary anomaly
6. Spontaneous coronary dissection

Question 23

What events modify the presentation of AMI?

Answer 23

Time of day

Inflammatory activity

Infection esp. Respiratory

Elevation of blood pressure

Catacholamines

Question 24

How do we classify myocardial infarctions

Answer 24

• By site of infarction - pathology
– Full thickness, transmural
– Sub endocardial

• By ECG - Clinical
– ST Elevation myocardial infarction (STEMI)
– Non-ST elevation myocardial infarction (non- STEMI)

• By cause
– Type 1-4

Question 25

Discuss the relation between anatomy and ECG in AMI

Answer 25

* STEMI implies transmural myocardial infraction | * NSTEMI will include subendocardial infraction but does not exclude transmural infraction in regions remote from ECG

Question 26

What are the type categories of myocardial infarction

Answer 26

Type 1 - spontaneous MI related to schema due to primary coronary event like plaque erosion +/or rupture, fissuring or dissection Type 2 - MI secondary to ischaemia due to either increased O2 demand or decreased supply Type 3 - Sudden unexpected cardiac death often with symptoms suggestive of myocardial ischaemia Type 4 - MI associated with percutaneous coronary intervention (4a) or stent thrombosis (4b) Type 5 - Myocardial infarction associated w cardiac surgery

Question 27

How does one diagnose myocardial infarction

Answer 27

• A Clinical History with: – ECG Changes, defining sub-classification of: • STEMI • NSTEMI * And raised cardiomyocyte markers in blood * Troponin T or I * Creatine kinase MB isoform (CKMB) * Creatine Phosphokinase (CPK) * AST * Myoglobin

Question 28

Discuss STEMI management

Answer 28

Antiplatelet agents Aspirin + Clopidogrel or other antiplatelet (P2Y12 inbibitor) Immediate revascularisation Primary PCI (percutaneous coronary intervention) (Thrombolysis – clot busting)

Question 29

What is adjunctive therapy for STEMI

Answer 29

• After anti-platelets agents and revascularisation – Statin drugs (reduce cholesterol – plaque passivation) – ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle) – Beta blockers (reduce myocardial infarction)

Question 30

What are the complications of a STEMI

Answer 30

• Immediate Complications of STEMI – Ventricular Arrhythmia and death – Acute Left Heart Failure ``` • Early (Day 2-7) – Myocardial Rupture – Mitral valve insufficiency – Ventricular Septal defect – Mural thrombus and emobolisation ``` • Late (beyond day 7) – LV dilatation and heart failure – Arrhythmia – Recurrent myocardial infarction

Question 31

Discuss the causes of NSTEMI

Answer 31

• Implies sub-endocardial ischaemia • Caused by: – Threatened STEMI – Small branch occlusion – Occlusion of well collateralised vessel – Lateral STEMI in territory not well seen by ECG

Question 32

Discuss treatment of non-STEMI

Answer 32

* Antiplatelet therapy (Aspirin and clopidogrel) * Anti-ischaemics (beta blockers and nitrates) * Statin drugs * ACE inhibitors • Coronary angiography and revascularisation – Early if symptoms continue – Early if Troponin raised – Risk score (eg GRACE)