20 Coronary Heart Disease, Angina, MI, Embolism Flashcards
How does coronary artery disease present
1) Sudden cardiac death
2) Acute coronary syndrome (acute MI and unstable angina)
3) Stable angina
4) Heart failure
5) Arrhythmia
What are the lifestyle risk factors and how do they increase the risk of coronary artery disease
Smoking Alcohol Physical inactivity Unhealthy diet These contribute to hyperlipidaemia, obesity, diabetes and hypertension which contribute to 80% of CHD
What is the world mortality rate caused by CHD
17 million per year
True or false: CHD is the leading cause of death in developing countries but not developed countries
False, it is the world leading cause of death in both
What is the incidence of CHD
88,000 CHD deaths / year
True or false: The death rate of CHD in the UK is decreasing
True, but the UK has higher death rates than the rest of Europe
Is the incidence of angina in the UK increasing or decreasing
Increasing
What is the pathophysiology of myocardial ischaemia
Mismatch between myocardial oxygen supply and metabolic demand. The heart is unable to increase flow to match increased demand
What are prearteriols and arterioles sensitive to
Prearterioles: flow/BP
Arterioles: metabolites
What is the role of coronary arteries and how does the coronary circulation ensure this
Maintains flow under a range of perfusion pressure
Epicardial artery and intramyocardial arteries are in concert. If there is coronary stenosis in the epicardial region, intramyocardial arteries will dilate to maintain flow under the control of autonomic nervous system
At what extent of stenosis will the coronary flow be affected and severely reduced
50% stenosis will cause a small reduction in flow
70% stenosis will cause a huge disruption in flow
Define coronary flow reserve
The ratio between resting coronary flow rate to the flow rate under maximal stress
State the stages of ischaemic cascade
Normal function Perfusion abnormality Regional diastolic dysfunction Regional systolic dysfunction Ischaemic ECG changes Angina pectoris
What is angina pectoris
Caused by exertion or emotional stress
Discomfort in shoulder, chest, jaw, arms and back
Treatment: rest
Why is investigation of angina important
To confirm diagnosis
To calculate the risk of future adverse CVD
Choice of test dependent on clinical probability of CHD
What are the investigations for CHD
Non-invasive/functional: exercise ECG
Non-invasive/anatomical: CT coronary angiogram
Invasive/functional: CFR
Invasive/anatomical: coronary angiogram
What is the management for CHD
- Prevent progression of atherosclerosis
- education
- lifestyle modification
- statins, aspirin - Reduce myocardial oxygen demand
- HR: beta blocker, Ca2+ channel antagonist
- Wall stress: ACE inhibitor (captopril) - Improve blood supply
- Vasodilators: nitrates
- Revascularisation (PCI and CABG)
What are the mechanisms underlying MI
- Disrupted blood flow: coronary plaque erosion and rupture, dissection
- Myocardial cell death by: apoptosis and oncosis
*plaque rupture more frequently seen
Differentiate between two types of thomboses
White thrombus: - Occurs in arteries/higher pressure - Platelet rich - Benefit from antiplatelet therapy Red thrombus: - Occurs in veins/lower pressure - Fibrin rich and trapped erythrocytes - Benefit from anticoagulant
What is the universal definition of acute MI
Rise or fall of cTn I/T AND one of the below:
- symptoms suggestive of ischaemia
- New ST-T changes or LBBB on ECG
- Development of pathological Q wave
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
- Identification of intracoronary thrombus on angiography or at autopsy
State two types of acute coronary syndromes and how are they differentiated
Acute MI: ST elevation due to complete blockage of coronary artery
Unstable angina: No ST elevation (ST depressoin or T inversion or even normal ECG) due to partial occlusion which embolises distal capillaries
How does acute MI develop
Necrotic zone initiates from intramyocardium. Particularly, subendocardium is most at risk and is important in heart function
Differentiate between transmural endocardial infarction and sub-endocardial infarction
Transmural endocardial infarction: entire muscle
Sub-endocardial infarction: only inner muscle wall
How much cell death does reperfusion injury account for
40%
What is the mechanism of left ventricular wall remodelling
- Infarct thinning, elongation, expansion
- LV dilatation
– Minimise the increase in wall tension
– Maintains cardiac output - Non-infarcted myocardium
– LVH + myofilament dysfunction
– Altered electromechanical coupling
– Myocardial fibrosis
– Apoptosis
– Inflammation
What are the consequences of left ventricular remodelling
- Increased wall tension
- Increased myocardial oxygen demand
- Reduce myocyte shortening
- Dysynchronous depolarisation/contraction
- Reduced subendocardial perfusion
- Mitral regurgitation
What is the management to stabilise plaque
Mechanical: stent
Drug: ACE inhibitor (captopril) and statins
What is are the drugs for LV remodelling
Beta blockers
ACE inhibitors
Angiotensin receptor blockers
Aldosterone receptor antagonists
What is the management for thrombolytic burden
Thrombectomy
Anti-coagulent (Factor Xa inhibitor)
Anti-platelets
What is the management for embolism
Thrombectomy
Fibrinolysis
Antiplatelet
