Chronic Stable Angina Flashcards
What is stable angina?
Stable angina is cardiac chest pain which comes on in a predictable manner e.g exertion and goes away with rest.
Caused by a demand for increased cardiac work in the presence of decreased perfusion
What is the typical history of someone with stable angina?
I was walking up a hill when I had to stop because I had a severe crushing central chest pain. When I stopped and sat down for a few minutes it went away.
What is the underlying pathology and causes of angina?
Causes:
Coronary aa disease:
Atherosclerosis of the coronary aa therefore cannot meet the demand of the heart during exertion.
Valvular heart disease:
Aortic stenosis: increased pressure for the heart to push against, during exertion it becomes too much therefore ischaemia and angina.
Cardiomyopathy:
HCM (hypertrophic cardiomyopathy)
Genetic disorder can be inherited or a de novo mutation.
Causes hypertrophy of the heart muscle causing a functional impairment. It is the must common cause of sudden cardiac death in the young.
Anaemia:
If you reduce the amount of hb and therefore the Oxygen carrying capability in times of exertion not enough oxygen will be taken to the heart causing angina.
Smasm of inflammation of coronary aa (cocaine can cause)
Carboxyhaemoglobinaemia
Describe the following clinical features and how they relate to angina? Xanthalasmata Tendon xanthoma Hypertension Anaemia Hyperthyroidism Aortic stenosis
Xanthalasma: yellow flat plaques on the upper or lower eyelid caused by lipid containing macrophages. Associated with hyperlipidaemia which is a rf for atherosclerosis.
Tendon xanthoma: nodules found in the hands, feet and ankles, associated with familial hypercholestrolaemia.
Hypertension: a major risk factor for atherosclerosis, also puts extra afterload on the heart both of which contribute to angina and CAD.
Anaemia: reduced Hb therefore reduced oxygen delivery to heart.
Hyperthyroidism: T3 causes increased transcription of myosin heavy chain alpha gene. This causes the heart to contract faster. Faster contraction can sometimes manifest as AF and palpitations. The increased heart rate means the heart is having to work hard therefore in the presence of any atherosclerosis in the coronary aa this can cause angina.
Aortic stenosis:
Narrowing of the aortic valve therefore it increases pressure and cardiac work, in times of exertion can cause angina.
Define the following terms: arteriosclerosis, atherosclerosis and atheroma?
Arteriosclerosis: thickening and hardening of the walls of arteries. Causes a reduction in lumen size and a loss of elasticity. In small vessels hypertension is the most common cause.
Atheroma:
A disease of medium and large aa, which only occurs in high pressure systems (arterial). Affects the tunica intima and eventually the tunics media.
Atherosclerosis:
Arteriosclerosis due to atheroma.
Describe the pathology of coronary artery disease and development of an atheroma?
The most common cause of angina is atherosclerosis of the coronary aa aka coronary aa disease.
Development of an atheroma:
- Lipids enter intima through endothelial damage.
- Lipids are phagocytosis by macrophages in the intima to make raised ‘fatty streaks’.
- Some lipids are released by the macrophages forming a ‘lipid plaque’.
Macrophages secrete cytokines which stimulate myofibroblasts to secrete collagen. Damage to the elastic lamina and media occur. - Collagen covers the plaque surface forming a ‘fibrolipid plaque’
Media wall thins with muscle being replaced by collagen, - Lipid in the intima becomes calcified. Surface of plaque ulcerates. Thinning of the media leads to vessel weakness and inelasticity.
What are the risk factors for coronary artery disease?
Non modifiable:
Age
Male
FH of a 1st degree relative who developed IHD
Modifiable: Smoking Obesity Sedentary lifestyle Diabetic control
Describe the investigations you would do with someone with suspected angina?
FBC: to check Hb
ECG: to rule out ACS
Use the NICE tool to determine likelyhood and guide further investigations
> 90% treat as stable angina
60-90% do a angiogram
30-60% imaging e.g. exercise echo, stress MRI, SPECT scan
<10% investigate for another cause
How is angina managed pharmacologically?
Reduce demand on heart:
-Beta blockers 1st line
OR
-Rate limiting ca channel blockers 2nd line (verapamil)
Increase supply to the heart (vasodilators)
- Issosorbide (long acting nitrate)
- Nifedipine (Ca channel blocker)
GTN for short term pain relief
NEVER GIVE
Beta-blocker + rate limiting Cachannel blocker (verapamil) together can cause a life threatening bradycardia. (can give beta blocker with non rate limiting ca channel blocker aka amlodipine)
When is angioplasty or coronary aa bypass grafts indicated?
Coronary revascularisation is required in:
- High risk patients*
- Failure to be controlled by medical therapy.
*May be indicated following angiography results
What are the driving limitations (car/lorry) with stable angina?
Type 1 drivers (car and motorbike):
Driving must cease when symptoms occur at rest, with emotion, or at the wheel.
The DVLA do not need to be informed.
Driving may recommence when symptoms are controlled adequately.
Type 2 drivers (lorry/buses):
Revocation of a driver’s licence may occur if symptoms (treated or untreated) continue.
Relicensing can occur if person has been free from angina for at least six weeks and passes exercise/functional tolerance tests.
Describe the variants of angina
Decubitus angina: associated with LVF, precipitated by lying down
Prinzmetal: as a result of coronary aa spasm, happens at rest (consider if ST elevation but no trop rise)
