Chronic stable angina pectoris Flashcards
Define stable angina
Episodic pain that takes place when there is increased myocardial demand, usually upon exercise, in the presence of impaired perfusion by blood. relieved by rest. Usually fades within minutes
Describe the typical history of a patient with stable angina
- Ischaemic pain of the myocardium, varying from a mild ache to a severe pain that provokes sweating and fear
- The pain is provoked by exercise, especially after meals, in the cold, and if the patient is angry/excited
- It fades quickly with rest, and in some patients the pain occurs predictably at certain levels of exertion
- There may be associated breathlessness
Usually no abnormal findings on examination, occasionally a 4th heart sound
What are the potenial underlying causes of angina?
- Coronary artery disease
- causes a decrease in blood flow reaching areas of myocardium
- Valvular heart disease
- increases cardiac workload
- Cardiomyopathy
- interferes with cardiac contractility
- Anaemia
- reduces oxygenation
What are the causes myocardial ichaemia?
- Reduced perfusion:
- Atheroma
- Embolus
- Thrombosis
- Spasm or inflammation of coronary arteries
- Generalised hypotension
- Reduced blood oxygenation
- Anaemia
- Carboxyhaemoglobinaemia
- Increased tissue demands
- Increased CO
- Cardiac hypertrophy
What clinical signs may be present in chronic stable angina pectoris?
- Xanthelasmata (cholesterol deposits around the eyes)
- tendon xanthoma (cholesterol deposits in the hands/skin)
- hypertension
- anaemic signs
- hyperthyroidism signs
- aortic stenosis (ejection systolic murmur radiating into neck)
List recognised risk factors for coronary artery disease
- Increasing age
- Male gender
- Family history
- Smoking
- Diet: high fat, low fruit and veg
- Obesity
- Hypertension
- Hyperlipidaemia
- Diabetes Mellitus
- type A personality
- haemostatic factors
What is coronary heart disease?
Also known as ischemic heart disease (IHD), is a group of diseases that includes: stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is within the group of cardiovascular diseases of which it is the most common type.
Define arteriosclerosis?
- Non-specific thickening and hardening of the walls of arteries causing a loss of contractility and elasticity, and decreased blood flow
- Often due to prolonged hypertension in smaller arteries
What is atheroma?
- Specific degenerative disease affecting large/medium sized arteries
- When this leads to thickening and hardening of the arterial wall, it is termed atherosclerosis: most common cause of arteriosclerosis affecting large/medium arteries
- Atherosclerosis reduces tissue perfusion, as well as predisposing to thrombus and aneurysm formation
Describe the pathology of atheroma formation
- Damage to the endothelium due to a variety of risk factors allows entry of LDLs into the intima
- This lipid is taken up by macrophages in the intima, and accumulates excessively as it is able to bypass normal receptor mediated uptake, forming a ‘fatty streak’
- As the macrophages take up more and more lipid, they release free lipid into the intima
- The macrophages also stimulate cytokines, which leads to collagen deposition by inflammatory cells, and the intimal lipid plaques becomes fibrotic
- At this stage it appears raised and yellow, and leads to pressure atrophy of the media and disruption of the elastic lamina
- Increased secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white
- Advanced places also show free lipid as well as lipid in macrophages
- The endothelium is fragile and often ulcerates, allowing platelet aggregation
What investigations would you do on a patient with suspected angina?
Clinical assessment alone can be sufficient to confirm stable angina
- Exclude other causes: FBC, glucose, lipids, thyroid function test
- Resting 12-lead ECG: usually normal, may be signs of previous MI (consider aortic stenosis if LVH/LBBB)
- Then use clinical assessment and ECG findings to estimate the likelihood of CAD using NICE tool:
- If >90% treat as stable angina
- If 61-90%, coronary angiography is indicated
- If 31-60% functional imaging is indicated
- SPECT myocardial perfusion scan, exercise echo, stress MRI
- If 10-30% CT calcium scoring is used
- If <10% investigate for another cause
What drugs are used to treat angina?
Symptomatic treatment:
- GTN spray + B-blocker or calcium inhibitor as first line
- Combination therapy, or nicorandil for refractory disease
Secondary prevention:
- Statin
- Low dose aspirin
- ACE inhibitor if co-morbid diabetes
What combination therapy is used for refractory disease (doesn’t respond to the 1st line treatment - in this case of GTN spray and b-blocker or calcium channel blocker) of angina?
What shouldn’t never be used?
B-blockers and dihydropyridines such as amlodipine are the combination used
NEVER combine a rate-limiting calcium channel blocker and a B-blocker, this can cause asystole (heart stops beating)
How should nitrates be used to treat angina?
Mechanism of action?
Side effects?
- Sub-lingual spray is first line for symptom relief
- spray under tongue, wait 5 minutes and spray again. If pain after 10 minutes call 999
- Can be used prior to performing activities that provoke angina
- They cause marked venorelaxation, thus reducing pre-load on the heart
- This can cause venous pooling on standing, thus can cause postural hypotension and dizziness
- They also affect large muscular arteries, reducing aaortic pressure and cardiac afterload, as well as dilating coronary vessels
- Decreased pre-load and after-load decreases the oxygen requirement of the myocardium and coronary vasodilation leads to increased oxygen delivery
How do B-blockers treat angina? - mechanism of action
Side effects?
- ß1 adrenoceptors are found mainly on the heart, acting to increase heart rate and stroke volume
- ß2 adrenoceptors act to cause smooth muscle relaxation in many organs, e.g. the trachea
- In ischaemic heart disease, ß1 selective ß-blockers are used to reduce cardiac rate and force (reduce myocardial oxygen consumption) with little broncho-constrictive effect as possible
- They also have an anti-hypertensive effect by reducing cardiac output, and decrease renin release from juxta-glomerular cells
- They also have class two anti-arrhythmic effects
Side effects:
- Bronchoconstriction: contradiction in asthma, caution in COPD
Cardiac depression/bradycardia: can be critical if combined with other rate limiting agents - Hypoglycaemia: impair the sympathetic warning signs of hypo’s
- Fatigue
What is the framingham risk score?
The Framingham Risk Score is a gender-specific algorithm used to estimate the 10-year cardiovascular risk of an individual.
Assessment for primary prevention of CHD
What is QRISK 2?
QRISK2 (the most recent version of QRISK) is a prediction algorithm for cardiovascular disease (CVD) that uses traditional risk factors (age, systolic blood pressure, smoking status and ratio of total serum cholesterol to high-density lipoprotein cholesterol) together with body mass index, ethnicity, measures of deprivation, family history, chronic kidney disease, rheumatoid arthritis, atrial fibrillation, diabetes mellitus, and antihypertensive treatment.
(better than framingham)
