ANGINA PECTORIS
DEFINITION
Refer acute coronary syndromes for
detail of coronary atheromatous syndromes.
This card discusses causes, symptoms, classification of angina.
Stable angina (related to chronic stable plaques) is also discussed
here.
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INCIDENCE
Variable with cause.
Risk Factors
Refer atherosclerosis.
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AETIOLOGY
Can be due to decreased oxygen delivery to, or increased oxygen demand
by, the myocardium.
Resulting in compromise to nutrient supply.
Coronary artery disease almost always the culprit.
Delivery Issues
Congenital
Variant coronary vessels / masses.
Congenital hypercoagulable states.
Inflammatory
Arteritides.
Degenerative
Systemic emboli & sieve.
Aneurysms, dissections & sieves.
Idiopathic
Vasospasm.
"Prinzmetal's angina"- occurs at rest due to coronary artery spasm
(responds to vasodilators)
Emotional apoplexy.
Insufficient oxygen
Anaemia & sieve.
Hypoxia & sieve.
Shock & sieve.
Increased oxygen demand
Hypertrophic cardiomyopathies & sieve.
Hypertensive heart disease & sieve.
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BIOLOGICAL BEHAVIOUR
Only atheroma will be discussed here.
Pathogenesis
All new onset angina is 'unstable'
by definition.
Chronic stable angina is caused by chronic stable plaques.
Oxygen supply exceeds demand.
If plaques are chronic a precipitating agent often precipitates
symptoms (e.g. anaemia).
- or classically on exercise, especially if vigorous, up hills, in cold
weather.
- also with stress or other animation.
Pathophysiology
First felt as a dull visceral pain.
If worse, a deep referred pain develops.
Cause of pain
Perhaps from mechanoreceptors following loss of contractility in
distended
muscle.
Coronary artery vasoreceptors may react to hypotension.
Secondary pain due to lactic acid, K+ and kinins.
Ischaemic neuropathy of cardiac nerves may contribute.
Complications
A historically confusing disease in that it occurs in paroxysms, with
no sequelae, then leads to sudden death or arrhythmia.
Plaques may destabilise leading to acute
coronary syndromes.
Natural History
1 in 4 men with angina, and 1 in 8 women pts will have an MI within
5 years.
About 30% of pts over 55 will die in 8 years, half suddenly.
This generally reflects poor management.
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MANIFESTATIONS
Symptoms
Local
Classically tightness, pressure, heaviness in chest.
Can be burning, aching or crushing.
But can also vary from pins and needles, to vague discomfort to severe
pain.
Usually recognised as deep.
Generally located in the chest, often mid-sternum.
Is said "anywhere from mouth to anus".
May radiate to epigastrium, up neck and jaw, down left arm (atypically
right).
Referral pattern
First a dull vague ache with strong autonomic reaction
If worse a deep referred pain develops, better localised to muscle/bone
T2-4.
20% have cutaneous dysaesthesia in C8-T1 dermatomes.
Systemic
Major apprehension is classical.
Ie 'angina animi' (imminent fear of impending doom)
Rarely fainting, dyspnoea (more apparent to bystanders).
Signs
Observe
Pain often described with hands rubbing across chest.
Especially up and down with a clenched fist.
Note anxiety.
Can be sweating, apparent dyspnoea, eructation (belching).
Exam
Careful evaluation.
Specific reference to cardiac evaluation.
Canadian Cardiovascular Society Classification
Class 0
No angina
Class I
'No angina on ordinary physical activity'
- angina on rapid, strenous prolonged exertion.
Class II
'Slight limitation to ordinary activity'
- walking two blocks
- climbing >1 flight of stairs
- physical activity in cold, after eating.
Class III
'Marked limitation of ordinary activity'
- pain occurs on ordinary activity
Class IV
'Can't carry out any physical activity'
- angina even at rest.
Also Assess
1. Risk factors
Eg high cholesterol, hyperthyroidism, diabetic & hypertensive
changes.
2. Other Vascular Problems
Eg cerebral, peripheries.
3. Comorbidities
Resp, renal, haematological.
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INVESTIGATIONS
See acute coronary syndromes
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MANAGEMENT
See
acute coronary syndromes
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