ANGINA
▪ A form of coronary artery disease (CAD)
▪ Classic cardiac pain that is felt when there is a reduction in blood supply to the myocardium.
PATHOPHYSIOLOGY
→ the main symptom of myocardial ischaemia, usually secondary due to coronary artery disease (CAD) but can
also be caused by coronary spasms, severe ventricular hypertrophy or severe aortic stenosis.
▪ Most commonly due to CAD
▪ CAD → atherosclerotic plaques developing within the coronary vessels
▪ This limits blood flow and precipitates symptoms
▪ On exertion there is increased oxygen demand within cardiomyocytes
▪ The narrowing of the coronary vessels means blood flow cannot be increased to meet this demand
o It may be obstructive (>50% of vessel lumen)
o May be non-obstructive (<50% of vessel lumen)
▪ This results in myocardial ischaemia which is experienced as pain.
There are other conditions that can cause ischaemia and angina due to reduced coronary artery blood flow or an
increased oxygen supply/demand mismatch. These include:
Prinzmetal angina (coronary artery spasm)
Microvascular angina → diffuse vascular disease within the microvasculature of the coronary circulation
Vasculitis → Kawasaki disease, polyarteritis nodosa
Anaemia → oxygen supply/demand mismatch
Severe left ventricular hypertrophy → reduced subendocardial blood flow and increased susceptibility to
ischaemia
Severe aortic stenosis → increases myocardial oxygen demand.
There are two main types of lesion:
1. Stable/stenotic plaque – has a thick fibrous cap
▪ These are slow growing
▪ Fibrin cap matures and isn’t prone to rupture
▪ This will cause stable angina
▪ This can only be seen on exertional studies
→ occurs predictably with exertion and lasts <10 minutes.
2. Unstable/non-stenotic plaque – has a thin cap which is susceptible to rupture.
▪ Grow rapidly due to rapid lipid deposition
▪ Have a thin fibrin cap which is fragile and prone to rupture easily
▪ Haemorrhage from the plaque also occurs
o This releases platelet tissue factor → stimulates clotting cascade
o Exposed collagen → platelet aggregation
o Thrombus formation occurs
o This reduces lumen diameter and may occlude it entirely causing an MI
▪ This is called unstable angina.
→ a sudden new onset of angina or a significant and abrupt deterioration in angina that was previously stable
e.g. pain that is increased in frequency and severity or pain at rest.
→ these px need urgent admission to hospital for exclusion of ACS.
, CLINICAL PRESENTATION
→ ‘classic central crushing/constricting chest pain’e
▪ Central chest pain that occurs only on exertion
o Site – central chest
o Onset – after exertion (emotional or physical), resolves upon rest, can be worse after eating
o Characteristic – crushing, pressing, squeezing, constricting in nature
▪ Seems as if they are going to die
o Radiation – can commonly radiate to the shoulder, left arm, jaw and neck
o Associated symptoms –
o Time – usually lasts about 5-10 minutes, typically <10
o Exacerbating/relieving factors – GTN spray will alleviate the pain, as will resting
o Severity – may be very severe
▪ Dyspnoea
▪ Palpitations – angina may be precipitated by tachyarrhythmias (e.g. AF)
▪ Syncope – may be suggestive of dangerous valvular or cardiac muscle disease causing angina
3 CLASSIC FEATURES
1. Constricting pain in the central chest +/- typical radiation to arm/neck/jaw
2. Precipitated by physical exertion
3. Relived by rest or GTN within 5 mins.
Classification → 3 types:
▪ Typical – all 3 of above features
▪ Atypical – 2 of the above features
▪ Non-anginal – 1 or less of the above features.
Grading → Canadian Cardiovascular Society
▪ Grade I – angina with strenuous activity (limitation on strenuous or prolonged ordinary activity)
▪ Grade II – angina with moderate activity (slight limitation if normal activities performed rapidly
▪ Grade III – angina with mild exertion (difficulty climbing one flight of stairs at normal pace)
▪ Grave IV – angina at rest (no exertion needed).
Non-anginal chest pain includes:
▪ Continuous or very prolonged pain
▪ Unrelated to activity
▪ Brought on by breathing
▪ Associated with dizziness, palpitations, paraesthesia, swelling difficulties.
(!) Worrying chest pain (!)
Chest pain lasting >10 mins
Chest pain not relieved by 2 doses of GTN taken 5 minutes apart
Significant worsening/deterioration in angina.
Risk factors → high cholesterol, hypertension, smoking, diabetes, obesity, age, family history, male, premature
menopause.
It is a dynamic process and can be broadly grouped into two categories:
Acute coronary syndrome (ACS)
Chronic coronary syndrome (CCS)
a. Includes six clinical presentations of CAD:
i. Suspected CAD with stable angina and/or dyspnoea
ii. Suspected CAD and new heart failure (or LV dysfunction)
iii. Known CAD (asymptomatic or symptomatic) within 1 year of ACS or revascularisation
iv. Known CAD (asymptomatic or symptomatic (1 year after initial diagnosis or
revascularisation
v. Angina secondary to vasospasm or microvascular disease
vi. CAD detected at screening (asymptomatic).
▪ A form of coronary artery disease (CAD)
▪ Classic cardiac pain that is felt when there is a reduction in blood supply to the myocardium.
PATHOPHYSIOLOGY
→ the main symptom of myocardial ischaemia, usually secondary due to coronary artery disease (CAD) but can
also be caused by coronary spasms, severe ventricular hypertrophy or severe aortic stenosis.
▪ Most commonly due to CAD
▪ CAD → atherosclerotic plaques developing within the coronary vessels
▪ This limits blood flow and precipitates symptoms
▪ On exertion there is increased oxygen demand within cardiomyocytes
▪ The narrowing of the coronary vessels means blood flow cannot be increased to meet this demand
o It may be obstructive (>50% of vessel lumen)
o May be non-obstructive (<50% of vessel lumen)
▪ This results in myocardial ischaemia which is experienced as pain.
There are other conditions that can cause ischaemia and angina due to reduced coronary artery blood flow or an
increased oxygen supply/demand mismatch. These include:
Prinzmetal angina (coronary artery spasm)
Microvascular angina → diffuse vascular disease within the microvasculature of the coronary circulation
Vasculitis → Kawasaki disease, polyarteritis nodosa
Anaemia → oxygen supply/demand mismatch
Severe left ventricular hypertrophy → reduced subendocardial blood flow and increased susceptibility to
ischaemia
Severe aortic stenosis → increases myocardial oxygen demand.
There are two main types of lesion:
1. Stable/stenotic plaque – has a thick fibrous cap
▪ These are slow growing
▪ Fibrin cap matures and isn’t prone to rupture
▪ This will cause stable angina
▪ This can only be seen on exertional studies
→ occurs predictably with exertion and lasts <10 minutes.
2. Unstable/non-stenotic plaque – has a thin cap which is susceptible to rupture.
▪ Grow rapidly due to rapid lipid deposition
▪ Have a thin fibrin cap which is fragile and prone to rupture easily
▪ Haemorrhage from the plaque also occurs
o This releases platelet tissue factor → stimulates clotting cascade
o Exposed collagen → platelet aggregation
o Thrombus formation occurs
o This reduces lumen diameter and may occlude it entirely causing an MI
▪ This is called unstable angina.
→ a sudden new onset of angina or a significant and abrupt deterioration in angina that was previously stable
e.g. pain that is increased in frequency and severity or pain at rest.
→ these px need urgent admission to hospital for exclusion of ACS.
, CLINICAL PRESENTATION
→ ‘classic central crushing/constricting chest pain’e
▪ Central chest pain that occurs only on exertion
o Site – central chest
o Onset – after exertion (emotional or physical), resolves upon rest, can be worse after eating
o Characteristic – crushing, pressing, squeezing, constricting in nature
▪ Seems as if they are going to die
o Radiation – can commonly radiate to the shoulder, left arm, jaw and neck
o Associated symptoms –
o Time – usually lasts about 5-10 minutes, typically <10
o Exacerbating/relieving factors – GTN spray will alleviate the pain, as will resting
o Severity – may be very severe
▪ Dyspnoea
▪ Palpitations – angina may be precipitated by tachyarrhythmias (e.g. AF)
▪ Syncope – may be suggestive of dangerous valvular or cardiac muscle disease causing angina
3 CLASSIC FEATURES
1. Constricting pain in the central chest +/- typical radiation to arm/neck/jaw
2. Precipitated by physical exertion
3. Relived by rest or GTN within 5 mins.
Classification → 3 types:
▪ Typical – all 3 of above features
▪ Atypical – 2 of the above features
▪ Non-anginal – 1 or less of the above features.
Grading → Canadian Cardiovascular Society
▪ Grade I – angina with strenuous activity (limitation on strenuous or prolonged ordinary activity)
▪ Grade II – angina with moderate activity (slight limitation if normal activities performed rapidly
▪ Grade III – angina with mild exertion (difficulty climbing one flight of stairs at normal pace)
▪ Grave IV – angina at rest (no exertion needed).
Non-anginal chest pain includes:
▪ Continuous or very prolonged pain
▪ Unrelated to activity
▪ Brought on by breathing
▪ Associated with dizziness, palpitations, paraesthesia, swelling difficulties.
(!) Worrying chest pain (!)
Chest pain lasting >10 mins
Chest pain not relieved by 2 doses of GTN taken 5 minutes apart
Significant worsening/deterioration in angina.
Risk factors → high cholesterol, hypertension, smoking, diabetes, obesity, age, family history, male, premature
menopause.
It is a dynamic process and can be broadly grouped into two categories:
Acute coronary syndrome (ACS)
Chronic coronary syndrome (CCS)
a. Includes six clinical presentations of CAD:
i. Suspected CAD with stable angina and/or dyspnoea
ii. Suspected CAD and new heart failure (or LV dysfunction)
iii. Known CAD (asymptomatic or symptomatic) within 1 year of ACS or revascularisation
iv. Known CAD (asymptomatic or symptomatic (1 year after initial diagnosis or
revascularisation
v. Angina secondary to vasospasm or microvascular disease
vi. CAD detected at screening (asymptomatic).
