Stable Angina
Stable angina is a predictable pattern of chest pain or discomfort caused by myocardial ischemia that occurs with exertion or emotional stress and is relieved by rest or nitroglycerin.
Stable angina — or more precisely, stable angina pectoris — is the clinical symptom complex arising from reversible myocardial ischaemia that occurs predictably when myocardial oxygen (O₂) demand exceeds supply, typically provoked by exertion or emotional stress, and relieved by rest or sublingual nitrates [1][2].
Let's break the name down:
- Angina (Latin: angere = to squeeze/choke) — refers to the strangling, constricting quality of the chest discomfort
- Pectoris (Latin: pectus = chest) — localises it to the chest
So angina pectoris literally means "a choking sensation in the chest."
The word "stable" is critical — it distinguishes this from acute coronary syndromes (ACS). In stable angina, the pattern of symptoms is reproducible and predictable over weeks to months: the same level of exertion provokes pain, and it relieves the same way each time. This implies a fixed, flow-limiting coronary stenosis rather than an acutely disrupted plaque [1][2].
Key Conceptual Distinction
The underlying condition is chronic coronary syndromes (CCS) — the 2019 ESC terminology that replaced the older "stable ischaemic heart disease" (SIHD) or "stable coronary artery disease" [3]. This updated terminology reflects the understanding that coronary artery disease (CAD) is a dynamic, lifelong process that may be stable for prolonged periods but can become unstable at any time due to plaque rupture or erosion.
Indicates: myocardial O₂ supply < demand [1]
Global and Hong Kong Context
- Angina is most common in middle-aged and elderly men [3]
- Among persons 60–79 years of age, approximately 25% of men and 16% of women have coronary heart disease; these figures rise to 37% and 23% among men and women > 80 years of age, respectively [3]
- The incidence of coronary heart disease and angina in women after menopause is similar to that of men [3] — because loss of oestrogen's protective effect on the vasculature (oestrogen promotes NO-mediated vasodilation and has favourable lipid effects)
- Although the survival rate has steadily improved over time, IHD remains the number one cause of death in men and women (27% of deaths) [3]
- The initial manifestation of IHD is angina pectoris in ~50%, and about 50% of patients presenting to the hospital with ACS have preceding angina [3]
- In the US, the annual rate of MI in patients with symptomatic angina is 3–3.5%/year [3]
- Within 12 months of initial diagnosis, 10–20% of patients with a diagnosis of stable angina progress to MI or unstable angina [3]
In Hong Kong specifically:
- IHD is among the top 3 leading causes of death (alongside cancer and cerebrovascular disease)
- High prevalence of cardiovascular risk factors: Hong Kong has increasing rates of diabetes mellitus (~10% of the population), hypertension (~27%), and obesity, partly driven by a westernising diet and sedentary lifestyles
- Smoking prevalence in HK is relatively lower (~10%) compared to other regions but still a significant contributor
- The ageing population in HK amplifies the burden of CAD
High Yield Epidemiology Points
Key exam points:
- IHD is the #1 killer globally and in HK
- Stable angina is the first manifestation of IHD in ~50% of patients
- Post-menopausal women "catch up" to men in incidence
- 10–20% of newly diagnosed stable angina patients progress to MI/UA within 12 months — this underscores why risk stratification and optimal medical therapy are essential
Risk Factors
Risk factors for stable angina are essentially the risk factors for atherosclerosis — because the pathological substrate is coronary atheroma.
| Factor | Mechanism / Why |
|---|---|
| Advanced age | Cumulative endothelial damage + longer exposure to risk factors; arterial stiffening |
| Male sex | Earlier onset than females by ~10 years; pre-menopausal oestrogen is protective (↑NO, ↑HDL, ↓LDL) |
| Family history of premature CVD (1st degree relative: male < 55y, female < 65y) | Genetic susceptibility to dyslipidaemia, endothelial dysfunction, inflammation; familial hypercholesterolaemia (FH) is a key example [4][5] |
| Factor | Mechanism / Why |
|---|---|
| Cigarette smoking | Endothelial damage via oxidative stress; ↑platelet aggregation; ↑fibrinogen; ↓HDL; promotes a pro-inflammatory, pro-thrombotic state |
| Hypertension | Shear stress damages endothelium → promotes atheroma formation; LV hypertrophy → ↑O₂ demand; target < 130/80 mmHg per 2023 ESH guidelines |
| Dyslipidaemia (↑LDL, ↓HDL, ↑TG) | LDL oxidation in arterial wall is the initiating event of atherosclerosis; HDL performs reverse cholesterol transport (protective). Familial hypercholesterolaemia (FH) causes extremely high LDL and premature ASCVD [4][5] |
| Diabetes mellitus | Chronic hyperglycaemia → advanced glycation end-products (AGEs) → endothelial dysfunction + oxidative stress; insulin resistance → dyslipidaemia (↑TG, ↓HDL, small dense LDL) + pro-inflammatory state [6] |
| Obesity (esp. abdominal/central) | Adipocytes release FFAs → insulin resistance; adipokines promote inflammation; metabolic syndrome clustering [6] |
| Sedentary lifestyle / lack of exercise | Physical inactivity → ↓AMPK activation → ↓glucose uptake, ↓FFA oxidation → insulin resistance; exercise also ↑HDL, ↓BP, ↓weight [6] |
| Unhealthy diet | High saturated fat/trans fat → ↑LDL; high sodium → ↑BP; low fruit/vegetable → ↓antioxidants |
These don't cause atherosclerosis per se but can unmask or worsen stable angina:
| Factor | Why it matters |
|---|---|
| Anaemia | ↓ O₂ carrying capacity → ↓ O₂ supply to myocardium even at rest or lower exertion thresholds [1][2] |
| Thyrotoxicosis | ↑ metabolic rate → ↑ HR, ↑ contractility → ↑ myocardial O₂ demand; may precipitate angina in previously compensated patients [1][2] |
| Aortic stenosis (AS) | ↑ afterload → LV hypertrophy → ↑ O₂ demand + ↓ coronary perfusion (compressed subendocardial vessels) [1] |
| Hypertrophic cardiomyopathy (HCMP/HOCM) | Massive LV hypertrophy → ↑ O₂ demand; dynamic LVOT obstruction → ↓ coronary perfusion; abnormal intramural coronary arteries [1] |
| Tachyarrhythmias (esp. AF) | ↑ HR → ↑ O₂ demand + ↓ diastolic filling time (coronary perfusion occurs primarily in diastole) |
Exacerbating Factors — Why They Matter
A common exam pitfall: Students list risk factors for atherosclerosis but forget about conditions that exacerbate angina without necessarily causing new atheroma. Always consider anaemia, thyrotoxicosis, aortic stenosis, and tachyarrhythmias as precipitating/aggravating factors in a stable angina patient — these are treatable and their correction may relieve symptoms without revascularisation.
Anatomy and Function — Coronary Arterial Supply
Understanding coronary anatomy is essential because stable angina results from fixed stenosis in these vessels.
The heart receives its blood supply from the left coronary artery (LCA) and right coronary artery (RCA), both arising from the aortic root just above the aortic valve cusps (the left and right coronary sinuses of Valsalva).
| Artery | Branches | Territory Supplied |
|---|---|---|
| Left Main Stem (LMS) | Divides into LAD and LCx | Very short (0.5–2 cm); stenosis here = "left main disease" → high mortality |
| Left Anterior Descending (LAD) | Diagonal branches, septal perforators | Anterior wall of LV, anterior 2/3 of interventricular septum, apex |
| Left Circumflex (LCx) | Obtuse marginal (OM) branches | Lateral wall of LV; inferior wall if left-dominant |
| Right Coronary Artery (RCA) | Posterior descending artery (PDA), AV nodal artery, acute marginal | Inferior wall of LV, posterior 1/3 of interventricular septum, RV, SA and AV nodes (in right-dominant circulation) |
- Right dominant (~85%): PDA arises from RCA → RCA supplies inferior wall and AV node
- Left dominant (~8%): PDA arises from LCx
- Co-dominant (~7%): PDA supplied by both
Why dominance matters clinically: An inferior MI from RCA occlusion may cause AV nodal ischaemia → heart block (because the AV nodal artery usually comes off the RCA).
This is the fundamental concept underlying stable angina:
Myocardial O₂ Supply depends on:
- Coronary blood flow (main determinant)
- Occurs predominantly in diastole (during systole, the contracting myocardium compresses intramural vessels)
- Regulated by coronary vascular resistance → mediated by metabolic autoregulation (adenosine, NO, prostacyclin)
- O₂ content of blood (Hb concentration × SaO₂)
Myocardial O₂ Demand depends on:
- Heart rate — the single most important determinant (more beats = more O₂ consumed, and ↓ diastolic time = ↓ coronary filling)
- Myocardial wall tension (= afterload, related to systolic BP)
- Contractility (inotropy)
- Preload (ventricular volume → wall stress via Laplace's law: Wall tension = Pressure × Radius / 2 × Wall thickness)
The rate-pressure product (RPP = HR × systolic BP) is a clinical surrogate for myocardial O₂ demand. In stable angina, symptoms characteristically occur at a reproducible RPP threshold — i.e., the same level of exertion causes the same angina every time.
Why Coronary Flow Reserve Matters
At rest, coronary arteries can dilate 4–6× their baseline calibre (coronary flow reserve). A stenosis of ~50% diameter starts to impair maximal flow reserve. A stenosis of ~70% diameter significantly limits flow during exertion. A stenosis of ~90% may limit flow even at rest. In stable angina, the stenosis is typically ≥ 70% (or ≥ 50% for left main), enough to limit flow when demand increases but not at rest.
Etiology (with Hong Kong Focus) and Pathophysiology
Etiology
The overwhelmingly dominant cause of stable angina is coronary atherosclerosis — the fixed, flow-limiting atherosclerotic plaque [1][7].
However, a comprehensive list of aetiologies includes:
This is a chronic, progressive, inflammatory disease of the arterial wall. In stable angina, the plaque is characteristically:
- Fixed (not acutely ruptured)
- Has a thick fibrous cap (stable plaque) with a relatively small lipid core
- Causes luminal narrowing ≥ 70% → haemodynamically significant stenosis
Why does atherosclerosis preferentially affect certain coronary sites?
- Atheroma forms at branch points and bifurcations (e.g., LAD/LCx bifurcation, proximal LAD) due to disturbed laminar flow → oscillatory shear stress → endothelial dysfunction
Hong Kong relevance:
- The high prevalence of diabetes, hypertension, and dyslipidaemia in Hong Kong's ageing population drives atherosclerotic burden
- Dietary westernisation (more red meat, processed foods) alongside a traditionally high-sodium Chinese diet compounds risk
- Familial hypercholesterolaemia (FH), prevalence ~1/250–1/500, is significantly underdiagnosed in HK; these patients develop premature severe CAD [4][5]
| Cause | Mechanism |
|---|---|
| Coronary vasospasm (Prinzmetal/variant angina) | Focal coronary artery spasm → transient ↓ supply; can occur at rest (typically nocturnal); more common in East Asian populations including Hong Kong (higher prevalence of CYP2C19 polymorphisms that affect endothelial NO pathways) |
| Coronary microvascular disease (cardiac syndrome X) | Dysfunction of small intramural coronary arterioles → impaired microvascular vasodilation; more common in women; normal epicardial coronary arteries on angiography |
| Myocardial bridging | A segment of epicardial coronary artery (usually mid-LAD) dips into the myocardium → systolic compression; usually benign but can cause exertional ischaemia |
| Coronary artery anomalies | Anomalous origin/course (e.g., interarterial course between aorta and pulmonary artery) → compression during exertion |
| Coronary arteritis | Takayasu, giant cell arteritis, Kawasaki disease (important in paediatrics) → coronary inflammation and stenosis |
| Cause | Mechanism |
|---|---|
| Aortic stenosis (AS) | ↑ afterload → LVH → ↑ O₂ demand; ↓ coronary perfusion pressure gradient |
| Hypertrophic cardiomyopathy (HCMP) | Massive LVH + LVOT obstruction → supply-demand mismatch |
| Severe anaemia | ↓ O₂ carrying capacity |
| Thyrotoxicosis | ↑ HR, contractility → ↑ demand |
| Severe hypertension | ↑ afterload → ↑ wall tension → ↑ O₂ demand |
Pathophysiology of Stable Angina
The pathophysiology can be understood as a chain of events:
When myocardial ischaemia develops, events do NOT occur simultaneously — they follow a temporal sequence called the ischaemic cascade:
- Metabolic abnormalities (↓ ATP, lactate accumulation) — earliest
- Diastolic dysfunction (impaired relaxation — because active relaxation requires ATP)
- Systolic dysfunction (regional wall motion abnormalities — hypokinesis/akinesis)
- ECG changes (ST-segment depression in stable angina — because ischaemia is subendocardial)
- Angina (chest pain/discomfort) — latest
Why is this important? Because ECG changes and wall motion abnormalities precede symptoms. A patient may have "silent ischaemia" detectable on stress testing before they ever feel chest pain. This is particularly common in diabetics (autonomic neuropathy impairs pain perception) and the elderly.
Pathophysiology: myocardial ischaemia → metabolite accumulation → stimulation of cardiac sympathetic nerves → pain [1][2]
The subendocardium (innermost layer of the myocardium) is most vulnerable to ischaemia because:
- It experiences the highest wall tension (highest intramyocardial pressure during systole → most compressed)
- It has the longest intramural vessels → flow is most impeded
- It receives blood last in the myocardial perfusion sequence
In stable angina with a fixed stenosis, ischaemia during exertion is characteristically subendocardial → this explains why the ECG shows ST-segment depression (not ST elevation, which indicates transmural ischaemia as in STEMI).
The cardiac sympathetic afferent nerve fibres (C-fibres) that transmit ischaemic pain enter the spinal cord at C8–T4 segments. These same spinal segments also receive somatic sensory input from the:
- Chest wall
- Left arm (especially medial aspect — T1 dermatome)
- Jaw (via trigeminal-spinal connections at upper cervical levels)
The brain cannot distinguish between cardiac and somatic pain at the same spinal level → convergence-projection theory → the brain "projects" the pain to the somatic territory → referred pain.
Since atherosclerosis is the primary cause, understanding its pathogenesis is fundamental:
- Endothelial injury/dysfunction: Risk factors (shear stress, smoking, HTN, hyperglycaemia, hyperlipidaemia) → endothelial damage → ↑ permeability, ↓ NO production
- Lipid infiltration: LDL crosses damaged endothelium → becomes trapped in the subintima → oxidised (ox-LDL)
- Inflammatory response: ox-LDL triggers monocyte recruitment → monocytes differentiate into macrophages → engulf ox-LDL → become foam cells → fatty streak
- Smooth muscle cell migration: SMCs migrate from media to intima, proliferate, and produce extracellular matrix (collagen, proteoglycans) → formation of a fibrous cap
- Mature plaque: Lipid core covered by fibrous cap → progressive luminal narrowing
- Stable vs. unstable plaque:
- Stable plaque: thick fibrous cap, small lipid core, predominantly collagen-rich → causes fixed stenosis → stable angina
- Unstable/vulnerable plaque: thin fibrous cap, large lipid core, rich in macrophages/inflammatory cells → prone to rupture → thrombus formation → ACS
Classification
This is the standard classification used for grading the severity of stable angina [1][2]:
| CCS Grade | Description | Functional Impact |
|---|---|---|
| I | Angina with strenuous exertion only | Ordinary physical activity (walking, climbing stairs) does NOT cause angina |
| II | Angina with moderate exertion (slight limitation of ordinary activities) | Walking > 2 blocks on level ground or climbing > 1 flight of stairs at a normal pace |
| III | Angina with mild exertion (e.g., 100–200 m, 1 flight of stairs) — great limitation | Marked limitation of ordinary physical activity |
| IV | Angina at rest (cannot carry out any exertion) | Inability to perform any physical activity without discomfort; angina may be present at rest |
CCS Class IV vs. Unstable Angina
CCS class IV describes angina at rest that occurs in a predictable, chronic pattern as part of severe stable CAD. This is different from unstable angina (ACS), where rest angina represents a new or worsening pattern due to acute plaque disruption. The distinction is about the tempo and trajectory: stable CCS IV = chronic and unchanging; unstable = acute change in character, frequency, or threshold.
| Type | Mechanism | Notes |
|---|---|---|
| Type 1: Classic exertional angina | Fixed epicardial coronary stenosis (atherosclerosis) | Most common; demand-driven ischaemia |
| Type 2: Vasospastic angina (Prinzmetal/variant) | Coronary artery spasm | Rest angina, often nocturnal; ST elevation during episodes; more common in East Asians |
| Type 3: Microvascular angina | Coronary microvascular dysfunction | Angina with positive stress test but normal coronary angiogram; more common in women |
The ESC 2019 guidelines define six clinical scenarios under chronic coronary syndromes (CCS):
- Patients with suspected CAD and "stable" anginal symptoms and/or dyspnoea
- Patients with new onset of HF or LV dysfunction and suspected CAD
- Asymptomatic and symptomatic patients with stabilised symptoms < 1 year after ACS or recent revascularisation
- Asymptomatic and symptomatic patients > 1 year after initial diagnosis or revascularisation
- Patients with angina and suspected vasospastic or microvascular disease
- Asymptomatic subjects in whom CAD is detected at screening
Stable angina primarily falls under scenarios 1 and 4.
Clinical Features
Symptoms
The hallmark symptom is chest discomfort — note that patients often resist calling it "pain" and prefer terms like "discomfort," "pressure," or "tightness."
| Feature | Description | Pathophysiological Basis |
|---|---|---|
| Onset / Provocation | Builds up gradually in proportion to intensity of exertion [1][2]; provoked by the "4 Es": Eating, Exertion, Emotion, Environment (cold) [2] | Exertion ↑ HR and BP → ↑ O₂ demand → exceeds supply from fixed stenosis. Cold weather causes coronary vasoconstriction + ↑ afterload (peripheral vasoconstriction). Heavy meals redirect blood to splanchnic circulation → "coronary steal" + ↑ cardiac workload |
| Quality | Typically dull, constricting, choking, 'heavy'; described as squeezing, crushing, burning, aching or even as breathlessness [1][2]; patients often emphasise it is a discomfort not a pain [1][2]; Levine's sign: characteristic gesture of a clenched fist on chest when describing angina [1][2] | Visceral pain from cardiac sympathetic C-fibre activation → poorly localised, deep, visceral quality (not sharp/well-localised like somatic pain) |
| Region and Radiation | Retrosternal/central chest; ± radiation to arms (especially left), shoulder, jaw, neck, epigastrium [1] | Referred pain via convergence of cardiac sympathetic afferents (C8–T4) with somatic afferents at the same spinal segments |
| Severity | Variable; typically graded by CCS classification (I–IV) [2]; generally less severe than ACS | Degree of ischaemia depends on severity of stenosis and extent of demand increase |
| Timing / Duration | Usually lasts 2–10 minutes [2]; relieved by rest or cessation of activity/stress, or by sublingual nitrates (relieved ≤ 5 min after rest) [2] | Rest → ↓ HR, BP → ↓ demand → supply meets demand again. Nitrates → venodilation → ↓ preload → ↓ wall tension → ↓ demand (+ some coronary vasodilation) |
| Associated features | Mild dyspnoea (angina equivalent), fatigue | Ischaemia → diastolic dysfunction → ↑ LVEDP → pulmonary congestion → dyspnoea |
Angina Equivalents
25% of patients with myocardial ischaemia may not suffer from angina (especially elderly and diabetics). They may present with angina equivalents — meaning these symptoms represent myocardial ischaemia even without classic chest pain [2]. These include:
- Exertional dyspnoea (most common equivalent)
- Fatigue / exercise intolerance
- Epigastric discomfort
- Syncope / dizziness
Why diabetics? Diabetic autonomic neuropathy damages cardiac sensory afferents → "silent ischaemia."
- Angina decubitus: Angina occurring when lying supine due to ↑ venous return (VR) → ↑ preload → ↑ O₂ demand [2]. This is a sign of more severe disease.
- Walk-through angina: Angina that occurs at the start of exertion but eases with continued activity → thought to be due to coronary vasodilation with sustained exercise (ischaemic preconditioning)
- First-effort angina: Worse with first effort of the day, then improves — related to ischaemic preconditioning
- Post-prandial angina: Worsened after large meals (splanchnic blood diversion)
- Cold-weather angina: Cold → peripheral vasoconstriction → ↑ afterload → ↑ demand; also direct coronary vasoconstriction
A chest pain is classified as [1][3]:
| Classification | Criteria Met |
|---|---|
| Typical angina | All 3 of: (1) Constricting discomfort in the chest, neck, jaw, shoulder, or arm; (2) Provoked by physical exertion or emotional stress; (3) Relieved by rest and/or GTN within 5 minutes |
| Atypical angina | 2 of 3 criteria |
| Non-cardiac chest pain | ≤ 1 criterion |
Signs
Physical examination is frequently unremarkable in stable angina [1]. However, a thorough examination may reveal:
| Sign | What It Tells You | Pathophysiological Basis |
|---|---|---|
| Evidence of VHD, esp. AS, AR, HOCM [1] | Non-coronary cause of angina or exacerbating factor | AS: ↑ afterload + LVH → ↑ demand; AR: volume overload → LV dilatation → ↑ wall tension; HOCM: massive LVH + dynamic obstruction |
| Risk factors: HTN, DM [1] | Underlying atherosclerotic risk | Confirm modifiable risk factors for targeted management |
| LV dysfunction: cardiomegaly, gallop rhythm (S3/S4) [1] | Previous MI with LV remodelling | S4 = non-compliant, stiff LV (diastolic dysfunction from chronic ischaemia/LVH); S3 = volume overload (systolic dysfunction, HF) |
| Xanthomas, xanthelasma, corneal arcus (< 45 y) | Hypercholesterolaemia, possibly FH [4] | Lipid deposition in tendons (tendon xanthomas), skin (xanthelasma), cornea (arcus) — markers of severely elevated LDL |
| Other arterial diseases: carotid bruit, signs of PVD (presence of all peripheral pulses) [1] | Generalised atherosclerosis | Atherosclerosis is a systemic disease — if it's in the coronaries, it's likely elsewhere (carotids, aorta, lower limbs) |
| Conditions that may exacerbate angina: anaemia (pallor, tachycardia), thyrotoxicosis (tremor, goitre, AF) [1] | Treatable exacerbating factors | Anaemia → ↓ O₂ supply; thyrotoxicosis → ↑ O₂ demand |
| Fundoscopy: hypertensive/diabetic retinopathy | Evidence of microvascular end-organ damage | Confirms chronicity and severity of HTN/DM |
| Nicotine staining of fingers | Active smoking | Modifiable risk factor |
| BMI / waist circumference | Central obesity | Metabolic syndrome, insulin resistance |
| Blood pressure measurement | Hypertension | Direct risk factor; also determines afterload (O₂ demand) |
Why Examine Peripheral Pulses in a Cardiac Patient?
Atherosclerosis is a systemic arterial disease. If a patient has coronary atherosclerosis, they likely have atherosclerosis in:
- Carotid arteries → bruits → stroke risk
- Abdominal aorta → AAA
- Lower limb arteries → peripheral arterial disease (PAD) → absent/reduced pulses, intermittent claudication [7]
Finding PVD in a stable angina patient escalates their risk category and mandates more aggressive risk factor management.
These signs may be transiently present:
- Tachycardia (sympathetic activation)
- Hypertension (sympathetic activation)
- S4 gallop (atrial contraction into stiff, ischaemic LV)
- Transient mitral regurgitation murmur (ischaemia of papillary muscles)
- Dyskinetic apex beat (ischaemic segment)
- Bibasal crackles (acute ischaemia-induced diastolic dysfunction → ↑ LVEDP → pulmonary congestion)
All of these resolve when ischaemia resolves (after rest or GTN) — which is what makes them useful confirmatory signs.
The clinical likelihood of CAD is determined by demographics, symptom profile, and cardiovascular risk factors [3].
Updated ESC 2019 Pre-Test Probability (PTP)
The ESC 2019 guidelines updated the classic Diamond-Forrester model, which significantly overestimated PTP of CAD. The new PTP table integrates:
- Age (30–39, 40–49, 50–59, 60–69, 70+)
- Sex (male vs. female)
- Symptom type (typical angina, atypical angina, non-anginal pain, dyspnoea only)
Clinical Likelihood of CAD is further modified by [3]:
| Decreases Likelihood | Increases Likelihood |
|---|---|
| Normal exercise ECG | Risk factors for CVD (dyslipidaemia, DM, HTN, smoking, family history) |
| Coronary calcium score (Agatston) = 0 | Resting ECG changes (ST-segment/T-wave changes) |
| LV dysfunction on echo | |
| Abnormal exercise ECG | |
| Coronary calcium on CT (Agatston > 0) |
The principle:
- If PTP < 5%: CAD unlikely → defer testing [3]
- If PTP 5–15%: low probability → consider testing only if clinical likelihood modifiers increase it [3]
- PTP 15–85%: testing most useful → choose test based on patient factors [1]
- PTP > 85%: CAD can be assumed → proceed directly to invasive coronary angiography (ICA) if symptoms warrant [1]
High Yield Summary
Definition: Stable angina = predictable, exertional chest discomfort from reversible myocardial ischaemia due to fixed coronary stenosis; relieved by rest/GTN within 5 minutes.
Epidemiology: IHD is #1 cause of death globally and in HK. Angina is the first manifestation of IHD in ~50%. 10–20% progress to MI/UA within 12 months.
Risk Factors: Modifiable (smoking, HTN, DM, dyslipidaemia, obesity, sedentary lifestyle) and non-modifiable (age, sex, family history). Exacerbating factors: anaemia, thyrotoxicosis, AS, HCMP, tachyarrhythmias.
Pathophysiology: Fixed coronary stenosis → ↓ coronary flow reserve → O₂ supply-demand mismatch during exertion → subendocardial ischaemia → ischaemic cascade (metabolic changes → diastolic dysfunction → RWMA → ECG changes → angina).
Clinical Features:
- Symptoms: Central, constricting chest discomfort; provoked by 4 Es (exertion, emotion, eating, environment); relieved by rest/GTN in ≤ 5 min; duration 2–10 min; Levine's sign; angina equivalents (dyspnoea, fatigue) in elderly/DM.
- Signs: Often unremarkable. Look for: signs of VHD (AS, HOCM), LV dysfunction (S3/S4, displaced apex), generalised atherosclerosis (carotid bruits, PVD), risk factors (HTN, xanthomas, corneal arcus), exacerbating conditions (anaemia, thyrotoxicosis).
Classification: CCS grading I–IV; ESC 2019 Chronic Coronary Syndromes framework.
Pre-Test Probability: Use ESC 2019 PTP tables + clinical likelihood modifiers to determine need/type of diagnostic testing.
Active Recall - Stable Angina (Definition, Epidemiology, Risk Factors, Anatomy, Etiology, Pathophysiology, Classification, Clinical Features)
[1] Senior notes: Ryan Ho Cardiology.pdf (Section 3.2.1 Stable Angina and Ischaemic Heart Disease, pp. 115–120) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1 Chest Pain / Angina Pectoris, pp. 199–203) [3] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (pp. 9, 27, 76) [4] Senior notes: Ryan Ho Chemical Path.pdf (pp. 46–48 — Lipid Profile, Familial Hypercholesterolaemia) [5] Senior notes: Ryan Ho Endocrine.pdf (pp. 125–131 — Dyslipidaemia, FH, ASCVD Risk Assessment) [6] Senior notes: Ryan Ho Endocrine.pdf (p. 77 — Type 2 DM, Metabolic Syndrome) [7] Senior notes: felixlai.md (Chronic Arterial Insufficiency — Atherosclerosis as commonest cause of PAD)
Differential Diagnosis of Stable Angina
When a patient presents with chest pain on exertion, the primary clinical task is to determine whether this is truly stable angina (i.e., exertional myocardial ischaemia from fixed coronary stenosis) or something else mimicking it. The differential diagnosis is best approached by system, because chest pain has cardiac, pulmonary, vascular, gastrointestinal, musculoskeletal, and psychological aetiologies [1][2][3].
The thinking framework is straightforward: you classify the patient's pain as typical angina, atypical angina, or non-cardiac chest pain [1][2] based on the three ESC criteria (constricting quality, provoked by exertion/emotion, relieved by rest/GTN). Then you systematically consider mimics.
Unlike ACS — where the urgency is ruling out myocardial necrosis — in stable chest pain the stakes are different. You have more time, but you must not:
- Miss a serious alternative (e.g., subacute PE, aortic stenosis, pulmonary hypertension, malignancy)
- Misattribute a benign condition to the heart (e.g., GERD, musculoskeletal pain), leading to unnecessary invasive testing
- Miss exacerbating factors that are worsening angina in someone with known CAD (e.g., new anaemia, thyrotoxicosis)
Systematic Differential Diagnosis by System
The main differentials for stable (chronic/recurrent) chest pain from the lecture slides and senior notes are [1][2]:
| System | Differential | Key Distinguishing Features | Why It Mimics Stable Angina |
|---|---|---|---|
| CVS | Stable ischaemic heart disease | The diagnosis itself — exertional, predictable, relieved by rest/GTN ≤ 5 min [1][2] | — |
| CVS | Aortic valve stenosis (AS) [1][3] | Exertional chest pain + exertional syncope + exertional dyspnoea (classic triad); ejection systolic murmur radiating to carotids; slow-rising pulse | AS causes angina even with normal coronaries → ↑ afterload + LVH → ↑ O₂ demand + ↓ subendocardial perfusion. The pain is genuinely ischaemic but the primary problem is valvular, not coronary |
| CVS | Hypertrophic cardiomyopathy (HCMP/HOCM) [1][3] | Exertional chest pain + syncope; jerky pulse; double apex beat; systolic murmur ↑ with Valsalva; family history of sudden cardiac death | Massive LVH + dynamic LVOT obstruction → supply-demand mismatch. Pain is truly ischaemic but from myopathy, not epicardial CAD |
| CVS | Pulmonary hypertension [1][5] | Progressive exertional dyspnoea > chest pain; loud P2, RV heave, signs of right HF; exertional syncope | ↑ RV wall stress → subendocardial RV ischaemia; ↓ LV filling from RV failure → ↓ coronary perfusion. Pain is exertional and can be mistaken for angina |
| Pulmonary | Subacute/chronic pulmonary embolism [1] | Pleuritic chest pain, exertional dyspnoea, risk factors for VTE (immobilisation, OCP, malignancy); may present insidiously | Recurrent small PEs can cause chronic exertional dyspnoea and chest discomfort mimicking angina. But pain is usually pleuritic (sharp, ↑ with inspiration), not constricting |
| Pulmonary | Malignancy with pleural/chest wall involvement [1] | Progressive, constant or positional pain; weight loss, haemoptysis; history of smoking/malignancy | Chest wall invasion or pleural involvement causes persistent/progressive pain. Unlike angina, it is not clearly linked to exertion |
| System | Differential | Key Distinguishing Features | Why It Mimics Stable Angina |
|---|---|---|---|
| GI | GERD and other oesophageal pathologies [1][2][3] | Retrosternal burning [2]; worse when lying flat, after meals; relieved by antacids/PPI; may be provoked by certain foods; no relation to physical exertion | Oesophagus shares spinal afferent innervation with the heart (T1–T5) → referred pain to the same retrosternal area. Trap: GERD can also respond to GTN (because GTN relaxes oesophageal smooth muscle) → false reassurance that "it's cardiac" |
| MSK | Musculoskeletal chest pain (costochondritis, Tietze syndrome) [1][2][3] | Sharp pain a/w specific movement or with palpation [2]; pain after exertion (not during) [2]; reproducible on chest wall palpation; localised tenderness at costochondral junctions | Pain from costal cartilage inflammation or intercostal muscle strain. Can be confusing because patients may report it "gets worse with activity" — but the timing is different (after, not during, and not relieved by rest within 5 min). The key is reproducibility with palpation |
| Psych | Psychogenic chest pain / Panic disorder [1][6] | Chest pain or discomfort is one of the DSM-5 panic attack criteria [6]; associated with palpitations, sweating, trembling, SOB, paraesthesias, fear of dying; episodes peak in minutes; history of anxiety/depression | Panic attacks cause sympathetic surge → ↑ HR, ↑ BP → ↑ myocardial O₂ demand; also hyperventilation → chest wall muscle spasm. The patient genuinely feels "cardiac" symptoms. Distinguished by: (1) unpredictable, not clearly linked to physical exertion; (2) peak within minutes then resolve; (3) associated with cognitive symptoms (depersonalisation, fear of dying) |
| Neuro | Herpes zoster [1][3] | Dermatomal pain (burning, sharp) that precedes vesicular rash by days; unilateral; pain persists beyond what exertion would explain | Reactivation of VZV in thoracic dorsal root ganglia → neuropathic pain in a dermatomal distribution. Before the rash appears, it is a diagnostic challenge. Look for allodynia/hyperaesthesia in a band-like distribution |
This is the single most important differentiation in any patient presenting with chest pain suggestive of ischaemia [1][2][3][4]:
| Feature | Stable Angina | Acute Coronary Syndrome (ACS) |
|---|---|---|
| Pattern | Occurs only at exertion and relieved by rest or nitrates [2] | Angina at rest, new-onset (≥ CCS II), increasing angina (↑ frequency/↑ duration/↓ threshold), post-infarct angina [4] |
| Duration | < 5–10 min [2] | > 20–30 min [2] |
| Onset | Builds up gradually in proportion to intensity of exertion [2] | Typically takes minutes to develop, may occur at rest or with exertion [2] |
| Response to rest/GTN | Relieved ≤ 5 min [2] | No relief after resting [2] |
| Autonomic features | Typically absent | Diaphoresis, N/V may occur [2] |
| Severity | Usually milder | Typically more severe in ACS than in stable angina [2] |
| ECG | May be normal at rest; ST depression with stress | ST elevation (STEMI), ST depression/T-wave inversion (NSTEMI), or normal/non-diagnostic (UA) |
| Troponin | Normal (no myocardial necrosis) | Elevated in NSTEMI/STEMI; normal in UA |
| Unstable Angina | NSTEMI | STEMI | |
|---|---|---|---|
| Clinical | New onset and severe; at rest or minimal exertion; crescendo pattern [3] | Features of UA + elevated cardiac markers (myocardial necrosis) [3] | Features of MI + ST-segment elevation on 12-lead ECG [3] |
| Troponin | Negative | Positive | Positive |
| ECG | Normal / ST depression / T-wave changes | Persistent ST/T abnormalities [4] | Persistent ST elevation [4] |
When Does Stable Angina Become Unstable?
A patient with known stable angina should be suspected of having transitioned to ACS if any of the following develop [4]:
- Rest angina: pain at rest lasting > 20 min
- New-onset angina: ≥ CCS II severity
- Crescendo angina: ↑ frequency, ↑ duration, or ↓ threshold of previously stable angina (to ≥ CCS III)
- Post-infarct angina: recurrent angina after recent MI
This is a medical emergency — the plaque has likely ruptured/eroded with superimposed thrombosis.
The ESC 2020 table of differential diagnoses lists comprehensive mimics that apply to chest pain in general [3]:
| Cardiac | Pulmonary | Vascular | Gastrointestinal | Orthopaedic | Other |
|---|---|---|---|---|---|
| Myopericarditis | Pulmonary embolism | Aortic dissection | Oesophagitis, reflux, or spasm | Musculoskeletal disorders | Anxiety disorders |
| Cardiomyopathies | (Tension) pneumothorax | Symptomatic aortic aneurysm | Peptic ulcer, gastritis | Chest trauma | Herpes zoster |
| Tachyarrhythmias | Bronchitis, pneumonia | Stroke | Pancreatitis | Muscle injury/inflammation | Anaemia |
| Acute heart failure | Pleuritis | Cholecystitis | Costochondritis | ||
| Hypertensive emergencies | Cervical spine pathologies | ||||
| Aortic valve stenosis | |||||
| Takotsubo syndrome |
Prevalence data from Fruergaard et al. (Eur Heart J 1996) cited in the lecture slides [3]:
- Gastrointestinal: 42%
- Ischaemic heart disease: 31%
- Chest wall syndrome: 28%
- Pericarditis: 4%
- Pleuritis: 2%
- Pulmonary embolism: 2%
- Lung cancer: 1.5%
- Aortic aneurysm: 1%
- Aortic stenosis: 1%
- Herpes zoster: 1%
This is striking — GI causes are actually the most common cause of chest pain in general! But in a cardiology clinic or in a patient with risk factors, IHD is more likely. Context matters.
| Feature | Stable Angina | Pericarditis [7] | Aortic Dissection [7] | PE [7] | GERD | MSK |
|---|---|---|---|---|---|---|
| Quality | Dull, constricting, heavy | Sharp, knife-like [7] | Ripping or tearing [7] | Pleuritic (sharp) | Burning | Sharp, localised |
| Provocation | Exertion, emotion | Inspiration, lying flat | Sudden onset, maximal at onset [2] | Inspiration, cough | Meals, lying flat | Movement, palpation |
| Radiation | L arm, jaw, neck | Trapezius ridge (characteristic) [7] | Back (interscapular) [7] | Usually none | Throat | Along chest wall |
| Relief | Rest, GTN ≤ 5 min | Sitting up, leaning forward | Nothing relieves | Nothing specific | Antacids, PPI | Analgesics, rest |
| Duration | 2–10 min | Hours–days | Sudden, persistent | Persistent | Hours | Variable |
| Associated | ± dyspnoea | Pericardial rub, fever | Pulse deficit, new AR murmur, wide mediastinum | Haemoptysis [7], tachycardia, DVT signs | Regurgitation, dysphagia | Tenderness on palpation |
Key Differentials — Detailed Pathophysiological Explanation
Why this is the trickiest differential:
- Both cause retrosternal discomfort
- Both can occur after meals (angina: ↑ cardiac output to splanchnic bed; GERD: acid reflux)
- GERD can respond to GTN (GTN relaxes lower oesophageal sphincter smooth muscle → ↓ reflux transiently → pain relief → false "positive" GTN test)
- Oesophageal spasm can cause intense, squeezing retrosternal pain that is almost indistinguishable from angina
How to tell them apart: GERD is rarely exertion-related, typically worse lying flat, worse with certain foods/alcohol, associated with regurgitation/waterbrash/dysphagia, and responds to PPIs over days to weeks.
- Costochondritis ("costo" = rib, "chondr" = cartilage, "itis" = inflammation) — inflammation at the costochondral or costosternal joints
- Tietze syndrome: costochondritis + visible swelling at the joint
- Key differentiator: reproducible on palpation. Angina is NEVER reproducible by pressing on the chest wall (because the pain comes from the heart, not the chest wall)
- Timing: MSK pain is often after exertion (not during), and may persist for hours [2]
Panic disorder (Latin: panikos = of the god Pan, who caused sudden terror) [6]:
- Chest pain/discomfort is one of the DSM-5 criteria for panic attacks (along with ≥ 3 of: palpitations, sweating, trembling, SOB, choking sensation, nausea, dizziness, paraesthesias, derealisation, fear of losing control, fear of dying) [6]
- Recurrent, unexpected panic attacks — at least one followed by ≥ 1 month of persistent concern about further attacks [6]
- Important: panic disorder is a diagnosis of exclusion — always rule out cardiac and other organic causes first, especially in patients with cardiovascular risk factors
- Young women with no risk factors who present with episodes of chest tightness + hyperventilation + tingling in hands/feet (respiratory alkalosis from hyperventilation → ↓ ionised Ca²⁺ → paraesthesias) + fear of dying → think panic disorder
- This is technically angina (genuine myocardial ischaemia), but the mechanism is coronary artery spasm rather than fixed stenosis
- Occurs at rest, typically nocturnal/early morning (circadian variation in vasomotor tone)
- ECG during episode shows ST elevation (transmural ischaemia from complete spasm), not ST depression
- More common in East Asian populations (including Hong Kong) — partly due to CYP2C19 polymorphisms affecting endothelial NO metabolism
- Responds to calcium channel blockers and nitrates, NOT beta-blockers (which can worsen spasm by unopposed alpha-receptor-mediated vasoconstriction)
- Typical angina + positive stress test (ST depression) + normal coronary angiogram
- Due to coronary microvascular dysfunction — the small intramural arterioles cannot dilate appropriately
- More common in post-menopausal women
- Now recognised under ESC 2019 as a specific entity requiring targeted evaluation (acetylcholine provocation testing, coronary flow reserve measurement)
Features that RULE IN stable angina:
- Predictable, reproducible exertional chest discomfort
- Constricting/heavy quality
- Relieved by rest/GTN within 5 minutes
- Duration 2–10 minutes
- Associated cardiovascular risk factors
- Abnormal stress test / CT coronary findings
Features that RULE OUT stable angina (suggest alternative diagnosis):
- Sudden onset, maximal at onset → aortic dissection, PE, pneumothorax [2]
- Sharp, stabbing, ↑ with inspiration → pleuritic (PE, pericarditis, pneumothorax) [2]
- Tearing pain radiating to back → aortic dissection [2][7]
- Retrosternal burning → GERD [2]
- Pain reproduced by palpation/movement → musculoskeletal [2]
- Pain after exertion (not during) → musculoskeletal, psychogenic [2]
- Radiation to trapezius ridge → pericarditis [7]
- Associated with haemoptysis → PE [7]
- Dermatomal vesicular rash → herpes zoster
- Panic symptoms (depersonalisation, fear of dying, tingling) → panic disorder [6]
- Pain lasting seconds → rarely cardiac; pain lasting hours → consider MSK, pericarditis, or aortic dissection
High Yield Summary
Differential diagnosis of stable angina is organised by system:
Cardiac: ACS (the most critical distinction — change in pattern/rest pain = emergency), aortic stenosis, HOCM, pericarditis, cardiomyopathies, tachyarrhythmias, Takotsubo
Pulmonary: Chronic/subacute PE, pulmonary hypertension, pleuritis, pneumonia
Vascular: Aortic dissection (sudden, tearing, radiates to back)
GI: GERD (most common non-cardiac cause of chest pain overall — 42%), oesophageal spasm, peptic ulcer, pancreatitis, cholecystitis
MSK: Costochondritis, Tietze, cervical spine pathology — reproduced by palpation
Other: Panic disorder, herpes zoster, anaemia (exacerbating factor)
Key discriminators: Onset pattern, quality, provocation/relief, duration, radiation, associated features, and physical examination findings
Most important distinction: stable angina vs. ACS — the question is always "has this changed?" New onset, rest, crescendo, or post-infarct angina = ACS until proven otherwise.
Active Recall - Differential Diagnosis of Stable Angina
References
[1] Senior notes: Ryan Ho Cardiology.pdf (Section 2.1 Chest Pain, pp. 54–58; Section 3.2.1 Stable Angina, pp. 115–116) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1 Chest Pain, pp. 199–203) [3] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (pp. 15–17 — ACS presentation, differential diagnosis table, Fruergaard prevalence data) [4] Senior notes: Ryan Ho Cardiology.pdf (Section B. Approach to ACS, p. 128 — clinical features distinguishing ACS from stable angina) [5] Senior notes: Ryan Ho Respiratory.pdf (pp. 137–138 — Pulmonary hypertension classification and clinical features) [6] Senior notes: Ryan Ho Psychiatry.pdf (pp. 178–179 — Panic disorder, DSM-5 criteria, differential diagnosis) [7] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (p. 13 — Differential diagnosis of acute pericarditis, PE, aortic dissection; p. 57 — ACS spectrum)
Diagnostic Criteria for Stable Angina
Unlike ACS or MI, stable angina does not have a single set of "diagnostic criteria" like the universal definition of MI. Instead, the diagnosis of stable angina (and its underlying chronic coronary artery disease) rests on a stepwise, probability-based approach that integrates clinical assessment, baseline investigations, and targeted diagnostic testing. Let me walk you through this systematically.
The question is not simply "does this patient have angina?" (that is a clinical/symptom diagnosis). The real question is: "Does this patient have obstructive coronary artery disease causing their symptoms?" — because the answer determines prognosis and the need for revascularisation [1][8].
The diagnostic process therefore has two linked goals:
- Establish the diagnosis of CAD — is there haemodynamically significant coronary stenosis?
- Risk-stratify — what is this patient's annual mortality risk, and does it warrant revascularisation?
Diagnosis based on history alone may be difficult [1][2] — but it is the essential starting point.
Classify the chest pain using the three ESC criteria (covered in prior sections):
| Classification | Criteria Met | Clinical Implication |
|---|---|---|
| Typical angina | All 3: constricting quality, provoked by exertion/emotion, relieved by rest/GTN ≤ 5 min | Highest PTP → may proceed directly to invasive angiography if very high |
| Atypical angina | 2 of 3 | Intermediate PTP → non-invasive diagnostic testing most useful |
| Non-cardiac chest pain | ≤ 1 of 3 | Low PTP → consider non-cardiac causes; testing may not be needed |
Also consider the patient's demographic profile (age, sex) and cardiovascular risk factors [1][8]:
Determinants of clinical likelihood of CAD [8]:
| Decreases Likelihood | Increases Likelihood |
|---|---|
| Normal exercise ECG | Risk factors for CVD (dyslipidaemia, DM, HTN, smoking, family history) |
| Coronary calcium score (Agatston) = 0 | Resting ECG changes (ST-segment/T-wave changes) |
| Abnormal exercise ECG | |
| LV dysfunction suggestive of CAD | |
| Coronary calcium on CT |
Pre-Test Probability — Why It Matters
Different tests have different sensitivity and specificity → suitable for different groups of patients [1].
The test of choice depends on the clinical pre-test probability (PTP) of CAD [1]:
- PTP < 5%: CAD very unlikely → defer testing (more harm than good from false positives)
- PTP 5–15%: Low probability → consider testing only if clinical likelihood modifiers increase it
- PTP 15–85%: This is where diagnostic testing is most useful — both anatomical and functional tests have their greatest discriminating power here
- PTP > 85%: Assume CAD — testing for diagnosis adds little; proceed to risk stratification (consider direct invasive coronary angiography if symptoms warrant)
Most imaging-based testing has sensitivity and specificity of ~85% → if PTP > 85%, then assuming all to be diseased will be superior to performing testing for all individuals; if PTP < 15%, assuming all to be without disease will be superior [1].
Before any diagnostic test, every patient with suspected stable angina needs a baseline workup [1]:
| Investigation | What to Look For | Why |
|---|---|---|
| Blood tests: CBC, ± TFT [1] | Anaemia and thyrotoxicosis may exacerbate IHD [1] | Anaemia → ↓ O₂ supply; thyrotoxicosis → ↑ O₂ demand. Treating these may resolve "angina" without needing cardiac intervention |
| Fasting glucose, HbA1c, ± OGTT [1] | Screen for T2DM | DM is a major risk factor and a "coronary equivalent"; changes management (SGLT2i, GLP-1a have cardioprotective effects) |
| Fasting lipid profile [1] | Screen for dyslipidaemia | Determines need for and intensity of statin therapy; LDL target depends on risk |
| RFT [1] | Baseline renal function (renal dysfunction has negative effect on prognosis of CAD) [1] | eGFR affects choice of investigations (contrast nephrotoxicity) and drug dosing |
| LFT, CK [1] | Baseline before starting statin [1] | Statins can cause transaminitis and myopathy; need baseline for monitoring |
| 12-lead ECG at rest [1][2] | Evidence of previous MI or myocardial damage: pathological Q waves, ST/T changes [1]; evidence of myocardial ischaemia: reversible ST/T changes, esp. a/w symptoms [1]; other evidence of cardiac disease: LVH, pre-excitation, arrhythmias, AF [2] | May provide clues to CAD (old infarct, LVH from HTN), alternative diagnoses (pre-excitation → WPW), or factors that affect test choice (LBBB makes exercise ECG uninterpretable) |
| Resting echocardiography [1] | Determine LVEF: important prognostic factor in stable CAD [1]; Detect underlying structural heart disease, esp. VHD and HCMP [1]; Detect any RWMA as evidence of previous silent infarct [1] | LVEF is the strongest predictor of long-term survival [1]. RWMA at rest = prior infarct. Also identifies non-coronary causes of angina (AS, HOCM). Routine baseline echocardiography recommended for all patients [1] |
| Additional [1] | Resting cardiac MRI as alternative to echo [1]; Ambulatory ECG monitoring if suspicion of arrhythmia or vasospastic angina [1]; CXR if suspicious of pulmonary problems or HF [1][2] | Holter captures transient ST changes in vasospastic angina (nocturnal); CXR for cardiomegaly, pulmonary congestion, or non-cardiac causes |
This is where the PTP guides your test choice. The ESC 2019 guidelines provide a clear framework [8]:
The Two Diagnostic Pathways
There are two main diagnostic pathways [8]:
-
Anatomical pathway — visualise the coronary arteries directly
- CT coronary angiography (CTCA) — first-line anatomical test
- Invasive coronary angiography (ICA) — gold standard but invasive
-
Functional pathway — detect ischaemia (supply-demand mismatch under stress)
- Exercise tolerance test (ETT / exercise ECG)
- Stress imaging: stress echocardiography, stress cardiac MRI, stress myocardial perfusion imaging (SPECT/PET)
The fundamental distinction: Anatomical tests tell you "is there a stenosis?" while functional tests tell you "is the stenosis causing ischaemia?" These are complementary questions — a 60% stenosis visible on CT may or may not be haemodynamically significant.
The ESC 2019 diagnostic approach [8]:
Step 1: Assess symptoms and signs Step 2: Assess comorbidities and quality of life Step 3: Basic testing (ECG, blood tests, echo) Step 4: Assess PTP and clinical likelihood Step 5: Offer diagnostic testing — coronary CTA or testing for ischaemia (imaging testing preferred) — choice of test based on clinical likelihood, patient characteristics and preference, availability, as well as local expertise [8] Step 6: Choose appropriate therapy based on symptoms and event risk [8]
Two main diagnostic pathways from ESC 2019 [8]:
| Coronary CTA preferentially considered if | Functional imaging preferentially considered if | Invasive coronary angiography preferentially considered if |
|---|---|---|
| Low clinical likelihood | High clinical likelihood | High clinical likelihood and severe symptoms inadequately responding to medical therapy |
| Patient characteristics suggest high image quality | Revascularisation likely | Typical angina at low level of exercise and clinical evaluation indicates high risk of events |
| Local expertise and availability | Local expertise and availability | LV dysfunction suggestive of CAD |
| No history of CAD | Viability assessment also required | Uncertain diagnosis on non-invasive testing |
Investigation Modalities — Detailed Explanations
A. Anatomical Tests
What it is: A contrast-enhanced, ECG-gated CT scan that produces high-resolution 3D images of the coronary arteries. "CTA" = CT Angiography — "angio" (Greek: angeion = vessel) + "graphy" (graphein = to write/image) [8][9].
How it works: A large IV bolus of iodinated contrast is injected, and rapid helical CT acquisition is timed to the arterial phase, with ECG gating to minimise cardiac motion artefact. Beta-blockers and GTN are often given pre-scan to slow heart rate and dilate coronaries, improving image quality.
Often used as a screening test to evaluate coronary artery disease before catheterisation [9].
What it shows:
- Coronary artery stenoses (location, severity, length)
- Plaque characterisation (calcified vs. non-calcified/soft plaque)
- Coronary anomalies
- Bypass graft patency
Key findings and interpretation:
| Finding | Interpretation |
|---|---|
| No stenosis (< 50%) | Obstructive CAD effectively excluded (very high NPV ~95–99%) |
| 50–70% stenosis | Indeterminate — needs functional assessment to determine if haemodynamically significant |
| Stenosis > 90% [8] | Highly likely to be haemodynamically significant → consider ICA |
| Non-calcified ("soft") plaque | May indicate higher-risk plaque morphology (more prone to rupture) |
| Heavily calcified arteries | "Blooming artefact" may overestimate stenosis severity — limits diagnostic accuracy |
Advantages: Non-invasive; very high negative predictive value (NPV) → excellent for ruling out CAD in low-to-intermediate PTP patients; fast acquisition.
Limitations: Ionising radiation; IV contrast (nephrotoxicity, allergy); image quality degraded by: high heart rate (need beta-blockers), arrhythmias (esp. AF), heavy calcification, obesity, inability to breath-hold.
What it is: Non-contrast CT used to assess degree of calcification of coronary arteries [9].
Principle: Coronary artery calcification (CAC) is a marker of atherosclerotic plaque burden. The Agatston score quantifies the total calcium in the coronary tree.
Interpretation:
| Agatston Score | Interpretation |
|---|---|
| 0 | Agatston score = 0 → decreases likelihood of CAD [8]; very low probability of significant obstructive CAD (NPV ~95–99% for obstructive disease) |
| 1–99 | Mild atherosclerosis |
| 100–399 | Moderate atherosclerosis; increased ASCVD risk |
| ≥ 400 | Severe atherosclerosis; high probability of significant CAD |
Use: Primarily a screening/risk stratification tool rather than a diagnostic test. Most useful in asymptomatic patients for ASCVD risk reclassification. In symptomatic patients, a score of 0 effectively rules out obstructive CAD (but not vasospastic or microvascular disease).
Calcium Score = 0
A coronary calcium score of zero has excellent NPV for obstructive CAD and is one of the "decreases likelihood" modifiers in the ESC 2019 PTP framework. However, young patients can have significant non-calcified ("soft") plaque with zero calcium — so a zero score does NOT exclude ALL coronary disease, just makes significant obstructive CAD very unlikely.
What it is: The gold standard for defining coronary anatomy. A catheter is threaded (usually via radial or femoral artery) into the coronary ostia, and contrast is injected directly under fluoroscopy.
What it shows: Precise luminal anatomy — location, severity (% stenosis), and extent (1-vessel, 2-vessel, 3-vessel, left main disease) of coronary stenoses.
Indications for invasive coronary angiography for risk stratification [1]:
- Clinically severe angina (≥ CCS III) or high event risk especially if not responding to OMT [1]
- Inconclusive diagnosis on non-invasive testing [1]
- High clinical likelihood and symptoms inadequately responding to medical treatment [8]
- High event risk based on clinical evaluation (e.g., ST-segment depression combined with symptoms at a low workload or systolic dysfunction indicating CAD) [8]
Key findings and interpretation:
| Finding | Prognostic Significance |
|---|---|
| Normal coronaries | Excellent prognosis; consider microvascular/vasospastic angina |
| 1-vessel disease (1VD) | Lower risk |
| 2-vessel disease (2VD) | Intermediate risk |
| 3-vessel disease (3VD) | High risk |
| Left main stem (LMS) disease | Highest risk [1] — mortality of 1VD < 2VD < 3VD < LMS disease [1] |
| Proximal LAD stenosis | Significantly worse prognosis than distal disease |
Adjunct — Fractional Flow Reserve (FFR) / Instantaneous Wave-Free Ratio (iFR):
- Performed during ICA by passing a pressure wire across a stenosis
- FFR: ratio of pressure distal to stenosis vs. pressure proximal, measured during maximal hyperaemia (adenosine-induced)
- FFR ≤ 0.80 = haemodynamically significant → revascularisation indicated
- iFR ≤ 0.89 = equivalent significance (measured at rest, no adenosine needed)
- Why this matters: A 60% stenosis on angiography may or may not be functionally significant — FFR/iFR tells you whether it actually limits flow
Risks: Invasive procedure — vascular access complications (haematoma, pseudoaneurysm), contrast nephropathy, stroke, coronary dissection, MI (~0.1%), death (~0.05%).
B. Functional Tests (Tests for Ischaemia)
What it is: The patient exercises on a treadmill (Bruce protocol) or bicycle ergometer with continuous 12-lead ECG monitoring, BP, and symptom assessment.
Principle: Exercise ↑ HR and BP → ↑ myocardial O₂ demand → if a fixed stenosis exists, it cannot augment supply → subendocardial ischaemia → ST-segment depression on ECG.
Protocol (Bruce Protocol): Incremental stages every 3 minutes with increasing speed and gradient. Target is ≥ 85% of age-predicted maximum HR (220 − age).
Key findings and interpretation:
| Parameter | Positive for Ischaemia | Prognostic Significance |
|---|---|---|
| ST-segment changes | ≥ 1 mm horizontal or downsloping ST depression (measured 60–80 ms after J-point) | ST depression is subendocardial ischaemia; ST elevation (rare in ETT) = transmural ischaemia (severe stenosis or spasm) |
| Exercise capacity | Poor exercise tolerance [1] = poor prognosis | Inability to complete Stage 2 Bruce (< 6.5 METs) is associated with worse outcomes |
| BP response | Drop in systolic BP > 10 mmHg during exercise | Suggests severe LV dysfunction or multivessel disease — the failing heart cannot augment cardiac output |
| Symptoms | Reproduction of typical angina during test | Confirms symptoms are ischaemic |
| Arrhythmias | Exercise-induced ventricular arrhythmias | Poor prognosis |
Duke Treadmill Score (DTS) — integrates exercise duration, ST deviation, and angina index:
- DTS = exercise time (min) − (5 × max ST deviation in mm) − (4 × angina index)
- Angina index: 0 = no angina, 1 = non-limiting angina, 2 = exercise-limiting angina
- DTS ≥ +5: low risk (annual mortality < 1%)
- DTS −10 to +4: intermediate risk
- DTS ≤ −11: high risk (annual mortality ≥ 3%)
Advantages: Widely available, inexpensive, no radiation, provides functional information (exercise capacity, haemodynamic response).
Limitations:
- Sensitivity ~68%, specificity ~77% — moderate at best
- Cannot be interpreted if baseline ECG is abnormal: LBBB, paced rhythm, LVH with strain, digoxin use, WPW, > 1 mm baseline ST depression
- Cannot perform if patient unable to exercise adequately (arthritis, peripheral vascular disease, deconditioning)
- Lower sensitivity in women (more false positives)
When NOT to Use Exercise ECG
Exercise ECG is uninterpretable if baseline ECG has: LBBB, paced rhythm, pre-excitation (WPW), LVH with repolarisation abnormalities, digoxin effect, or > 1 mm resting ST depression. In these patients, you MUST use stress imaging instead.
If the patient cannot exercise (e.g., severe PVD, orthopaedic limitations), use pharmacological stress with imaging.
What it is: Echocardiography performed at rest and during/after stress (exercise or pharmacological with dobutamine).
Principle: Ischaemic myocardium loses contractile function → new or worsening regional wall motion abnormalities (RWMA) appear under stress. This exploits the ischaemic cascade — wall motion abnormalities occur BEFORE ECG changes and symptoms.
What to look for:
| Rest | Stress | Interpretation |
|---|---|---|
| Normal wall motion | Normal wall motion | Normal — no significant ischaemia |
| Normal wall motion | New hypokinesis/akinesis | Inducible ischaemia — haemodynamically significant stenosis in the territory |
| Akinesis at rest | Improves with low-dose dobutamine → worsens at high dose | Viability — hibernating myocardium (stunned but alive) → may benefit from revascularisation |
| Akinesis at rest | Remains akinetic | Scar/infarct — non-viable → revascularisation unlikely to help |
Risk stratification by stress imaging [1]:
- High risk = area of ischaemia > 10% (≥ 3 LV segments for echo) [1]
- Intermediate risk = area of ischaemia 1–10%
- Low risk = no ischaemia [1]
Advantages: No radiation; assesses both wall motion and valve function; good for viability assessment.
Limitations: Operator-dependent; poor acoustic windows in obese/COPD patients; lower sensitivity for single-vessel disease; dobutamine contraindicated in severe arrhythmias.
Indication: screening and diagnosis of coronary artery disease [10].
What it is: Nuclear imaging using radiotracers (Thallium-201 or 99mTc-sestamibi [10]) that are taken up by viable myocardium in proportion to blood flow. Images are acquired at rest and after stress.
Principle — the coronary steal phenomenon [10]:
At rest [10]:
- Partial coronary stenosis limits blood flow to affected myocardium
- Blood flow remains substantial due to collaterals and ischaemia-induced vasodilation
With stress [10]:
- Vessels supplying normal myocardium also dilate
- Blood siphoned to normal myocardium ("steal")
- → ↓↓ perfusion of affected myocardium → appears as "cold spots" in perfusion scan
Interpretation [10]:
- Normal → homogenous perfusion
- Ischaemia → cold spots when under stress (but fills in at rest — "reversible defect")
- Infarct → cold spots at rest + under stress ("fixed defect")
Stress can be induced by [10]:
- Exercise
- Drugs, including vasodilators (e.g., adenosine, dipyridamole) or inotropes (e.g., dobutamine + atropine)
This is important because compensatory vasodilation in response to hypoxaemia means that significant ischaemia will not set in with < 50% stenosis despite presence of structural lesions detected in anatomical imaging. This gives an advantage to MPI as a functional test over anatomical tests such as cardiac MRI, CT coronary angiography or calcium score [10].
Risk stratification [1]:
- High risk = area of ischaemia > 10% on SPECT [1]
Advantages: Quantitative assessment of ischaemic burden; high sensitivity (~85–90%); useful in patients who cannot exercise (pharmacological stress); PET offers superior spatial resolution and attenuation correction.
Limitations: Ionising radiation; longer acquisition time; expensive (especially PET); lower specificity than CTCA for anatomy; attenuation artefacts (e.g., breast tissue in women, diaphragm in obese men).
What it is: Cardiac MRI with pharmacological stress (adenosine for perfusion or dobutamine for wall motion).
Principle: Similar to stress echo and MPI — detects either perfusion defects (adenosine stress CMR) or RWMA (dobutamine stress CMR) indicative of ischaemia.
What it shows:
- First-pass perfusion: Subendocardial hypoperfusion during stress → bright normal myocardium vs. dark ischaemic territory
- Late gadolinium enhancement (LGE): Gadolinium accumulates in fibrotic/scarred tissue → bright signal = infarct scar → viability assessment (< 50% transmural LGE = viable → may benefit from revascularisation)
- Wall motion: Dobutamine stress CMR detects RWMA
Advantages: No radiation; excellent spatial resolution; multiparametric (perfusion + wall motion + viability + anatomy in one scan); best for viability assessment.
Limitations: Expensive; time-consuming; limited availability; claustrophobia; contraindicated in certain implants (non-MRI-conditional pacemakers, metallic devices); gadolinium contraindicated in severe CKD (nephrogenic systemic fibrosis risk).
| Modality | What It Detects | Sensitivity | Specificity | Radiation | Best For |
|---|---|---|---|---|---|
| Exercise ECG | ST changes (ischaemia) | ~68% | ~77% | None | First-line if can exercise + interpretable ECG; prognostic (Duke score) |
| CTCA | Coronary anatomy (stenosis) | ~95–99% | ~64–83% | Yes (low) | Rule out CAD in low-intermediate PTP; very high NPV |
| CT calcium score | Plaque burden | N/A (screening) | N/A | Yes (very low) | Risk stratification; score = 0 ↓ likelihood |
| Stress echo | RWMA (ischaemia) | ~80–85% | ~80–88% | None | Good all-rounder; viability; valve assessment |
| SPECT MPI | Perfusion defects | ~85–90% | ~70–75% | Yes | Quantitative ischaemia burden; pharmacological stress |
| PET MPI | Perfusion defects | ~90–95% | ~85–90% | Yes | Best nuclear test; quantitative flow reserve; obese patients |
| Stress CMR | Perfusion + RWMA + scar | ~86–90% | ~82–86% | None | Viability; comprehensive assessment; good spatial resolution |
| Invasive angiography | Coronary anatomy (gold standard) | ~100% (for anatomy) | ~100% | Yes | Definitive anatomy; FFR for functional significance; high-risk patients |
Once CAD is diagnosed, every patient must be risk-stratified to guide management (medical therapy alone vs. revascularisation) [1]:
Risk stratification for all-cause mortality in all diagnosed CAD patients → guide need of revascularisation [1]:
- High risk: mortality ≥ 3%/year → OMT + invasive coronary angiography ± revascularisation [1]
- Intermediate risk: mortality ≥ 1% but < 3%/year → OMT + consider ICA based on comorbidities and patient preferences [1]
- Low risk: mortality < 1%/year → trial of OMT only [1]
Prognostic factors [1]:
| Factor | Details |
|---|---|
| Clinical evaluation | S/S of HF, pattern and severity of angina [1]; poor prognosis in recent onset or unstable, poor exercise tolerance [1]; clinical risk factors: CKD, PVD, prior MI, current smoking, background HTN [1]; baseline investigations: old infarct on ECG, diabetes, ↑ total cholesterol [1] |
| LVEF | Strongest predictor of long-term survival [1]; LVEF < 50% a/w ↑↑ event risk regardless of severity of ischaemia [1]; baseline echocardiography recommended for all patients [1] |
| Stress testing | Exercise ECG: exercise capacity, BP response, exercise-induced ischaemia, Duke score [1]; Stress imaging: High risk = area of ischaemia > 10% (> 10% for SPECT, ≥ 3 LV segments for echo) [1]; Intermediate risk = area of ischaemia 1–10% [1]; Low risk = no ischaemia [1] |
| Coronary anatomy | Number of vessels: mortality of 1VD < 2VD < 3VD < LMS disease [1]; evaluated by CTCA or ICA |
Roadmap to stable IHD (ESC 2013/2019) [1]:
- Clinical assessment for clinical presentation and risk factors for IHD [1]
- Baseline evaluation: basic blood tests, resting 12-lead ECG, ± echo/cardiac MRI [1]
- Diagnostic evaluation: modality of choice based on pre-test probability of CAD [1]
- Prognostic evaluation: risk of all-cause mortality determines the need of revascularisation after institution of OMT [1]
- Basis: (1) clinical evaluation (2) LVEF (3) stress testing response (4) coronary anatomy [1]
- Management: appropriate management (medical vs revascularisation) based on risk of event [1]
A Note on Troponin in Stable Angina
Troponin should be normal in stable angina. Elevated troponin indicates myocardial necrosis (i.e., MI, not stable angina). If troponin is elevated in someone you thought had stable angina, reclassify as NSTEMI and manage as ACS. This is a critical distinction:
The universal definition of MI requires: detection of rise and/or fall of cardiac biomarkers (preferably cTn) with ≥ 1 value above 99th percentile URL [1] — stable angina, by definition, does NOT meet this criterion.
High Yield Summary
Diagnostic approach to stable angina is stepwise and probability-based:
- Clinical assessment: Classify symptoms (typical / atypical / non-cardiac); assess risk factors → determine PTP
- Baseline investigations: Blood tests (CBC, TFT, HbA1c, lipid, RFT, LFT/CK), resting ECG, resting echocardiography (LVEF is the strongest prognostic predictor)
- Diagnostic testing (PTP 15–85%):
- Anatomical: CTCA (excellent NPV for ruling out CAD in low-intermediate PTP); ICA (gold standard for anatomy + FFR)
- Functional: ETT (first-line if interpretable ECG + can exercise), stress echo, stress MPI (SPECT/PET), stress CMR
- Choice depends on PTP, patient characteristics, local expertise
- Risk stratification: High risk (≥ 3%/y mortality) → OMT + ICA ± revascularisation; Intermediate (1–3%) → OMT + consider ICA; Low (< 1%) → OMT alone
- Key prognostic factors: LVEF (strongest), stress test response (ischaemic burden), coronary anatomy (LMS > 3VD > 2VD > 1VD), clinical factors
Critical points:
- Troponin is NORMAL in stable angina (elevated = MI → reclassify)
- Exercise ECG is uninterpretable with LBBB, pacing, WPW, LVH, digoxin
- Calcium score = 0 has high NPV for obstructive CAD
- MPI uses coronary steal principle: stress causes blood to be "stolen" from diseased territory → cold spots
- FFR ≤ 0.80 during ICA = haemodynamically significant → revascularise
Active Recall - Diagnosis and Investigations for Stable Angina
[1] Senior notes: Ryan Ho Cardiology.pdf (Section 3.2.1 Stable Angina — Evaluation, pp. 115–120) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1 Chest Pain, pp. 199–203) [8] Lecture slides: GC 032. Chest pain on exertion_ischaemic heart disease; angina pectoris.pdf (pp. 27, 45, 79 — Clinical likelihood of CAD, ESC 2019 diagnostic approach, diagnostic pathways) [9] Senior notes: Ryan Ho Diagnostic Radiology.pdf (pp. 43, 57 — CT angiography, cardiac CT, myocardial perfusion imaging) [10] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p. 57 — MPI technique, coronary steal phenomenon, interpretation)
The management of stable angina has two parallel and equally important goals [1]:
- Improve prognosis → reduce the risk of MI and death (prognostic therapy)
- Improve symptoms → relieve angina, improve exercise tolerance and quality of life (symptomatic therapy)
Think of it this way: even if a patient feels perfectly fine on anti-anginal drugs, they still need prognostic medications (aspirin, statin) because the underlying atherosclerosis is a systemic, progressive disease that can kill silently. Conversely, even if prognosis is excellent, a patient who can't walk 200 m without chest pain needs symptomatic relief.
The ESC 2023 framework emphasises thinking in a structured way [11]:
Think 'A.C.S.' at initial assessment → Think antithrombotic therapy → Think revascularisation → Think secondary prevention [11]
For stable angina, the same secondary prevention principles apply — long-term Rx: antithrombotic therapy, lipid-lowering therapy, smoking cessation, cardiac rehabilitation, risk factor management, psychosocial considerations [11].
Step 1: General Measures
These are the foundations of management — no drug or stent can substitute for lifestyle modification and risk factor control [1].
| Measure | Detail | Why |
|---|---|---|
| Stop smoking [1] | Refer to smoking cessation programme; offer NRT, varenicline, or bupropion | Drastic ↓ MI risk after just 1 year of smoking cessation; smoking doubles 5-year mortality [1]. Smoking promotes endothelial dysfunction, ↑ platelet aggregation, ↑ fibrinogen, ↓ HDL |
| Regular exercise [1] | But not beyond point of discomfort [1]; 150 min/week moderate-intensity aerobic exercise | Exercise ↑ coronary flow reserve, ↑ HDL, ↓ BP, ↓ insulin resistance, ↑ endothelial function, promotes collateral development |
| Healthy diet | Mediterranean diet (high fruits/vegetables/olive oil/fish, low saturated fat/red meat/salt) | Mediterranean diet [1] reduces ASCVD events by ~30% (PREDIMED trial). ↓ Sodium → ↓ BP; ↓ saturated fat → ↓ LDL |
| Maintain ideal body weight [1] | BMI target < 25 kg/m²; waist circumference < 94 cm (M), < 80 cm (F) for Asians | Central obesity → insulin resistance → metabolic syndrome → accelerated atherosclerosis |
| Limit alcohol | ≤ 14 units/week, no binge drinking | Excess alcohol → HTN, cardiomyopathy, arrhythmia |
Treat precipitating factors: thyrotoxicosis, anaemia [1]:
| Factor | Action | Why |
|---|---|---|
| Anaemia | Investigate and treat cause (iron deficiency, chronic disease, etc.) | ↓ O₂ carrying capacity → ↓ supply → angina at lower thresholds |
| Thyrotoxicosis | Carbimazole/propylthiouracil + beta-blocker | ↑ HR + ↑ contractility → ↑ O₂ demand; tachycardia also ↓ diastolic filling time |
| Tachyarrhythmia | Rate control (BB, non-DHP CCB) or rhythm control | ↑ HR → ↑ demand + ↓ diastolic coronary filling |
| Uncontrolled HTN | Antihypertensive therapy | ↑ Afterload → ↑ wall tension → ↑ O₂ demand |
Manage risk factors [1]:
| Risk Factor | Target | Agent/Approach |
|---|---|---|
| DM | Aim HbA1c < 7% [1]; consider SGLT2i or GLP-1a [1] | SGLT2 inhibitors (empagliflozin, dapagliflozin) and GLP-1 receptor agonists (semaglutide, liraglutide) have proven cardiovascular benefit — ↓ MACE, ↓ HF hospitalisations |
| HTN | Aim < 140/90 [1] (ESC 2023 recommends < 130/80 if tolerated); use BB if indicated [1] | BB achieves dual goals in stable angina: ↓ BP + anti-anginal |
| Lipids | ↓ LDL to < 1.8 mmol/L [1] (ESC 2019/2023: < 1.4 mmol/L for very high risk + ≥ 50% reduction from baseline) | High dose statins for aggressive ↓ lipid (regardless of serum cholesterol level) → ↓ mortality [1]; add ezetimibe then PCSK9 inhibitor if target not met [12] |
LDL Targets — Know the Numbers
Target LDL-C [12]:
- Very high risk (established ASCVD): < 1.4 mmol/L (ESC 2019/2023) — previously 1.8, now lower
- High risk: < 1.8 mmol/L (or ≥ 50% reduction if baseline 1.8–3.5)
- Low/moderate risk: < 3.0 mmol/L
In stable angina with confirmed CAD, the patient is automatically very high risk → target < 1.4 mmol/L. Statins are recommended in all patients [1].
Step 2: Pharmacological Therapy
A. Prognostic Drugs (Disease-Modifying — Given to ALL Patients)
These drugs reduce MI and death. They treat the underlying atherosclerotic disease process, not the symptoms.
Aspirin is recommended for all patients without contraindications at dose of 75–100 mg daily [1][11].
| Drug | Mechanism | Dose | Notes |
|---|---|---|---|
| Aspirin | Irreversibly inhibits COX-1 → ↓ thromboxane A₂ (TXA₂) synthesis → ↓ platelet aggregation | 75–100 mg daily [11] | Low-dose (75–325 mg daily) prescribed for all patients with CAD indefinitely [1]. Higher doses do not add efficacy but increase bleeding risk. The COX-1 inhibition is permanent for the platelet's 7–10 day lifespan |
| Clopidogrel (Plavix) | Irreversibly blocks P2Y₁₂ ADP receptor on platelets → ↓ ADP-mediated platelet activation | 75 mg daily [11] | Equally/more effective, used as alternative to aspirin if intolerant (↑ cost) [1]. Clopidogrel 75 mg daily when aspirin is not tolerated because of hypersensitivity or GI intolerance [11] |
Important nuance for stable angina specifically [1]:
- Combination therapy (DAPT) is standard of care post-ACS/PCI, but NOT associated with benefit in stable CAD [1] — i.e., do NOT give DAPT routinely for stable angina without prior PCI/ACS
- Newer P2Y₁₂ inhibitors (prasugrel, ticagrelor): not evaluated by studies in stable CAD [1] — these are reserved for ACS
Post-PCI in stable angina: If a patient with stable angina undergoes elective PCI with stenting, DAPT (aspirin + clopidogrel) is given for a defined period (typically 6 months for drug-eluting stent), then aspirin monotherapy indefinitely.
Caveat: clopidogrel interacts with PPI [1] — PPIs inhibit CYP2C19/3A4 activation of clopidogrel prodrug → treatment failure [1]. Use pantoprazole (least CYP2C19 interaction) if PPI is needed.
Why aspirin works in stable angina from first principles: Atherosclerotic plaque, even when "stable," has an endothelial surface that is dysfunctional. Platelets adhere more readily, and even without frank rupture, there is ongoing low-grade platelet activation at the plaque surface. Aspirin suppresses this, reducing the risk of acute thrombosis (which would convert stable angina to ACS/MI).
Low-dose rivaroxaban consideration (2019 COMPASS trial) [11]: For patients with stable CAD at high ischaemic risk but acceptable bleeding risk, consider rivaroxaban 2.5 mg BID added to aspirin — this reduces MACE but increases bleeding. Not yet universally adopted but referenced in ESC 2023 guidelines.
Statins: recommended in all patients [1][12].
| Drug | Mechanism | Dose | Target |
|---|---|---|---|
| Atorvastatin (Lipitor) | Inhibits HMG-CoA reductase → ↓ hepatic cholesterol synthesis → ↑ hepatic LDL receptor expression → ↑ LDL clearance from blood | 40–80 mg (high intensity) | LDL < 1.4 mmol/L and/or ≥ 50% reduction [1][12] |
| Rosuvastatin (Crestor) | Same mechanism | 20–40 mg (high intensity) | Same |
Statin effects beyond lipid-lowering ("pleiotropic effects") [12]:
- Plaque stabilisation — ↑ fibrous cap thickness, ↓ lipid core
- ↓ Inflammation — ↓ CRP, ↓ macrophage activity
- Reversal of endothelial dysfunction — ↑ NO bioavailability
- ↓ Thrombogenicity — ↓ tissue factor, ↓ platelet reactivity
Side effects [12]:
- Myopathy: ranges from myalgia, myopathy, myositis to rhabdomyolysis [12]
- Transaminitis (check LFT at baseline and if symptomatic)
- New-onset DM (slight increase, but cardiovascular benefit far outweighs)
Dosing: generally more conservative in Asians (higher plasma concentration with same dose) [12].
If LDL target not met with maximally tolerated statin [12]:
- Add ezetimibe (blocks intestinal cholesterol absorption via NPC1L1 transporter)
- Add PCSK9 inhibitor (evolocumab or alirocumab — monoclonal antibodies that ↓ PCSK9 → ↑ hepatic LDL receptor recycling → dramatic ↓ LDL)
ACEI/ARB: evidence unclear in stable CAD alone without comorbidities [1].
| Indication | Why |
|---|---|
| When comorbidities are present: DM, HTN, LV HF [1] | ACEI/ARBs: ↓ afterload, ↓ ventricular remodelling, ↓ proteinuria (in DM nephropathy), cardioprotective via ↓ RAAS activation |
| Either one is used (combination a/w ↑ adverse events w/o ↑ benefits) [1] | NEVER combine ACEI + ARB — ↑ hyperkalaemia, ↑ renal failure, no additional CV benefit |
Bottom line: In a stable angina patient who also has DM, HTN, or HFrEF → give ACEI (e.g., ramipril, perindopril) or ARB (e.g., valsartan, losartan). If none of these comorbidities, the evidence does not strongly support routine use.
B. Symptomatic Drugs (Anti-Anginal — For Symptom Relief)
These drugs reduce the frequency and severity of angina episodes. They do NOT modify the disease course or improve survival (with the possible exception of beta-blockers).
First-Line: Beta-Blockers and/or Calcium Channel Blockers
β-blockers: blocks β receptors → ↓ HR, ↓ contractility, ↓ AVN conduction, ↓ ectopic activity [1].
Role: potential prognostic effect renders BB as the 1st-line anti-anginal Tx in patients without contraindications [1]:
- Anti-anginal: clearly effective in ↓ exercise-induced angina, ↑ exercise tolerance, limit ischaemic episodes [1]
- Prognostic Tx: definitely prognostic in post-MI, but effect unclear in patients with stable CAD only [1]
| Property | Detail |
|---|---|
| Mechanism (anti-anginal) | ↓ HR → ↓ O₂ demand (most important); ↓ contractility → ↓ O₂ demand; ↑ diastolic filling time → ↑ coronary perfusion (coronaries fill in diastole). Together, this restores the supply-demand balance |
| Choice | β₁-selective: metoprolol (Betaloc), bisoprolol (Zebeta); α₁β-selective: carvedilol [1]. β₁-selective preferred to avoid bronchospasm from β₂ blockade |
| Dose | Metoprolol (Betaloc) 25–100 mg BD [1]; titrate to resting HR 55–60 bpm |
| Side effects | Precipitates ADHF, bronchospasm, exacerbate PAD, fatigue, sexual dysfunction, hypoglycaemia, hyperkalaemia [1] |
| Contraindications | Bradycardia, AVB, ↓ BP, asthma [1] |
| NOT contraindicated in | HF (actually indicated in HFrEF), COPD (use β₁-selective cautiously), peripheral vascular disease [1] |
Beta-Blockers in Asthma vs. COPD
BBs are absolutely contraindicated in asthma (β₂ blockade → unopposed bronchial smooth muscle constriction → severe bronchospasm → death). However, in COPD, cardioselective β₁-blockers (bisoprolol, metoprolol) can be used cautiously because the bronchospasm component in COPD is less β₂-dependent. This is a classic exam trap.
CCB: block Ca²⁺ channel → ↓ inward current during phase 2 action potential [1].
There are two fundamentally different subclasses, and understanding this is critical for safe prescribing:
| Property | Dihydropyridine (DHP) [1] | Non-DHP [1] |
|---|---|---|
| Examples | Amlodipine, nifedipine, felodipine | Diltiazem, verapamil |
| Main effect | Mainly vascular effects [1] — potent vasodilation | Vascular + cardiac effects [1] — vasodilation + ↓ HR + ↓ contractility |
| Mechanism (anti-anginal) | ↓ PVR → ↓ afterload → ↓ O₂ demand; coronary vasodilation → ↑ supply | ↓ HR → ↓ O₂ demand (similar to BB); ↓ afterload; coronary vasodilation |
| Characteristic | Little cardiac effects → safe in patients with poor cardiac function [1] | ↓ HR → anti-anginal properties (similar to BB) [1] |
| Use | Usually combined with BB [1] (complement each other — BB covers the reflex tachycardia from DHP vasodilation) | As alternative to BB in those who cannot take BB [1]; NOT combined with BB → third-degree heart block [1] |
| Side effects | Flushing, oedema, headache, palpitation [1] (all from vasodilation) | Heart block, bradycardia, heart failure [1] |
| Contraindications | Severe AS, HOCM [1] — ↓ PVR → ↓↓ BP because ↓ SV from fixed obstruction cannot compensate; avoid short-acting nifedipine (reflex tachycardia → ↑ demand) | HFrEF [1] — negative inotropy worsens pump failure; avoid with BB (additive negative chronotropy/dromotropy → complete heart block) |
For ACS/secondary prevention context: Calcium antagonists (diltiazem or verapamil) if contraindications to beta-blockers and no heart failure [11].
How to choose BB vs. CCB:
- BB preferred if: post-MI, HFrEF, tachyarrhythmia — offers both anti-anginal and prognostic benefit
- DHP-CCB + BB combination: excellent first-line combination — BB handles HR and contractility, DHP handles afterload and coronary tone
- Non-DHP CCB alone: only if BB is contraindicated AND patient does NOT have HFrEF
- NEVER: Non-DHP CCB + BB together (risk of complete heart block and severe bradycardia)
Short-acting nitrates: for ALL patients with symptomatic stable CAD [1].
Nitrates: mechanism is arteriovenous dilatation by release of NO [1]:
- ↑ Supply by: (1) dilating coronary arteries (2) redistributing perfusion from epicardial to endocardial sites [1]
- ↓ Demand by: (1) venodilation (major) → ↓ preload (2) arteriodilation (modest) → ↓ afterload [1]
| Formulation | Dose | Onset/Duration | Notes |
|---|---|---|---|
| Sublingual GTN | 0.3–0.6 mg Q5min, max 1.2 mg in 15 min [1] | Onset 1–2 min, lasts 20–30 min | During acute angina episode or prophylactically before exertion [1] |
| GTN spray | 1–2 sprays, up to 3 sprays in 15 min | Acts quicker [1] | Preferred by many patients; longer shelf life than tablets |
| Sublingual isosorbide dinitrate | 5 mg [1] | Slower onset (3–4 min) but effect can last ~1 hour [1] | Alternative |
Important: should rest sitting while taking nitrates [1]:
- Standing → syncope (vasodilation + gravity → postural hypotension)
- Supine → ↑ VR → ↑ preload (defeats the purpose of ↓ preload)
Patient education point: "If you get chest pain during exertion, stop, sit down, and take one GTN under the tongue. Wait 5 minutes. If pain persists, take a second. If still no relief after 3 doses in 15 minutes, call an ambulance — this may be a heart attack."
Second-Line Anti-Anginal Agents
If BB + CCB combination is insufficient, add second-line agents [1]:
Long-acting nitrates: for angina prophylaxis via regular use [1]:
- Indication: usually as 2nd line if BB/CCB are ineffective [1]
- Risk of worsening endothelial dysfunction with long-term use [1]
| Drug | Route | Key Point |
|---|---|---|
| Isosorbide mononitrate | Oral | Mononitrate has more reliable pharmacokinetics [1] than dinitrate (dinitrate requires hepatic conversion to active mononitrate) |
| Isosorbide dinitrate | Oral | Less predictable due to extensive first-pass metabolism |
| GTN patch | Transcutaneous | Convenient but must be removed for nitrate-free interval |
Critical concept — Nitrate tolerance and the nitrate-free interval [1]:
- Regimen: to be used daily with nitrate-free or nitrate-low interval of 8–10 hours [1]
- Why: Continuous nitrate exposure depletes intracellular sulfhydryl groups needed to convert nitrates to NO → ↓ efficacy (tolerance). A drug-free period allows regeneration. Typically, the patch is removed at night or the evening dose is omitted.
| Drug | Mechanism | Indication | Key Notes |
|---|---|---|---|
| Ranolazine | Inhibits late inward Na⁺ channel → ↓ Na⁺/Ca²⁺ exchange → ↓ intracellular Ca²⁺ → ↓ contractility → ↓ angina, ↓ recurrent ischaemia [1] | 2nd/3rd-line add-on | A/w ↑ QTc [1] — avoid with other QT-prolonging drugs; does NOT affect HR or BP (useful when BB not tolerated) |
| Trimetazidine (Vastarel) | ↓ fatty acid oxidation → protect myocardium from ischaemic injury [1] — shifts energy metabolism from FFA to glucose (more O₂-efficient) | 2nd-line add-on | Popular in Asia; no haemodynamic effects |
| Nicorandil | Opens K⁺ channel → arteriovenous + coronary dilatation [1]; also has nitrate-like action (NO donor) | 2nd-line add-on | Unique dual mechanism; can cause oral/GI ulceration |
| Ivabradine | Blocks HCN channel → ↓ Iꜰ → ↓ HR [1] | Used if sinus rhythm ≥ 70 bpm [1] | Should be limited to HF patients as latest trials showed possible ↑ CVD death and non-fatal MI [1] in non-HF; only works in sinus rhythm (useless in AF) |
Ivabradine — A Cautionary Tale
Ivabradine ("I-VA-BRA-dine" — think "I slow the heart rate") selectively blocks the funny current (Iꜰ) in the SA node, slowing HR without affecting contractility or BP. Sounds ideal for angina, but the SIGNIFY trial (2014) showed that in stable CAD patients without HF, ivabradine was associated with increased risk of cardiovascular death and MI in the subgroup with symptomatic angina (CCS ≥ II). It is now primarily reserved for HFrEF with HR ≥ 70 bpm in sinus rhythm (SHIFT trial).
Step 3: Revascularisation
Revascularisation means physically restoring blood flow to ischaemic myocardium — either by PCI (percutaneous coronary intervention) or CABG (coronary artery bypass grafting).
| Group | Purpose | Indication | Benefit |
|---|---|---|---|
| High-risk | Improve prognosis [1] | Annual mortality ≥ 3%; anatomy showing LMS disease, proximal LAD disease, 3VD (especially with LVEF < 50%), large area of ischaemia > 10% | Revascularisation ↓ mortality in these high-risk subgroups |
| Symptomatic despite OMT | Improve symptoms | Persistent symptoms despite adequate trial of guideline-directed medical therapy (GDMT) [11] | Revascularisation relieves angina and improves quality of life, even if it may not improve prognosis in lower-risk patients |
The lecture slide framework [11]:
Consider revascularisation to improve symptoms if: persistent symptoms despite adequate trial of GDMT [11] Potential revascularisation procedure warranted on the basis of assessment of coexisting cardiac and noncardiac factors and patient preferences [11] Perform coronary angiography → Heart team concludes that anatomy and clinical factors indicate revascularisation may improve symptoms → Heart team determines optimal method of revascularisation on the basis of patient preferences, anatomy, other clinical factors, and local resources and expertise [11]
Aim for complete revascularisation [11]. Consider adjunctive tests to guide revascularisation: intravascular imaging, intravascular physiology [11].
The decision is made by a Heart Team (interventional cardiologist + cardiac surgeon + clinical cardiologist) [11]:
| Factor | Favours PCI | Favours CABG |
|---|---|---|
| Anatomy | 1VD or 2VD without proximal LAD; low SYNTAX score (≤ 22) | LMS disease, 3VD, proximal LAD, high SYNTAX score ( > 32) |
| Comorbidities | High surgical risk, frailty, advanced age | DM (CABG has superior long-term outcomes in diabetics with multivessel disease — FREEDOM trial) |
| LVEF | Preserved | Reduced (CABG provides more complete revascularisation + ↓ remodelling) |
| Patient factors | Preference for less invasive; shorter recovery | Willing to accept surgical risk for more durable result |
| Previous | No prior CABG (PCI to native vessels) | Prior PCI with in-stent restenosis; prior CABG (redo CABG or PCI to grafts depending on anatomy) |
"Percutaneous" = through the skin; "coronary" = heart vessels; "intervention" = therapeutic procedure.
- Approach: Catheter inserted via radial (preferred — ↓ bleeding) or femoral artery → wire crosses stenosis → balloon angioplasty ± stent deployment
- Stent types:
- Bare-metal stent (BMS): Rarely used now; higher restenosis rate (~20–30%)
- Drug-eluting stent (DES): Coated with antiproliferative drug (everolimus, zotarolimus) → ↓ neointimal hyperplasia → ↓ restenosis (~5–10%); requires DAPT for 6 months minimum
- Post-PCI antiplatelet: DAPT (aspirin + clopidogrel) for 6 months (DES in stable angina), then aspirin monotherapy indefinitely. Duration may be shortened to 1–3 months if high bleeding risk.
"Bypass" = creates a new route around the obstruction; "grafting" = using a conduit (vein or artery) to bridge the blocked segment.
- Conduits:
- Left internal mammary artery (LIMA) → LAD: Gold standard graft; > 90% patency at 10 years (arterial conduit maintains endothelial function → ↓ atherosclerosis)
- Saphenous vein graft (SVG): Used for non-LAD targets; ~50% patency at 10 years (venous grafts are prone to intimal hyperplasia and accelerated atherosclerosis)
- Radial artery, right IMA (RIMA): Alternative arterial conduits for additional targets
- Post-CABG medications: Aspirin indefinitely; statins; ACEI/ARB if indicated; BB especially if reduced LVEF
| Drug Class | Specific Agents | Indication in Stable Angina | Mechanism | Key C/I | Key S/E |
|---|---|---|---|---|---|
| Aspirin | 75–100 mg daily | ALL patients, indefinitely [1] | Irreversible COX-1 inhibition → ↓ TXA₂ → ↓ platelet aggregation | Active GI bleeding, aspirin allergy, severe bleeding diathesis | GI bleeding, peptic ulcer, rarely bronchospasm (aspirin-sensitive asthma) |
| Clopidogrel | 75 mg daily | Alternative to aspirin if intolerant [1]; DAPT post-PCI | Irreversible P2Y₁₂ receptor blockade → ↓ ADP-mediated platelet activation | Active bleeding; interacts with PPI via CYP2C19 [1] | Bleeding, TTP (rare), rash |
| Statin | Atorvastatin 40–80 mg; Rosuvastatin 20–40 mg | ALL patients [1] | HMG-CoA reductase inhibition → ↓ LDL + pleiotropic effects | Active liver disease, pregnancy | Myopathy, transaminitis, new-onset DM |
| ACEI/ARB | Ramipril, perindopril / Valsartan, losartan | If DM, HTN, HF, CKD [1] | ↓ RAAS → ↓ afterload, ↓ remodelling | Bilateral RAS, pregnancy, angioedema (ACEI), hyperkalaemia | Cough (ACEI), hyperkalaemia, AKI |
| BB | Metoprolol, bisoprolol, carvedilol [1] | 1st-line anti-anginal [1] | ↓ HR, ↓ contractility → ↓ O₂ demand | Asthma, bradycardia, AVB, hypotension [1] | Fatigue, sexual dysfunction, cold extremities, masking hypoglycaemia |
| DHP-CCB | Amlodipine, nifedipine MR, felodipine | Combined with BB; or monotherapy if BB C/I + HFrEF | ↓ PVR → ↓ afterload; coronary vasodilation | Severe AS, HOCM [1]; avoid short-acting nifedipine | Flushing, ankle oedema, headache, palpitation |
| Non-DHP CCB | Diltiazem, verapamil [1][11] | Alternative to BB if C/I and no HF [1][11] | ↓ HR + ↓ afterload + coronary vasodilation | HFrEF [1]; NOT combined with BB [1] | Bradycardia, heart block, constipation (verapamil) |
| Short-acting nitrate | SL GTN 0.3–0.6 mg; GTN spray | ALL symptomatic patients, PRN [1] | NO → venodilation (↓ preload) + coronary dilation | Severe AS/HOCM (↓ preload → ↓↓ CO); concurrent PDE5i (sildenafil → profound hypotension) | Headache, flushing, hypotension |
| Long-acting nitrate | ISMN, ISDN, GTN patch | 2nd-line if BB/CCB insufficient [1] | Same as above, sustained release | Same as above; must have 8–10 h nitrate-free interval [1] | Tolerance, headache |
| Ranolazine | 375–500 mg BD | 2nd/3rd-line add-on | ↓ Late Na⁺ current → ↓ intracellular Ca²⁺ | ↑ QTc [1]; avoid with QT-prolonging drugs | QT prolongation, dizziness, nausea |
| Nicorandil | 10–20 mg BD | 2nd-line add-on | K⁺ channel opener + NO donor | Hypotension | Oral/GI ulceration, headache |
| Trimetazidine | 35 mg BD MR | 2nd-line add-on | Shifts myocardial metabolism from FFA to glucose | Parkinsonism | GI upset, rarely extrapyramidal symptoms |
| Ivabradine | 5–7.5 mg BD | If sinus rhythm ≥ 70 bpm [1]; best reserved for HF patients [1] | ↓ Iꜰ (funny current) → ↓ HR | AF/flutter (useless), severe bradycardia, severe HF (NYHA IV) | Visual disturbances (phosphenes), bradycardia |
High Yield Summary
Management of Stable Angina — The Three Pillars:
1. General Measures: Smoking cessation (most impactful lifestyle change), exercise (not beyond discomfort), Mediterranean diet, weight management, treat exacerbating factors (anaemia, thyrotoxicosis)
2. Pharmacological Therapy:
- Prognostic (ALL patients): Aspirin 75–100 mg daily (or clopidogrel if intolerant) + high-intensity statin (target LDL < 1.4 mmol/L for very high risk) + ACEI/ARB if DM/HTN/HF
- Symptomatic: Short-acting GTN PRN (all patients) → 1st-line BB ± DHP-CCB (or non-DHP CCB if BB C/I and no HF) → 2nd-line: long-acting nitrate, ranolazine, nicorandil, trimetazidine → If still symptomatic despite GDMT → consider revascularisation
- Key drug rules: Never combine non-DHP CCB + BB (→ heart block); BB absolutely C/I in asthma; nitrates need 8–10 h drug-free interval; GTN is C/I with PDE5 inhibitors; clopidogrel interacts with PPIs
3. Revascularisation (PCI or CABG):
- For prognosis: High-risk anatomy (LMS, 3VD, proximal LAD, large ischaemic burden > 10%, LVEF < 50%)
- For symptoms: Persistent angina despite adequate GDMT
- Heart team decision: PCI favoured for simpler anatomy (1–2VD, low SYNTAX); CABG favoured for complex anatomy (3VD, LMS, DM, high SYNTAX)
Active Recall - Management of Stable Angina
[1] Senior notes: Ryan Ho Cardiology.pdf (Section 3.2.1 Stable Angina — Management, pp. 120–124) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1 Chest Pain, pp. 199–203) [11] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (pp. 54–55, 60 — Secondary prevention: antiplatelet, anti-ischaemic therapy, ESC 2023 ACS framework with secondary prevention) [12] Senior notes: Ryan Ho Endocrine.pdf (pp. 128–131 — Statin therapy, LDL targets, management of dyslipidaemia)
When we talk about complications of stable angina, we are really talking about two overlapping categories:
- Complications of the underlying disease (progressive coronary atherosclerosis) — the natural history of stable angina if inadequately treated, including acute plaque events and chronic myocardial consequences
- Complications of treatment — adverse effects from medications, PCI, or CABG
The fundamental concept to grasp is that stable angina is not a static condition. The underlying atherosclerotic plaque is a living, dynamic structure subject to ongoing inflammation, lipid accumulation, and haemodynamic stress. At any point, a stable plaque can become unstable → rupture or erode → acute thrombosis → ACS. This is why prognostic therapy (aspirin, statin) is so critical — it modifies the biology of the plaque itself.
Atherothrombosis is a generalised and progressive process [13]:
Atherosclerosis → Stable angina / Intermittent claudication Atherothrombosis → Unstable angina / MI / Ischaemic stroke-TIA / Critical leg ischaemia → ACS [13]
A. Complications of the Underlying Disease (Natural History of Stable Angina)
Within 12 months of initial diagnosis, 10–20% of patients with stable angina progress to MI or unstable angina (from Part 1 epidemiology, GC 032 lecture slides).
Why does stable angina become unstable?
The key event is plaque disruption — either plaque rupture (fissuring of the fibrous cap) or plaque erosion (denudation of the endothelial surface). This exposes the thrombogenic lipid core and subendothelial collagen to circulating platelets and clotting factors → acute thrombus formation → partial or complete coronary occlusion.
The clinical spectrum of ACS [13][14]:
- Unstable angina (UA): new onset and severe; occurs at rest or minimal exertion; crescendo pattern [14]
- NSTEMI: Clinical features of UA + elevated cardiac markers (myocardial necrosis) [14]
- STEMI: Clinical features of MI + ST-segment elevation on 12-lead ECG [14]
The clinical spectrum spans from [13]:
- Oligo/asymptomatic → Increasing chest pain/symptoms → Persistent chest pain/symptoms → Cardiogenic shock/acute heart failure → Cardiac arrest [13]
Risk factors for plaque instability in a stable angina patient:
- Thin fibrous cap with large lipid-rich necrotic core
- Active plaque inflammation (macrophage-rich shoulder region)
- Inadequate medical therapy (no statin → no plaque stabilisation; no aspirin → no antiplatelet protection)
- Ongoing smoking, uncontrolled DM/HTN, non-adherence
- Haemodynamic stress (e.g., hypertensive crisis, severe anaemia, intercurrent illness)
Recognising the transition — the features that suggest a patient has moved from stable to unstable [1]:
- Angina at rest: prolonged > 20 min
- New-onset angina: ≥ CCS II
- Crescendo angina: ↑ frequency, ↑ duration, ↓ threshold to ≥ CCS III severity
- Post-infarct angina: recurrent angina after recent MI
Red Flag — When Stable Becomes Unstable
Any change in the pattern of previously stable angina is an ACS until proven otherwise. The patient should be treated with an acute pathway: ECG, troponin, anti-ischaemic therapy, dual antiplatelet, anticoagulation, and consideration of early invasive strategy. Do NOT reassure and send home.
2. Myocardial Infarction and Its Complications
If progression to ACS occurs and myocardial necrosis ensues, the patient is now dealing with the full spectrum of MI complications [1]. These are grouped by timing:
| Complication | Mechanism | Presentation | Key Points |
|---|---|---|---|
| Arrhythmias [1][15] | Ischaemic/infarcted myocardium is electrically unstable → acidosis → K⁺ influx + Ca²⁺ efflux → altered conduction and automaticity [1] | VF/pulseless VT (most common cause of sudden death in first hour); bradyarrhythmias; AV block (especially inferior MI → AV nodal ischaemia from RCA) | Coronary artery disease accounts for 85% of cardiac arrests [16]; VF/VT are shockable rhythms; AV block in inferior MI often transient |
| Pump failure [1] | ↓ Systolic function → ↓ coronary perfusion → ↓ supply → more ischaemia; ↓ diastolic function → ↑ pulmonary congestion → hypoxaemia → more ischaemia [1] — a vicious downward spiral | Acute pulmonary oedema, hypotension, cardiogenic shock | Indicates extensive myocardial damage → poor prognosis [1]; Killip classification grades severity |
| Sudden cardiac death | VF within minutes of coronary occlusion (before hospital arrival) | Patient found collapsed/dead | ~50% of MI deaths occur pre-hospital; this is why public-access defibrillators and bystander CPR are critical |
Assessing for complications on physical examination [13]:
| Complication | Mechanism | Presentation | Key Points |
|---|---|---|---|
| IV septal rupture [1] | Rupture at margin of necrotic and non-necrotic myocardium [1]; usually complicates anterior MI (LAD) [1] | L-to-R shunting → sudden haemodynamic deterioration + new onset pansystolic murmur (to RLSB) [1]; usually develops RV failure [1] | Occurs in ~0.1% of MI, usually ~24h but may occur up to 2 weeks [1]; Dx: echo, RH catheterisation |
| LV free wall rupture [1] | Necrotic myocardial wall ruptures under systolic pressure | Complete rupture: blood into pericardial cavity → cardiac tamponade → sudden profound RHF + shock → PEA and death [1]; Incomplete: persistent pleuritic chest pain (sealed by pericardium/thrombus) [1] | < 1%, 50% occurs ≤ 5 days, > 90% occurs ≤ 2 weeks [1]; emergency pericardiocentesis → surgical repair |
| Papillary muscle rupture → acute MR [15] | Ischaemic necrosis of papillary muscle (usually posteromedial, supplied by single artery — PDA from RCA) → complicates inferior MI [15] | Sudden severe pulmonary oedema + new loud pansystolic murmur (at apex, radiating to axilla) + haemodynamic collapse | D/dx from VSD (different murmur location and findings on echo); emergency surgical repair |
| Peri-infarction pericarditis (PIP) [1] | Transmural infarction → inflammation reaches epicardial surface → pericardial irritation | Development of a different pain: positional, sharp pleuritic, esp at trapezius ridge [1]; pericardial rub (diagnostic) [1] | Common on 2nd/3rd day post-MI, 1.2% of MI patients [1]; Mx: paracetamol ± aspirin; avoid NSAIDs/steroids 7–10 days after acute MI → ↑ risk of aneurysm/rupture [1] |
| Post-MI pericardial effusion [1] | Inflammatory exudate from pericarditis; or haemopericardium from incomplete rupture | Usually asymptomatic, detected incidentally [1] | ~1/3 of acute STEMI [1]; drain only if tamponade |
| Systemic embolism [1] | Ventricular thrombus due to wall motion abnormality/aneurysm [1]; atrial thrombus from AF | Stroke, ischaemic limb… classically occurring 1–3 weeks after MI [1] | Risk of embolisation in non-anticoagulated documented LV thrombus is 10–15% [1]; most common in anterior STEMI, LAD infarct, large infarct with EF < 30% [1] |
AMI complications listed in lecture slides [15]:
- Heart failure
- Arrhythmias
- VSD (anterior MI)
- Mitral regurgitation complicating papillary muscle dysfunction (inferior MI)
- Pericarditis
| Complication | Mechanism | Presentation | Key Points |
|---|---|---|---|
| Ventricular remodelling and chronic HF [1] | Infarct zone → fibrotic scar → non-contractile → remaining viable myocardium compensates by hypertrophy and dilatation (Frank-Starling) → over time, the ventricle dilates progressively → systolic dysfunction | Progressive dyspnoea, exercise intolerance, peripheral oedema, fluid retention | LVEF < 50% a/w ↑↑ event risk [1]; ACEI/ARB + BB + MRA + SGLT2i are the pillars of HFrEF therapy to slow remodelling |
| Ventricular aneurysm [1] | 70–85% at anterior or apical walls → due to LAD total occlusion w/o collateral [1]; thin, scarred, dyskinetic wall segment | Acute decompensated HF with angina (wasted mechanical energy) [1]; ventricular arrhythmia [1]; systemic embolisation (mural thrombus > 50%) [1] | Dx: ECG: persistent ↑ ST and Q despite reperfusion [1]; CXR: unusual bulge from cardiac silhouette [1]; echo is diagnostic. Mx: anticoagulation if mural thrombus; aneurysmectomy + CABG if intractable arrhythmia/HF |
| Dressler syndrome (post-cardiac injury syndrome) [1] | Probably autoimmunity due to release of cardiac antigens into pericardial space [1] | Persistent fever, pericarditis, pleurisy weeks to months post-MI [1]; ↑ inflammatory markers (WCC, CRP/ESR) ± pericardial/pleural effusion [1] | Mx: high-dose aspirin/NSAID (indomethacin 25–50 mg TDS), colchicine ± steroid [1] |
| Recurrent angina / Chronic ischaemia | Residual stenoses in other territories; progression of atherosclerosis; incomplete revascularisation | Return of exertional chest pain | Stress testing 2–3 weeks post-MI to assess residual ischaemia [1]; may need further revascularisation |
Even without a discrete MI, chronic repetitive subendocardial ischaemia from stable angina can lead to progressive myocardial dysfunction over years:
- Hibernating myocardium: Chronically underperfused but viable myocardium that has "downregulated" its contractile function to reduce O₂ demand — a survival adaptation. This is potentially reversible with revascularisation.
- Stunned myocardium: Myocardium that remains dysfunctional after a transient ischaemic episode despite restoration of flow — recovers spontaneously over days to weeks.
- Myocardial fibrosis: Repeated ischaemia-reperfusion cycles → progressive interstitial fibrosis → diastolic then systolic dysfunction → ischaemic cardiomyopathy → HFrEF.
Why this matters: A patient with stable angina, 3VD, and LVEF 35% may have significant hibernating myocardium. Viability assessment (stress echo with dobutamine, cardiac MRI with LGE) determines if revascularisation can recover function.
Chronic CAD is the substrate for arrhythmias even outside the acute MI setting:
| Arrhythmia | Mechanism | Clinical Significance |
|---|---|---|
| AF | Left atrial dilatation from ↑ LVEDP (diastolic dysfunction) + atrial ischaemia | ↑ Stroke risk; ↑ HR → worsens angina; requires anticoagulation if CHA₂DS₂-VASc ≥ 2 (men) or ≥ 3 (women) |
| VT/VF | Scar-related re-entry circuits from prior MI or chronic ischaemia | Risk of sudden cardiac death; consider ICD if LVEF ≤ 35% despite ≥ 3 months OMT (SCD-HeFT criteria) |
| Conduction disease | Fibrosis of conduction system from chronic ischaemia (LAD supplies proximal bundle of His and left anterior fascicle; RCA supplies AV node) | Bundle branch blocks, fascicular blocks, AV block; may need pacing |
Because atherosclerosis is a systemic disease, a patient with coronary atherosclerosis is at risk for atherosclerotic events in all vascular beds:
| Territory | Complication | Clinical Significance |
|---|---|---|
| Carotid/cerebral | Ischaemic stroke, TIA | Stable angina → intermittent claudication (atherosclerosis); atherothrombosis → unstable angina / MI / ischaemic stroke-TIA / critical leg ischaemia [13] |
| Aortic | Abdominal aortic aneurysm (AAA) | Screen with USS in men ≥ 65 with risk factors |
| Lower limb | Peripheral arterial disease (PAD), intermittent claudication, critical limb ischaemia | PAD: carotid bruits, peripheral pulses, peripheral skin discolouration or hair loss [13]; shares the same risk factor management as CAD |
| Renal | Renovascular disease, ischaemic nephropathy | May contribute to resistant hypertension; atherosclerotic renal artery stenosis |
B. Complications of Treatment
Mortality < 0.5% [1].
| Category | Complication | Mechanism and Detail |
|---|---|---|
| Coronary artery related [1] | Dissection and abrupt closure (rare with routine stenting) [1]; intramural haematoma (6.7%) [1]; perforation (0.2–0.6%) [1]; side branch occlusion (up to 19%) [1] | ALL can lead to myocardial ischaemia or infarction [1]; consider emergency CABG if haemodynamic compromise, ongoing ischaemia, or threatened occlusion with significant myocardium at risk [1] |
| Stent-related [1] | Stent thrombosis (1–2%): acute event, usually presents with severe STEMI or cardiac death [1]; due to thrombus at exposed stent surface before endothelialisation [1]; majority occurs < 30 days [1] | Prevention: DAPT (aspirin + clopidogrel) until endothelialisation [1] |
| In-stent restenosis (ISR): chronic event, usually presents with recurrent stable angina [1]; due to intimal proliferation leading to gradual re-stenosis [1]; usually ≥ 6–9 months after stenting [1] | Prevention: drug-eluting stent (DES) to prevent intimal proliferation [1] | |
| Others [1] | Access-related: bleeding, infection, atheroembolism [1]; other cardiac: arrhythmia, bradycardia [1]; systemic: AKI (contrast, haemodynamic instability, atheroembolism), stroke (mural thrombus), bacteraemia [1] | Radial access ↓ vascular complications vs. femoral; hydration ↓ contrast nephropathy risk |
Stent Thrombosis vs. In-Stent Restenosis — Critical Distinction
| Feature | Stent Thrombosis | In-Stent Restenosis |
|---|---|---|
| Timing | Acute to late (majority < 30 days) | Chronic (≥ 6–9 months) |
| Mechanism | Thrombus on exposed stent before endothelialisation | Neointimal hyperplasia (smooth muscle cell proliferation) |
| Presentation | Acute STEMI or sudden death — medical emergency | Recurrent stable angina — gradual return of symptoms |
| Prevention | DAPT | Drug-eluting stent (DES) |
| Treatment | Emergency PCI + thrombectomy | Repeat PCI (drug-coated balloon or new DES) |
This is a very high-yield exam distinction.
| Complication | Mechanism | Note |
|---|---|---|
| Perioperative mortality | ~1–2% for elective CABG; higher in emergency, elderly, reduced LVEF | Risk calculated by EuroSCORE or STS risk models |
| Perioperative MI | Graft occlusion, incomplete revascularisation, atheroembolism from aortic manipulation | Dx: ↑ cTn > 10× 99th URL + new Q waves or angiographic graft occlusion (Type 5 MI) |
| Stroke | Atheroembolism from aortic cross-clamping; hypoperfusion during bypass | ~1–2%; risk ↑ with age, aortic atherosclerosis, AF |
| AF | Post-operative inflammation, pericardial irritation, autonomic imbalance | ~30–40% of patients; usually self-limiting but ↑ stroke risk → anticoagulate |
| Mediastinitis / sternal wound infection | Surgical site infection; risk ↑ in DM, obesity, bilateral IMA harvest | Serious complication with high morbidity; requires IV antibiotics ± surgical debridement |
| Graft failure | SVG: intimal hyperplasia → atherosclerosis → occlusion (50% at 10 years); LIMA: > 90% patent at 10 years | Long-term aspirin + statin mandatory; LIMA to LAD is gold standard |
| Post-pericardiotomy syndrome | Similar to Dressler syndrome — autoimmune pericarditis post-cardiac surgery | Fever, pericarditis, pleurisy weeks post-surgery; Mx: NSAIDs + colchicine |
| Neurocognitive decline | Microemboli during cardiopulmonary bypass; hypothermic brain injury | Subtle cognitive changes in up to 50%; usually mild and improve over months |
| Drug | Complication | Mechanism | Prevention/Management |
|---|---|---|---|
| Aspirin | GI bleeding, peptic ulcer, aspirin-sensitive asthma | COX-1 inhibition → ↓ gastroprotective prostaglandins → mucosal injury; leukotriene shunting → bronchospasm | PPI prophylaxis in high-risk (age > 65, h/o peptic ulcer, concurrent anticoagulant); switch to clopidogrel if true aspirin allergy |
| Statin | Myopathy (myalgia → rhabdomyolysis), hepatotoxicity, new-onset DM | Myopathy: mitochondrial dysfunction in skeletal muscle (mechanism debated); DM: impaired insulin signalling | Monitor CK/LFT; switch to hydrophilic statin (pravastatin, rosuvastatin) if myopathy; CV benefit far outweighs DM risk |
| Beta-blocker | Bronchospasm, severe bradycardia, masking of hypoglycaemia, fatigue, depression, erectile dysfunction | β₂ blockade → bronchial constriction; β₁ blockade → ↓ HR excessively; β blockade suppresses sympathetic hypoglycaemia awareness | Use β₁-selective agents; avoid in asthma; warn diabetic patients; slow up-titration |
| CCB (non-DHP) | Heart block, HF exacerbation | Negative chronotropy + dromotropy + inotropy | Avoid with BB (risk of complete heart block); avoid in HFrEF |
| CCB (DHP) | Peripheral oedema, reflex tachycardia, flushing | Arteriolar vasodilation → capillary hydrostatic pressure ↑ → oedema (not fluid overload); baroreceptor reflex → ↑ HR | Combine with BB to blunt reflex tachycardia; use long-acting formulations |
| Nitrates | Tolerance, headache, hypotension, syncope | Nitrate tolerance from sulfhydryl depletion; vasodilation → ↓ BP | 8–10 h nitrate-free interval; take sitting (not standing/supine); absolute C/I with PDE5 inhibitors (sildenafil/tadalafil) → profound refractory hypotension |
| ACEI | Dry cough, angioedema, hyperkalaemia, AKI | ↓ Bradykinin degradation → cough/angioedema; ↓ aldosterone → ↑ K⁺; ↓ efferent arteriolar tone → ↓ GFR | Switch to ARB for cough; stop for angioedema (ARB with caution); monitor K⁺ and creatinine |
The overall annual mortality rate for stable angina is approximately 1–3% per year, but this varies enormously depending on risk factors [1]:
| Risk Category | Annual Mortality | Determinants |
|---|---|---|
| Low risk | < 1%/year [1] | 1VD, preserved LVEF, normal stress test, good exercise capacity |
| Intermediate risk | 1–3%/year [1] | 2VD, borderline LVEF, moderate ischaemic burden |
| High risk | ≥ 3%/year [1] | 3VD, LMS disease [1], LVEF < 50%, large ischaemic burden > 10%, poor exercise tolerance, HF symptoms |
Prognostic factors (recap) [1]:
- LVEF: strongest predictor of long-term survival [1]
- Coronary anatomy: mortality of 1VD < 2VD < 3VD < LMS disease [1]
- Clinical risk factors: CKD, PVD, prior MI, current smoking, background HTN [1]
High Yield Summary
Complications of Stable Angina — Organised Framework:
1. Progression to ACS (most feared): 10–20% of stable angina patients progress to MI/UA within 12 months. Plaque rupture/erosion → thrombosis → UA/NSTEMI/STEMI. Red flags: rest angina, new-onset, crescendo, post-infarct angina.
2. MI complications (if progression occurs):
- Acute: arrhythmias (VF/VT — most common cause of death), pump failure (cardiogenic shock), sudden death
- Subacute: mechanical complications (VSD in anterior MI, papillary muscle rupture/MR in inferior MI, free wall rupture → tamponade), pericarditis, systemic embolism
- Chronic: ventricular remodelling → HFrEF, ventricular aneurysm, Dressler syndrome, recurrent angina
3. Chronic consequences of stable CAD:
- Ischaemic cardiomyopathy (hibernating/stunned myocardium → progressive HF)
- Arrhythmias (AF, VT/VF from scar re-entry)
- Systemic atherosclerotic events (stroke, PAD, AAA)
4. Treatment complications:
- PCI: stent thrombosis (acute STEMI, < 30 days, prevented by DAPT) vs. in-stent restenosis (gradual angina, ≥ 6–9 months, prevented by DES)
- CABG: perioperative stroke, AF, mediastinitis, graft failure
- Medications: aspirin → GI bleeding; statin → myopathy; BB → bronchospasm; CCB → heart block (non-DHP + BB); nitrates → tolerance, C/I with PDE5i; ACEI → cough/angioedema
Active Recall - Complications of Stable Angina
[1] Senior notes: Ryan Ho Cardiology.pdf (Sections 3.2.1 Stable Angina pp. 115–124; Complications of MI pp. 139–144) [13] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (pp. 7, 11, 19 — Atherothrombosis as progressive process; clinical spectrum of ACS; physical examination for complications) [14] Lecture slides: GC 028. Accelerating chest pain_Acute coronary (1).pdf (p. 15 — ACS principal presentation: UA, NSTEMI, STEMI) [15] Lecture slides: GC 088. Sudden Severe Chest Pain.pdf (pp. 4, 56 — ACS as manifestation of atherothrombosis; AMI complications) [16] Senior notes: Ryan Ho Critical Care.pdf (p. 28 — Cardiac arrest: CAD accounts for 85%, shockable rhythms VF/pulseless VT)
High Yield Summary
Definition: Stable angina = predictable, exertional chest discomfort from reversible myocardial ischaemia due to fixed coronary stenosis; relieved by rest/GTN within 5 minutes.
Epidemiology: IHD is #1 cause of death globally and in HK. Angina is the first manifestation of IHD in ~50%. 10–20% progress to MI/UA within 12 months.
Risk Factors: Modifiable (smoking, HTN, DM, dyslipidaemia, obesity, sedentary lifestyle) and non-modifiable (age, sex, family history). Exacerbating factors: anaemia, thyrotoxicosis, AS, HCMP, tachyarrhythmias.
Pathophysiology: Fixed coronary stenosis → ↓ coronary flow reserve → O₂ supply-demand mismatch during exertion → subendocardial ischaemia → ischaemic cascade (metabolic changes → diastolic dysfunction → RWMA → ECG changes → angina).
Clinical Features:
- Symptoms: Central, constricting chest discomfort; provoked by 4 Es (exertion, emotion, eating, environment); relieved by rest/GTN in ≤ 5 min; duration 2–10 min; Levine's sign; angina equivalents (dyspnoea, fatigue) in elderly/DM.
- Signs: Often unremarkable. Look for: signs of VHD (AS, HOCM), LV dysfunction (S3/S4, displaced apex), generalised atherosclerosis (carotid bruits, PVD), risk factors (HTN, xanthomas, corneal arcus), exacerbating conditions (anaemia, thyrotoxicosis).
Classification: CCS grading I–IV; ESC 2019 Chronic Coronary Syndromes framework.
Pre-Test Probability: Use ESC 2019 PTP tables + clinical likelihood modifiers to determine need/type of diagnostic testing.
High Yield Summary
Differential diagnosis of stable angina is organised by system:
Cardiac: ACS (the most critical distinction — change in pattern/rest pain = emergency), aortic stenosis, HOCM, pericarditis, cardiomyopathies, tachyarrhythmias, Takotsubo
Pulmonary: Chronic/subacute PE, pulmonary hypertension, pleuritis, pneumonia
Vascular: Aortic dissection (sudden, tearing, radiates to back)
GI: GERD (most common non-cardiac cause of chest pain overall — 42%), oesophageal spasm, peptic ulcer, pancreatitis, cholecystitis
MSK: Costochondritis, Tietze, cervical spine pathology — reproduced by palpation
Other: Panic disorder, herpes zoster, anaemia (exacerbating factor)
Key discriminators: Onset pattern, quality, provocation/relief, duration, radiation, associated features, and physical examination findings
Most important distinction: stable angina vs. ACS — the question is always "has this changed?" New onset, rest, crescendo, or post-infarct angina = ACS until proven otherwise.
High Yield Summary
Diagnostic approach to stable angina is stepwise and probability-based:
- Clinical assessment: Classify symptoms (typical / atypical / non-cardiac); assess risk factors → determine PTP
- Baseline investigations: Blood tests (CBC, TFT, HbA1c, lipid, RFT, LFT/CK), resting ECG, resting echocardiography (LVEF is the strongest prognostic predictor)
- Diagnostic testing (PTP 15–85%):
- Anatomical: CTCA (excellent NPV for ruling out CAD in low-intermediate PTP); ICA (gold standard for anatomy + FFR)
- Functional: ETT (first-line if interpretable ECG + can exercise), stress echo, stress MPI (SPECT/PET), stress CMR
- Choice depends on PTP, patient characteristics, local expertise
- Risk stratification: High risk (≥ 3%/y mortality) → OMT + ICA ± revascularisation; Intermediate (1–3%) → OMT + consider ICA; Low (< 1%) → OMT alone
- Key prognostic factors: LVEF (strongest), stress test response (ischaemic burden), coronary anatomy (LMS > 3VD > 2VD > 1VD), clinical factors
Critical points:
- Troponin is NORMAL in stable angina (elevated = MI → reclassify)
- Exercise ECG is uninterpretable with LBBB, pacing, WPW, LVH, digoxin
- Calcium score = 0 has high NPV for obstructive CAD
- MPI uses coronary steal principle: stress causes blood to be "stolen" from diseased territory → cold spots
- FFR ≤ 0.80 during ICA = haemodynamically significant → revascularise
High Yield Summary
Management of Stable Angina — The Three Pillars:
1. General Measures: Smoking cessation (most impactful lifestyle change), exercise (not beyond discomfort), Mediterranean diet, weight management, treat exacerbating factors (anaemia, thyrotoxicosis)
2. Pharmacological Therapy:
- Prognostic (ALL patients): Aspirin 75–100 mg daily (or clopidogrel if intolerant) + high-intensity statin (target LDL < 1.4 mmol/L for very high risk) + ACEI/ARB if DM/HTN/HF
- Symptomatic: Short-acting GTN PRN (all patients) → 1st-line BB ± DHP-CCB (or non-DHP CCB if BB C/I and no HF) → 2nd-line: long-acting nitrate, ranolazine, nicorandil, trimetazidine → If still symptomatic despite GDMT → consider revascularisation
- Key drug rules: Never combine non-DHP CCB + BB (→ heart block); BB absolutely C/I in asthma; nitrates need 8–10 h drug-free interval; GTN is C/I with PDE5 inhibitors; clopidogrel interacts with PPIs
3. Revascularisation (PCI or CABG):
- For prognosis: High-risk anatomy (LMS, 3VD, proximal LAD, large ischaemic burden > 10%, LVEF < 50%)
- For symptoms: Persistent angina despite adequate GDMT
- Heart team decision: PCI favoured for simpler anatomy (1–2VD, low SYNTAX); CABG favoured for complex anatomy (3VD, LMS, DM, high SYNTAX)
High Yield Summary
Complications of Stable Angina — Organised Framework:
1. Progression to ACS (most feared): 10–20% of stable angina patients progress to MI/UA within 12 months. Plaque rupture/erosion → thrombosis → UA/NSTEMI/STEMI. Red flags: rest angina, new-onset, crescendo, post-infarct angina.
2. MI complications (if progression occurs):
- Acute: arrhythmias (VF/VT — most common cause of death), pump failure (cardiogenic shock), sudden death
- Subacute: mechanical complications (VSD in anterior MI, papillary muscle rupture/MR in inferior MI, free wall rupture → tamponade), pericarditis, systemic embolism
- Chronic: ventricular remodelling → HFrEF, ventricular aneurysm, Dressler syndrome, recurrent angina
3. Chronic consequences of stable CAD:
- Ischaemic cardiomyopathy (hibernating/stunned myocardium → progressive HF)
- Arrhythmias (AF, VT/VF from scar re-entry)
- Systemic atherosclerotic events (stroke, PAD, AAA)
4. Treatment complications:
- PCI: stent thrombosis (acute STEMI, < 30 days, prevented by DAPT) vs. in-stent restenosis (gradual angina, ≥ 6–9 months, prevented by DES)
- CABG: perioperative stroke, AF, mediastinitis, graft failure
- Medications: aspirin → GI bleeding; statin → myopathy; BB → bronchospasm; CCB → heart block (non-DHP + BB); nitrates → tolerance, C/I with PDE5i; ACEI → cough/angioedema
Nstemi
Non-ST-elevation myocardial infarction (NSTEMI) is an acute coronary syndrome characterized by myocardial necrosis with elevated cardiac biomarkers but without persistent ST-segment elevation on electrocardiography.
Stemi
ST-elevation myocardial infarction (STEMI) is an acute complete coronary artery occlusion causing transmural myocardial ischemia, identified by persistent ST-segment elevation on electrocardiogram and requiring emergent reperfusion therapy.