Angina Pectoris

Overview – Angina Pectoris

Angina pectoris refers to chest pain caused by transient myocardial ischaemia due to reduced coronary perfusion relative to myocardial oxygen demand. It is most commonly associated with coronary artery disease—particularly atherosclerosis—but may also result from vasospasm or embolism. Recognising and classifying angina is crucial, as certain forms (such as unstable angina) are early indicators of an impending myocardial infarction.

Definition

  • Angina pectoris is chest pain or discomfort due to transient myocardial ischaemia without myocardial infarction.

Aetiology

  • Decreased myocardial perfusion (relative to demand), most often due to:
  • Exacerbating conditions:
    • Left ventricular hypertrophy
    • Tachycardia
    • Hypoxia
    • Coronary arteritis (e.g. systemic lupus erythematosus)

Pathogenesis

  • Angina is typically a late manifestation of coronary artery disease, often signalling >70% vessel occlusion.
  • The core mechanism is insufficient coronary perfusion relative to myocardial demand.

Types of Angina

Stable Angina

  • Caused by: Fixed atherosclerotic obstruction
  • Symptoms: Chest pain during exertion → resolves with rest
  • No plaque rupture

Variant (Prinzmetal) Angina

  • Caused by: Transient coronary vasospasm, possibly without atheroma
  • Symptoms: Occurs at rest, not exertion-related

Unstable Angina

  • Caused by: Unstable atherosclerotic plaque, with/without thrombus
  • Symptoms: Prolonged or worsening chest pain at rest
  • Red flag for imminent myocardial infarction

Silent Ischaemia

  • Ischaemia without chest pain, often in patients with diabetic neuropathy or B12 deficiency
  • Symptoms may include: nausea, diaphoresis, vomiting
  • ECG may reveal abnormalities despite lack of pain

Clinical Features

Characteristic Pain

  • <15 minutes of central, crushing chest pain
  • Often radiates to arms, neck, jaw
  • Pain triggered by:
    • Exertion (Stable)
    • Rest (Prinzmetal/Unstable)
  • Associated symptoms:
    • Dyspnoea
    • Sense of impending doom

Signs

  • Sympathetic activation → Diaphoresis
  • Hypotension → Cool, clammy skin; thready pulse
  • Pulmonary congestion → Elevated JVP, dyspnoea

Investigations

1. Resting ECG

  • During attack: ST-depression, T-wave inversion
  • May be normal between episodes
  • Pathological Q-waves suggest previous infarction
Angina Pectoris ECG

2. Cardiac Stress Test + ECG

  • ST-depression indicates underlying coronary artery disease

3. Stress Echocardiography

  • Evaluates ventricular wall motion abnormalities

4. Coronary Angiography

  • Maps coronary anatomy prior to intervention (e.g. angioplasty)

5. Myocardial Perfusion Scans

  • Nuclear imaging used when stress testing is inconclusive

Management

Lifestyle & Risk Factor Modification

  • Smoking cessation
  • Weight loss
  • Management of:
    • Hypertension
    • Diabetes mellitus
    • Hyperlipidaemia

Medical Therapy

1. Anti-Anginal Agents

  • Nitrates (e.g. GTN) – Vasodilation to improve perfusion
  • β-Blockers (e.g. Metoprolol) – ↓Heart rate and myocardial workload
  • Calcium Channel Blockers (e.g. Verapamil, Diltiazem) – ↓Afterload and vasospasm

2. Antiplatelet Agents

3. Lipid-Lowering Therapy

  • Statins (e.g. Atorvastatin, Simvastatin)

Revascularisation – Optional Definitive Treatment

  • Percutaneous Coronary Intervention (PCI)
    • Balloon dilation and/or stent placement
  • Coronary Artery Bypass Grafting (CABG)
    • Typically using saphenous vein or radial artery

Summary – Angina Pectoris

Angina pectoris is a clinical syndrome characterised by transient myocardial ischaemia, most often due to atherosclerotic coronary artery disease. It presents with chest pain that varies depending on the subtype—stable, variant, unstable, or silent. Diagnosis relies on clinical history supported by ECG and cardiac imaging, and management includes lifestyle modification, pharmacological therapy, and revascularisation when indicated. For a broader context, see our Cardiovascular Overview page.

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