thee types angina

Also written as ischemic chest pain, angina pectoris.

Angina describes chest pain from myocardial oxygen shortage. Three main types—stable, unstable, and variant—differ in triggers, duration, and risk of imminent infarction.

Overview

Angina is a symptom of coronary artery disease. It signals an imbalance between myocardial oxygen demand and supply.

• Stable: predictable, triggered by exertion, relieved by rest or nitrates.
• Unstable: new or worsening pain at rest, high risk of MI.
• Variant (Prinzmetal): coronary spasm, often nocturnal, relieved by calcium‑channel blockers.

Key concepts

Understanding the pathophysiology guides urgency and treatment.

• ECG: Does the ECG show ischemic changes? ST depression suggests subendocardial ischemia; ST elevation suggests spasm or infarction.
• Troponin: Is there myocardial injury? Elevated troponin indicates unstable angina or MI.
• Coronary angiography: What is the anatomic severity? Shows obstructive lesions for revascularisation; if unavailable, use stress imaging.

• Demand‑supply mismatch → subendocardial ischemia.
• Coronary atherosclerosis → stable angina.
• Plaque rupture or spasm → unstable/variant angina.

Clinical relevance

Distinguish type to decide urgency, need for admission, and revascularisation.

• Unstable angina → admit, anti‑ischemic therapy, early invasive strategy.
• Stable angina → outpatient risk stratification, lifestyle, pharmacotherapy.
• Variant angina → avoid beta‑blockers, use calcium‑channel blockers.

Exam pearls

Examiners test pattern recognition, risk assessment, and immediate management.

• Identify red‑flag features: pain at rest, crescendo pattern, diaphoresis.
• Know first‑line drugs: nitrates, aspirin, beta‑blockers (except variant).
• Recall contraindications: beta‑blockers in variant, nitrates in hypotension.

Common mistakes

Pitfalls often stem from misclassifying the angina type.

• Treating variant angina with beta‑blockers – may worsen spasm.
• Assuming all chest pain is cardiac – miss pulmonary embolism, pericarditis.
• Relying on a normal ECG to rule out unstable angina – troponin needed.

Questions an examiner may ask

• A 58‑year‑old smoker presents with chest pain at rest for 30 min – what is your next step? — Admit, give aspirin, oxygen, nitrates, and obtain ECG/troponin.
• How does variant angina differ from stable angina on ECG? — Transient ST elevation during pain, resolves with nitroglycerin.
• Why are beta‑blockers contraindicated in Prinzmetal angina? — They can exacerbate coronary spasm by unopposed alpha‑mediated vasoconstriction.
• A patient with stable angina has a negative treadmill test but persistent symptoms – what is the next investigation? — Consider coronary CT angiography or stress myocardial perfusion imaging.
• What clinical features would shift management from outpatient to inpatient for angina? — New-onset pain, crescendo pattern, pain at rest, elevated troponin, or haemodynamic instability.
• Explain the rationale for dual antiplatelet therapy after PCI in unstable angina. — Reduces stent thrombosis by inhibiting platelet activation via two pathways.
• In a low‑resource setting without angiography, how would you risk‑stratify unstable angina? — Use TIMI score, bedside ECG, troponin, and clinical assessment to decide on transfer.
• What is the first pharmacologic agent to give in acute unstable angina and why? — Sublingual nitroglycerin for rapid relief of ischemia by dilating coronary vessels.

When to seek help

• Chest pain lasting >20 min at rest, radiating to arm/jaw, associated with sweating, nausea, or dyspnoea – call emergency services.

Quick questions

Can angina occur without coronary artery disease?

Yes, variant angina is caused by coronary spasm without fixed atherosclerosis.

Why is aspirin given to all angina patients?

It inhibits platelet aggregation, reducing thrombus formation on ruptured plaques.

Is a normal stress test enough to rule out coronary disease?

No; false‑negatives occur, especially in multi‑vessel disease or microvascular angina.