Ep 224 – Unstable angina

In this episode, Dr Roger Henderson discusses unstable angina and its place within the spectrum of acute coronary syndrome (ACS). Although advances in high-sensitivity troponin testing mean that unstable angina is diagnosed less frequently than in the past, recognising the clinical syndrome remains essential. For GPs, the challenge is distinguishing acute myocardial ischaemia from other causes of chest discomfort, while identifying those patients who require urgent investigation and treatment. The episode covers the underlying pathophysiology, the clinical features that should raise suspicion and the role of the electrocardiogram (ECG) and high-sensitivity troponin in contemporary diagnosis. It also explores risk stratification, antiplatelet and anticoagulant therapy, symptom management, indications for invasive assessment and secondary prevention. Most importantly, it considers how careful clinical reasoning can help GPs identify high-risk patients early and avoid missing alternative life-threatening diagnoses.

Key take-home points

• Unstable angina is part of the ACS spectrum, representing acute myocardial ischaemia without the biochemical evidence of myocardial necrosis required for myocardial infarction.
• High-sensitivity cardiac troponin has changed the diagnosis of unstable angina. Many patients who would previously have been diagnosed with unstable angina are now classified as having non-ST-elevation myocardial infarction because contemporary assays detect smaller degrees of myocardial injury.
• The most common underlying mechanism is disruption or erosion of an atherosclerotic coronary plaque, followed by platelet activation and formation of a usually non-occlusive thrombus.
• The clinical history is often more informative than the precise description of the pain. New-onset angina, increasing frequency or duration of symptoms, symptoms occurring with less exertion or pain at rest should raise concern for unstable coronary disease.
• Angina symptoms are not necessarily described as "pain". Patients may report pressure, tightness, heaviness, burning, dyspnoea, fatigue, nausea, diaphoresis or discomfort involving the chest, arms, jaw, neck, back or upper abdomen.
• Relief with rest or nitrates supports but does not establish the diagnosis of ACS. Conversely, failure to respond to nitrate therapy does not exclude myocardial ischaemia.
• The physical examination is often nonspecific but remains essential for risk assessment. Raised jugular venous pressure, pulmonary crackles, S3 or S4, hypotension, a new murmur or signs of poor perfusion may indicate a high-risk presentation or complications.
• A normal ECG does not exclude unstable angina or ACS. Ischaemic changes may be transient, so repeat ECGs are important when symptoms recur or clinical suspicion remains high.
• High-sensitivity troponin should be interpreted serially and in clinical context. Troponin elevation indicates myocardial injury, but myocardial infarction requires evidence that the injury is related to myocardial ischaemia.
• Risk stratification should integrate clinical features, ECG findings, troponin results and the patient's overall cardiovascular risk. Risk-scoring tools such as Thrombolysis In Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) can support clinical decision-making but should not replace clinical judgement.
• Antiplatelet therapy is a cornerstone of ACS management. Aspirin is generally combined with an appropriate P2Y12 inhibitor, with the choice of agent and duration influenced by ischaemic risk, bleeding risk, planned percutaneous coronary intervention, contraindications and concomitant anticoagulation.
• Anticoagulation may be required during the acute phase, particularly when an invasive strategy is planned, but the choice of agent should take renal function, bleeding risk and the overall treatment pathway into account.
• Nitrates and beta-blockers can reduce myocardial oxygen demand and improve symptoms in appropriately selected patients, but contraindications such as hypotension, bradycardia, conduction disease, right ventricular infarction or acute decompensated heart failure must be considered.
• Routine oxygen therapy is no longer recommended for every patient with suspected ACS. Oxygen should generally be reserved for patients who are hypoxaemic or have another clear clinical indication.
• Always consider dangerous alternative diagnoses and match the intensity of treatment to the patient's risk. Pulmonary embolism, aortic dissection, pneumothorax, pericarditis, myocarditis and other causes of chest pain can mimic ACS, while recurrent or refractory angina, haemodynamic instability, heart failure, significant arrhythmias or dynamic ECG changes should prompt urgent cardiology assessment and consideration of an invasive strategy.

Key references

1. Byrne RA, et al. Eur Heart J. 2023;44(38):3720-3826. doi: 10.1093/eurheartj/ehad191.
2. NICE. 2020. https://www.nice.org.uk/guidance/ng185.
3. Bergmark BA, et al. Lancet. 2022;399(10332):1347-1358. doi: 10.1016/S0140-6736(21)02391-6.
4. Chang AM, et al. Cardiol Clin. 2018;36(1):1-12. doi: 10.1016/j.ccl.2017.08.001.
5. Rao SV, et al. Circulation. 2025;151(13):e771-e862. doi: 10.1161/CIR.0000000000001309.