30th May 2026

Unstable Angina

Background

Unstable angina (UA) is myocardial ischemia occurring at rest or minimal exertion without acute cardiomyocyte injury or necrosis. Key features include:

• Prolonged (>20 minutes) angina at rest.
• New onset of severe angina.
• Increasing frequency, duration, or intensity of angina.
• Angina after a recent myocardial infarction.

Epidemiology

UA is a form of acute coronary syndrome (ACS) with rising prevalence, particularly among individuals with risk factors such as diabetes, hypertension, and smoking. It often indicates a higher risk of progression to myocardial infarction or other severe cardiac events.

Aetiology & Pathophysiology

UA is caused by a non-occlusive thrombus on a ruptured atherosclerotic plaque, leading to partial obstruction of the coronary artery and myocardial ischemia without infarction. The severity of symptoms is determined by the degree of ischemia, collateral circulation, and comorbidities. Key features include plaque rupture at thin-cap regions and thrombus formation that is typically non-occlusive.

Diagnosis

Investigations

• ECG: A 12-lead ECG should be performed within 10 minutes to identify changes such as ST depression, transient ST elevation, or T-wave inversion.
• Troponin: Troponin levels help differentiate UA from NSTEMI. Dynamic or persistently normal troponin levels can rule out myocardial infarction. If there is strong suspicion of unstable angina with negative ECG and troponin, serial measurements are essential to identify progression to NSTEMI and to help with risk stratification. 
• Chest X-ray: To rule out alternative diagnoses like pneumothorax or aortic dissection.
• Blood Tests: FBC, U&E, LFTs, glucose, and CRP to assess the patient’s overall health and detect complications.
• Echocardiography: Used to evaluate left ventricular (LV) function and identify regional wall motion abnormalities suggestive of ongoing ischemia.
• Risk Pathways: Troponin levels, clinical features, and ECG findings guide decisions regarding further testing and intervention, including coronary angiography.

Clinical Manifestations

Chest pain in UA is typically retrosternal, lasting for more than 20 minutes, and often occurs at rest or with minimal exertion. Symptoms are frequently accompanied by nausea, sweating, breathlessness, or dizziness.

• Red Flags: Hemodynamic instability, acute LV failure, or arrhythmias.

Management

Initial Treatment

• Aspirin: Administer a loading dose unless contraindicated.
• Anticoagulation: Fondaparinux or unfractionated heparin, especially in patients with renal impairment.
• Pain Relief: Glyceryl trinitrate (GTN) and morphine as needed.
• Monitoring: Continuous monitoring for symptom recurrence, dynamic ECG changes, or rising troponin levels.
• Antiplatelet Therapy: Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is recommended for high-risk patients. If severe thrombocytopaenia develops, alternative anticoagulation should be considered. In patients at high risk of thrombotic complications, a direct thrombin inhibitor such as bivalirudin should be considered.
• Invasive Strategy: Coronary angiography is indicated within 24-72 hours for high-risk patients based on clinical features and risk stratification.

Long-term Treatment

• Continue aspirin and P2Y12 inhibitors for up to 12 months.
• Consider ACE inhibitors/ARBs, beta-blockers, statins, and aldosterone antagonists for patients with heart failure or diabetes.
• SGLT2 inhibitors (e.g., dapagliflozin) may be used for patients with heart failure, regardless of ejection fraction.
• Stress-testing a few weeks after the event may guide the need for further invasive treatment.

Prevention & Follow-Up

• Primary Prevention: Smoking cessation, a healthy diet, weight management, and regular physical activity are crucial. Statins should be prescribed for high cardiovascular risk patients.
• Secondary Prevention: Cardiac rehabilitation and adherence to long-term medications, including antiplatelet therapy, statins, and ACE inhibitors.
• Follow-Up: Regular outpatient follow-up within 1-2 weeks post-discharge, with lipid monitoring every 6 months. Medication reviews should be conducted at each visit.

Complications

• Short-term: Cardiac arrhythmias, acute heart failure, cardiogenic shock, and post-ischemic pericarditis.
• Variable: Depression and in-stent thrombosis.
• Bleeding: Major bleeding events occur in 3.9% of ACS patients, especially those receiving anticoagulation therapy. Minor bleeding can be managed conservatively without halting anticoagulants or antiplatelet therapy. Major bleeding may require discontinuation of DAPT, as well as measures such as platelet transfusion and resuscitation.

Prognosis

Mortality

• Overall mortality in NSTE-ACS patients is 4.8% over 6 months.
• Mortality rates exceed those of STEMI after 6 months.
• At 12 months, adverse cardiovascular events (recurrent ischemia, MI, and death) occur in up to 10% of patients, likely reflecting widespread atherosclerotic disease.

Prognostic Factors

• Adverse markers include rest pain, comorbidities (e.g., diabetes, hypertension, chronic kidney disease), left ventricular failure, ST depression, raised biomarkers, and multi-vessel or left main disease.
• Short-term risk factors for death or non-fatal MI include:
  • Accelerated ischemic symptoms, prolonged rest pain, pulmonary oedema, new mitral regurgitation, age >75, and significant ECG changes (ST-T changes, new bundle branch block, sustained VT).

Risk Assessment

Risk models (e.g., GRACE Score) predict outcomes for up to 6 months and maintain predictive value for 1-year outcomes such as death or MI.

• The GRACE score takes into account factors such as patient age, cardiac history, ECG findings, signs and symptoms, and gives a score to estimate 6-month mortality.