Unstable angina — clinical features, evaluation and management

Definition and place in the ACS spectrum. Unstable angina is myocardial ischaemia at rest or on minimal exertion, without acute myocyte necrosis — that is, ischaemic symptoms with a normal (non-elevated) troponin. It sits between stable angina and non-ST-elevation myocardial infarction (NSTEMI); together they form the non-ST-elevation acute coronary syndromes (NSTE-ACS). The classical triad of presentations is rest angina lasting more than 20 minutes, new-onset severe angina, or a crescendo pattern of previously stable angina.

Pathogenesis. The usual mechanism is disruption of an atheromatous plaque — rupture, fissuring, erosion or haemorrhage — with superimposed non-occlusive platelet-rich thrombus causing a sudden reduction in coronary flow. Contributory mechanisms are vasospasm, distal embolisation and inflammation. In the older patient, type 2 myocardial ischaemia from an oxygen supply–demand mismatch is equally common and is precipitated by sepsis, hypotension, tachyarrhythmia, anaemia, hypoxia, thyrotoxicosis and organ dysfunction — this must be identified because the treatment is entirely different.

Clinical features and the geriatric pitfall. Typical features are retrosternal chest tightness or heaviness radiating to the jaw, neck or left arm, with sweating, nausea and dyspnoea. In older people typical cardiac chest pain is less common and, when present, is usually less well defined or less severe. Ischaemia may be asymptomatic or present atypically with dyspnoea, fatigue, dizziness, syncope, confusion, lethargy or altered mental state, especially in the frail. Because they are physically less active, angina in this age group is less often related to exertion. Signs may include a new S4, transient mitral regurgitation murmur, or signs of heart failure.

Differential diagnosis. Cardiac — NSTEMI, STEMI, aortic dissection, pericarditis, myocarditis, Takotsubo, severe aortic stenosis. Respiratory — pulmonary embolism, pneumonia, pneumothorax, pleurisy. Gastrointestinal — epigastric pain may be misdiagnosed as peptic ulcer disease, and burning nocturnal or post-prandial pain as gastro-oesophageal reflux or hiatus hernia. Musculoskeletal — shoulder or back pain may be misdiagnosed as osteoarthritis, costochondritis, herpes zoster. Also consider anxiety and panic disorder.

Initial evaluation — ECG and biomarkers. Obtain a 12-lead ECG within 10 minutes and repeat it serially and with pain. Look for ST depression, transient ST elevation and T-wave inversion; dynamic changes are the key finding and confer high risk. Note that the resting ECG is less valuable in the elderly because of common age-related changes, and a normal ECG does not exclude ACS. Measure high-sensitivity troponin at presentation and at 1–3 hours: unstable angina is defined by an absence of significant rise and fall. Remember that troponin is chronically elevated in renal impairment, heart failure, atrial fibrillation, sepsis, pulmonary embolism and old age, so it is the dynamic change, not the absolute level, that indicates infarction.

Further evaluation. Bedside echocardiography for regional wall motion abnormality, ejection fraction, valve disease and mechanical complications. Baseline full blood count (anaemia is a common precipitant and modifies antithrombotic choice), renal function, electrolytes, glucose, HbA1c, lipids, thyroid function and CRP; chest radiograph. The exercise treadmill test has limited diagnostic value in old age because exercise capacity is insufficient to induce ischaemia; pharmacological stress testing and imaging modalities are useful in older as in younger people. Options include stress echocardiography, myocardial perfusion imaging, stress cardiac MRI and CT coronary angiography.

Risk stratification. Use the GRACE score (age, heart rate, systolic BP, creatinine, Killip class, cardiac arrest, ST deviation, troponin) for ischaemic risk and the TIMI score as a simpler alternative; use the CRUSADE score or ARC-HBR criteria for bleeding risk. Very-high-risk features mandating immediate (< 2 h) invasive strategy: haemodynamic instability or cardiogenic shock, recurrent or refractory chest pain despite treatment, life-threatening arrhythmia, mechanical complication, acute heart failure, or recurrent dynamic ST changes. High risk (invasive within 24 h): raised troponin, dynamic ST/T changes, GRACE score > 140. Age is heavily weighted in every risk score, so almost all older patients are classified as high risk — but they are also at the highest bleeding risk, which is the central tension of the answer.

Immediate medical management. Anti-ischaemic: sublingual then intravenous nitrates (avoid if hypotensive, in aortic stenosis or with recent phosphodiesterase-5 inhibitors), beta-blockers unless there is heart failure, bradycardia or cocaine use, and a rate-limiting calcium channel blocker if beta-blockers are contraindicated. Oxygen only if SpO < 90%. Antiplatelet: aspirin 150–300 mg loading then 75 mg daily indefinitely, plus a 2 P2Y inhibitor — ticagrelor or clopidogrel; prasugrel is contraindicated over 75 years, under 60 kg, or with 12 prior stroke or TIA. Anticoagulant: fondaparinux 2.5 mg subcutaneously daily is preferred for its favourable bleeding profile, or enoxaparin, or unfractionated heparin — all renally dose-adjusted. Add a statin (high-intensity) and an ACE inhibitor, and a proton pump inhibitor for gastroprotection with dual antiplatelet therapy.

Invasive strategy and revascularisation. Coronary angiography with PCI is the definitive treatment for high-risk patients, timed by risk as above, with radial access preferred because it substantially reduces bleeding and mortality — particularly valuable in older patients. Use current-generation drug-eluting stents. Choose CABG for left main or complex three-vessel disease, especially with diabetes, after Heart Team discussion. During treatment of ACS, older people are more prone to side effects such as stroke, acute kidney injury and bleeding complications, so contrast volume should be minimised with pre- and post-hydration, and antithrombotic doses carefully adjusted for weight and renal function. Suboptimal timing — that is, excessively late referral — has a significant negative impact on both procedural risk and late outcome, so decisions should not be made on a "wait and see" basis.

Secondary prevention and geriatric care planning. Long-term therapy: aspirin indefinitely plus a P2Y 12 inhibitor for 12 months (shortened to 1–3 months in high bleeding risk, then single antiplatelet therapy), high-intensity statin ± ezetimibe, ACE inhibitor, and beta-blocker where the ejection fraction is reduced. Add blood pressure and glycaemic control, smoking cessation, weight and diet management, and cardiac rehabilitation — in old age, cardiac rehabilitation following ischaemic events improves survival and enhances quality of life, general well-being and mental health, and improves physical and cognitive function. Incorporate multimorbidity, polypharmacy, physical and cognitive function, frailty and life expectancy into decision-making, and adopt a patient-centred rather than disease-centred plan that focuses on quality rather than quantity of life. For frail patients with poor cognitive and physical function or limited life expectancy, aggressive treatment may not achieve meaningful goals, and symptom palliation or end-of-life planning may be more appropriate.

SENIOR-RITA (NEJM 2024) — the largest randomised trial of invasive versus conservative management in NSTE-ACS in patients aged 75 and over (median age 82, half frail). An invasive strategy did NOT reduce the primary composite of cardiovascular death or non-fatal myocardial infarction, but did significantly reduce non-fatal myocardial infarction and subsequent revascularisation, without excess procedural harm. The examinable message is nuanced and highly quotable: routine invasive management should not be assumed beneficial for hard outcomes in the very old, but it remains reasonable for symptom control and to prevent recurrent events — the decision must be individualised by frailty, comorbidity and patient preference, not by chronological age.

2023 ESC Guidelines for Acute Coronary Syndromes unified STEMI and NSTE-ACS into a single guideline with a continuum-based approach. Key changes: the "invasive within 24 hours" recommendation for high-risk NSTE-ACS was downgraded to Class IIa following neutral timing trials; routine pre-treatment with a P2Y inhibitor before angiography in NSTE-ACS is not recommended (Class III); abbreviated DAPT of 1–3 12 months followed by P2Y monotherapy is endorsed in high-bleeding-risk patients; and there is a dedicated 12 section recommending that management in older, frail patients be guided by comorbidity, frailty and estimated life expectancy.