Acute Coronary Syndrome
Spectrum of acute myocardial ischaemia encompassing unstable angina, NSTEMI, and STEMI. Caused by atherosclerotic plaque rupture with thrombus formation.
Key Facts
Spectrum: unstable angina → NSTEMI → STEMI, differentiated by ECG changes and troponin Immediate management: MONA — Morphine (if needed), Oxygen (only if SpO₂ <94%), Nitrates, Aspirin 300mg loading Dual antiplatelet therapy: aspirin 300mg + ticagrelor 180mg (or clopidogrel 300-600mg if ticagrelor contraindicated) STEMI: emergency PPCI within 120 minutes of first medical contact; if not feasible, thrombolysis within 12 hours NSTEMI: risk-stratify using GRACE score → angiography ± PCI within 72 hours for intermediate/high risk Troponin: high-sensitivity troponin (hs-cTn) at presentation and 3 hours; rule out with 0/1 hour algorithm NICE TA236: ticagrelor preferred over clopidogrel for ACS (based on PLATO trial) Post-ACS: DAPT for 12 months, high-dose statin, ACEi, beta-blocker, cardiac rehabilitation
Overview
Key Facts
Acute coronary syndrome (ACS) is an umbrella term for conditions caused by sudden reduction in coronary blood flow due to atherosclerotic plaque disruption with superimposed thrombus formation. It encompasses unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI).
Epidemiology
- ~100,000 hospital admissions per year in England for ACS
- Leading cause of death worldwide; ~70,000 deaths per year in the UK from coronary heart disease
- Male:female ratio ~2:1; women present ~10 years later than men
- In-hospital mortality: STEMI ~7%, NSTEMI ~5%, UA ~2%
Aetiology
- Atherosclerotic plaque rupture/erosion with superimposed thrombus formation (>90%)
- Less common: coronary artery spasm, coronary dissection (spontaneous or iatrogenic), coronary embolism, vasculitis, cocaine use, supply-demand mismatch (type 2 MI)
Pathophysiology
- Vulnerable plaque (thin fibrous cap, large lipid core, inflammatory cell infiltration) ruptures
- Exposed subendothelial collagen triggers platelet adhesion, activation, and aggregation
- Coagulation cascade activation forms fibrin-rich thrombus
- STEMI: complete occlusion → transmural infarction
- NSTEMI: subtotal occlusion or distal embolisation → subendocardial infarction
- UA: transient ischaemia without myocyte necrosis (troponin negative)
Clinical Presentation
Typical Presentation
- Acute-onset central chest pain: heavy, tight, crushing, or pressure-like
- Duration: >15 minutes, not relieved by rest or GTN
- Radiation to left arm, jaw, neck, back, or epigastrium
- Associated symptoms: sweating, nausea/vomiting, dyspnoea, palpitations, anxiety
Atypical Presentations
- More common in elderly, women, and diabetic patients
- Breathlessness without chest pain
- Epigastric pain mimicking indigestion
- Syncope or presyncope
- Acute confusion (elderly)
- Diabetic patients may have painless (silent) MI
Classification
- STEMI: ST elevation ≥2mm in ≥2 contiguous chest leads or ≥1mm in limb leads, or new LBBB
- NSTEMI: troponin elevation WITHOUT ST elevation; may have ST depression, T-wave inversion
- Unstable angina: typical ischaemic symptoms without troponin rise; may have ECG changes
Red Flags
- Ongoing chest pain despite initial management
- Haemodynamic instability (hypotension, tachycardia)
- Signs of cardiogenic shock
- Acute heart failure (pulmonary oedema)
- New murmur (VSD, mitral regurgitation from papillary muscle rupture)
- Cardiac arrest
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Aortic dissection | Tearing pain, BP differential, widened mediastinum | CT aortogram |
| Pulmonary embolism | Pleuritic pain, dyspnoea, risk factors for VTE | CTPA, D-dimer |
| Tension pneumothorax | Sudden pleuritic pain, absent breath sounds, tracheal deviation | Clinical + CXR |
| Acute pericarditis | Sharp pain, worse on inspiration, relieved sitting forward, saddle ST elevation | ECG, echo, inflammatory markers |
| GORD/oesophageal spasm | Burning/squeezing pain, postprandial, may respond to GTN | PPI trial, OGD |
| Musculoskeletal | Reproducible on palpation, positional | Clinical examination |
| Myocarditis | Chest pain, troponin rise, viral prodrome, no coronary disease | Cardiac MRI |
| Takotsubo cardiomyopathy | Post-emotional stress, apical ballooning, troponin rise, unobstructed coronaries | Angiography, echo, cardiac MRI |
Diagnosis / Investigation
Bedside
- ECG: 12-lead within 10 minutes of presentation
- STEMI: ST elevation, new LBBB, hyperacute T waves
- NSTEMI/UA: ST depression, T-wave inversion, or normal
- Continuous cardiac monitoring: arrhythmia detection
- Observations: BP, HR, SpO₂, RR
Bloods
- High-sensitivity troponin (hs-cTnT or hs-cTnI): at presentation and 3 hours (or 0/1h rule-out algorithm)
- FBC: anaemia
- U&Es: renal function (before contrast/ACEi)
- Glucose/HbA1c: diabetes
- Lipid profile: dyslipidaemia
- Coagulation screen: before anticoagulation
- BNP/NT-proBNP: heart failure assessment
Imaging
- Chest X-ray: pulmonary oedema, mediastinal widening (dissection)
- Echocardiography: regional wall motion abnormalities, LV function, mechanical complications
- Coronary angiography: gold standard for coronary anatomy; guides revascularisation
Special Tests
- GRACE score: risk stratification for NSTEMI/UA (predicts 6-month mortality)
- CT coronary angiography: if diagnosis uncertain in low-risk patients
Management
Non-pharmacological
- Bed rest during acute phase
- Continuous cardiac monitoring
- Supplemental oxygen ONLY if SpO₂ <94% (AVOID-trial: routine O₂ may be harmful)
Pharmacological
Immediate management (all ACS):
- Aspirin 300mg loading dose (chewed)
- Sublingual GTN 400mcg (if SBP >90 mmHg)
- Morphine 2-5mg IV titrated for pain (with antiemetic: metoclopramide 10mg IV)
- Fondaparinux 2.5mg SC OD (preferred anticoagulant in NSTEMI per NICE; or enoxaparin 1mg/kg BD)
STEMI-specific:
- Second antiplatelet: ticagrelor 180mg loading (or prasugrel 60mg if PCI-naïve, or clopidogrel 600mg)
- Primary PCI (PPCI): within 120 minutes of first medical contact (door-to-balloon <90 min)
- If PPCI not available within 120 min: thrombolysis (tenecteplase weight-adjusted IV bolus) within 12 hours of symptom onset
- Unfractionated heparin during PPCI
NSTEMI/UA-specific:
- Second antiplatelet: ticagrelor 90mg BD (PLATO trial) or clopidogrel 300mg if ticagrelor contraindicated
- Risk stratify with GRACE score:
- High risk (GRACE >140): angiography within 24 hours
- Intermediate (GRACE 109-140): angiography within 72 hours
- Low risk (GRACE <109): consider conservative management or non-invasive testing
Post-ACS (secondary prevention):
- DAPT: aspirin 75mg OD + ticagrelor 90mg BD for 12 months
- Atorvastatin 80mg OD (aim LDL <1.4 mmol/L or >50% reduction)
- ACE inhibitor: ramipril 1.25-10mg OD (especially if LV dysfunction, diabetes, HTN, CKD)
- Beta-blocker: bisoprolol 1.25-10mg OD (especially if LV dysfunction)
- Cardiac rehabilitation: all ACS patients
- Lifestyle: smoking cessation, exercise, diet, weight management
Landmark trials:
- PLATO: ticagrelor superior to clopidogrel in ACS
- CURE: clopidogrel + aspirin in NSTEMI
- TRITON-TIMI 38: prasugrel superior to clopidogrel in PCI
Surgical/Interventional
- PCI with drug-eluting stent (DES): standard for STEMI and high-risk NSTEMI
- CABG: if left main stem disease, complex multivessel disease, or PCI not feasible
- IABP/Impella: for cardiogenic shock
Referral Criteria
- All suspected ACS: call 999 for emergency admission
- Activate primary PCI pathway for STEMI
- Cardiology review within 24 hours for NSTEMI
Prognosis
- In-hospital mortality: STEMI ~7%, NSTEMI ~5%
- 30-day mortality: STEMI ~10%, NSTEMI ~6%
- 1-year mortality after ACS: ~10-15%
- GRACE score predicts 6-month post-discharge mortality
- Complications: heart failure (25-30%), arrhythmia, mechanical complications (papillary muscle rupture, VSD, free wall rupture), Dressler syndrome (2-10 weeks post-MI)
- Post-MI LV dysfunction: mortality increases with lower EF
- Modern PPCI and dual antiplatelet therapy have significantly improved outcomes
Other Relevant Information
GRACE Score Components
| Variable | Points |
|---|---|
| Age | 0-100 |
| Heart rate | 0-46 |
| Systolic BP | 0-63 |
| Creatinine | 0-28 |
| Killip class | 0-64 |
| Cardiac arrest at admission | 0-43 |
| ST deviation | 0-28 |
| Elevated cardiac enzymes | 0-15 |
Killip Classification (Heart Failure Post-MI)
| Class | Features | Mortality |
|---|---|---|
| I | No heart failure | ~6% |
| II | Crepitations, S3, elevated JVP | ~17% |
| III | Pulmonary oedema | ~38% |
| IV | Cardiogenic shock | ~81% |
Universal Definition of MI Types
| Type | Mechanism |
|---|---|
| 1 | Atherosclerotic plaque rupture/erosion |
| 2 | Supply-demand mismatch (secondary) |
| 3 | MI resulting in death without biomarkers |
| 4a | PCI-related MI |
| 4b | Stent thrombosis |
| 5 | CABG-related MI |