TextbookCardiologyAcute Coronary Syndrome

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

DiagnosisKey FeaturesInvestigation
Aortic dissectionTearing pain, BP differential, widened mediastinumCT aortogram
Pulmonary embolismPleuritic pain, dyspnoea, risk factors for VTECTPA, D-dimer
Tension pneumothoraxSudden pleuritic pain, absent breath sounds, tracheal deviationClinical + CXR
Acute pericarditisSharp pain, worse on inspiration, relieved sitting forward, saddle ST elevationECG, echo, inflammatory markers
GORD/oesophageal spasmBurning/squeezing pain, postprandial, may respond to GTNPPI trial, OGD
MusculoskeletalReproducible on palpation, positionalClinical examination
MyocarditisChest pain, troponin rise, viral prodrome, no coronary diseaseCardiac MRI
Takotsubo cardiomyopathyPost-emotional stress, apical ballooning, troponin rise, unobstructed coronariesAngiography, 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

VariablePoints
Age0-100
Heart rate0-46
Systolic BP0-63
Creatinine0-28
Killip class0-64
Cardiac arrest at admission0-43
ST deviation0-28
Elevated cardiac enzymes0-15

Killip Classification (Heart Failure Post-MI)

ClassFeaturesMortality
INo heart failure~6%
IICrepitations, S3, elevated JVP~17%
IIIPulmonary oedema~38%
IVCardiogenic shock~81%

Universal Definition of MI Types

TypeMechanism
1Atherosclerotic plaque rupture/erosion
2Supply-demand mismatch (secondary)
3MI resulting in death without biomarkers
4aPCI-related MI
4bStent thrombosis
5CABG-related MI