NSTEMI

Non-ST elevation myocardial infarction characterised by troponin elevation without persistent ST elevation, caused by subtotal coronary occlusion or distal embolisation.

Key Facts

Diagnosis: elevated high-sensitivity troponin with ischaemic symptoms BUT without persistent ST elevation on ECG ECG changes: ST depression, T-wave inversion, or may be normal; NEVER persistent ST elevation Risk stratification: use GRACE score to guide timing of invasive management NICE NG185: angiography within 72 hours for intermediate/high risk; within 24 hours if very high risk Antiplatelet: aspirin 300mg + ticagrelor 180mg loading (PLATO trial — superior to clopidogrel) Anticoagulation: fondaparinux 2.5mg SC OD preferred (OASIS-5 trial — lower bleeding vs enoxaparin) More common than STEMI and carries significant 6-month mortality (~12%) Post-NSTEMI: DAPT for 12 months, high-intensity statin, ACEi, beta-blocker, cardiac rehab

Overview

Key Facts

NSTEMI is a form of acute coronary syndrome characterised by myocardial necrosis (elevated troponin) in the setting of ischaemic symptoms, without persistent ST elevation on ECG. It is typically caused by subtotal coronary occlusion or distal microembolisation.

Epidemiology

  • NSTEMI is now more common than STEMI, accounting for ~60% of all acute MI
  • ~70,000 NSTEMI admissions per year in England
  • Incidence increasing, partly due to improved hs-troponin sensitivity
  • In-hospital mortality: ~5%; 6-month mortality: ~12%
  • Higher proportion of older patients and comorbidities compared to STEMI

Aetiology

  • Atherosclerotic plaque rupture/erosion with subtotal thrombotic occlusion
  • Distal microembolisation from unstable plaque
  • Type 2 MI: supply-demand mismatch (anaemia, sepsis, tachyarrhythmia, hypotension)

Pathophysiology

  • Subtotal coronary occlusion or intermittent occlusion causes subendocardial ischaemia and necrosis
  • Unlike STEMI, some residual flow is maintained, limiting the extent of infarction
  • Troponin release indicates myocyte death
  • Risk of progression to STEMI if thrombus propagates to complete occlusion

Clinical Presentation

Typical Presentation

  • Chest pain similar to STEMI but may be less severe
  • Rest pain, new-onset angina, or crescendo angina
  • Duration: usually >20 minutes
  • May wax and wane
  • Associated symptoms: dyspnoea, sweating, nausea

Differentiating Features from STEMI

  • No persistent ST elevation on ECG
  • ECG may show ST depression, T-wave inversion, or be normal
  • Troponin IS elevated (differentiates from unstable angina)

Risk Factors for Poor Outcome

  • Advanced age
  • Diabetes
  • Renal impairment
  • Heart failure
  • ST depression on ECG
  • Elevated troponin
  • Recurrent ischaemia

Red Flags

  • Ongoing or recurrent chest pain despite treatment
  • Haemodynamic instability
  • Dynamic ECG changes
  • Ventricular arrhythmia
  • Pulmonary oedema

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Unstable anginaIschaemic symptoms, normal troponinSerial troponin
STEMIPersistent ST elevation12-lead ECG
Type 2 MIDemand ischaemia (sepsis, anaemia, tachycardia)Clinical context, treat underlying cause
Acute pericarditisDiffuse ST elevation, sharp pain, friction rubECG, echo
MyocarditisTroponin rise, viral prodrome, chest painCardiac MRI
TakotsuboPost-emotional stress, apical ballooning, unobstructed coronariesAngiography, echo
Aortic dissectionTearing pain, BP differentialCT aortogram

Diagnosis / Investigation

Bedside

  • 12-lead ECG: ST depression, T-wave inversion, or normal (serial ECGs recommended)
  • Continuous cardiac monitoring
  • Observations: HR, BP, SpO₂, RR

Bloods

  • High-sensitivity troponin: at presentation and 3 hours (or 0/1 hour rule-out protocol)
  • FBC: anaemia (type 2 MI)
  • U&Es: renal function
  • Glucose, HbA1c: diabetes
  • Lipid profile: dyslipidaemia
  • BNP/NT-proBNP: heart failure
  • Coagulation screen: before anticoagulation

Imaging

  • Chest X-ray: pulmonary oedema
  • Echocardiography: LV function, regional wall motion abnormalities
  • Coronary angiography: timing guided by GRACE score

Special Tests

  • GRACE score: risk stratification (6-month mortality prediction)
    • Low risk (<109): consider non-invasive testing or conservative management
    • Intermediate risk (109-140): angiography within 72 hours
    • High risk (>140): angiography within 24 hours
  • hs-troponin 0/1h algorithm: rapid rule-out in selected patients

Management

Non-pharmacological

  • Bed rest during acute phase
  • Continuous cardiac monitoring
  • Oxygen only if SpO₂ <94%

Pharmacological

Acute management:

  • Aspirin 300mg loading (chewed)
  • Ticagrelor 180mg loading (PLATO trial; or clopidogrel 300mg if ticagrelor contraindicated)
  • Fondaparinux 2.5mg SC OD (OASIS-5 trial; preferred over enoxaparin — similar efficacy, less bleeding)
  • GTN sublingual/IV for ongoing pain (if SBP >90 mmHg)
  • Morphine 2-5mg IV titrated for pain + metoclopramide 10mg
  • Beta-blocker (if no contraindications): metoprolol 12.5-50mg TDS or bisoprolol

Invasive management (timing by GRACE score):

  • Very high risk (ongoing ischaemia, haemodynamic instability, arrhythmia): immediate angiography
  • High risk (GRACE >140): angiography within 24 hours
  • Intermediate risk (GRACE 109-140): angiography within 72 hours
  • Low risk: consider non-invasive functional testing or conservative approach

Post-NSTEMI (secondary prevention):

  • DAPT: aspirin 75mg OD + ticagrelor 90mg BD for 12 months
  • Atorvastatin 80mg OD
  • ACE inhibitor: ramipril titrated to 10mg OD
  • Beta-blocker: bisoprolol titrated if LV dysfunction
  • Eplerenone 25-50mg OD: if EF ≤40% + HF or diabetes
  • Cardiac rehabilitation

Landmark trials:

  • PLATO: ticagrelor vs clopidogrel — ticagrelor reduced CV death/MI/stroke
  • OASIS-5: fondaparinux vs enoxaparin — similar ischaemic outcomes, less bleeding
  • FRISC-II: early invasive strategy improved outcomes in NSTEMI
  • TIMACS: early angiography (<24h) beneficial in high-risk NSTEMI

Surgical/Interventional

  • PCI with DES: standard for significant single/double-vessel disease
  • CABG: left main stem disease, complex multivessel disease

Referral Criteria

  • All NSTEMI: immediate cardiology involvement
  • Cardiac rehabilitation post-discharge
  • Heart failure team if EF ≤40%

Prognosis

  • In-hospital mortality: ~5%
  • 6-month mortality: ~12% (GRACE score stratified)
  • 1-year mortality: ~15%
  • Higher mortality than STEMI at 6 months (older patients, more comorbidities)
  • With early invasive strategy and optimal medical therapy: significantly improved outcomes
  • Long-term risk: recurrent MI, heart failure, stroke
  • Prognosis depends on: age, LV function, GRACE score, completeness of revascularisation

Other Relevant Information

GRACE Score Risk Categories

GRACE ScoreRisk Category6-Month MortalityAngiography Timing
<109Low<3%Non-invasive testing or conservative
109-140Intermediate3-8%Within 72 hours
>140High>8%Within 24 hours

NSTEMI vs Unstable Angina

FeatureNSTEMIUnstable Angina
TroponinElevatedNormal
ECGST depression/TWI or normalST depression/TWI or normal
Myocyte necrosisPresentAbsent
ManagementMore aggressiveRisk-stratified