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Acute Coronary Syndrome (ACS)

NICE guideline [NG185] Acute coronary syndromes. Published: 18 November 2020

Background Information

ACS is the acute manifestation of coronary artery disease. This umbrella term includes the spectrum of STEMI, NSTEMI, and unstable angina.[ref]
 
 

Unstable angina 

NSTEMI

STEMI

Pathogenesis 

Partial occlusion → ischemia WITHOUT infarction 

Partial occlusion → partial thickness (subendocardial) infarction 

Complete occlusion → full-thickness (transmural) infarction 

ECG findings 

No ST elevation

Other ECG changes maybe present:

  • ST depression 
  • T wave abnormalities

ECG maybe normal 

ST elevation in at least 2 contiguous leads (see below for full criteria)

Cardiac troponin (T/I)

<99th centile 

 Rise and/or fall Rise and/or fall

Major risk factors:[ref]
  • Age (>65 y/o)
  • Male 
  • Cardiovascular risk factors
  • Family history of premature coronary artery disease
  • Presence of other cardiovascular diseases
  • Established coronary artery disease (e.g. previous MI, coronary revascularisation)

Other risk factors:[ref]
  • CKDChronic kidney disease
  • Chronic inflammatory conditions (e.g. rheumatoid arthritis, SLE)
  • Premature menopause
  • Pregnancy-related complications (e.g. pre-eclampsia, gestational diabetes)

Complications of MI can be organised by the time frame after the event:[ref, ref]
 
Timeframe Complication Presentation
Early (0-24 hours) Arrhythmia Common life-threatening arrhythmias:
  • Ventricular tachycardia
  • Ventricular fibrillation
Acute heart failure / cardiogenic shock  
Intermediate (0-1 week) Papillary muscle rupture Presents as acute mitral regurgitation
  • Left-sided heart failure features predominant - pulmonary oedema
  • New pansystolic murmur - best heard at the apex and radiates to the axilla
Ventricular septal rupture Presents as left-to-right shunting:
  • Bi-ventricular failure is common
    • Left-sided → pulmonary oedema
    • Right-sided → raised JVP, peripheral oedema
  • New pansystolic murmur - best heard at the left lower sternal border
  • New palpable thrill at the left sternal border
Ventricular free wall rupture Presents as cardiac tamponade (Beck's triad):
  • Muffled heart sound
  • JVP distension
  • Hypotension
Late (>1-2 weeks) Congestive heart failure Causes HFrEFHeart failure with reduced ejection fraction
Left ventricular aneurysm Presents as:
  • Heart failure features
  • Recurrent ventricular arrhythmias
  • Embolic complications (e.g. stroke, systemic emboli)
  • Persistent ST elevation in leads of prior infarct but NO reciprocal changes
Dressler syndrome Autoimmune pericarditis:
  • Pleuritic chest pain (worse with lying flat and relieved sitting forward)
  • Fever
  • Pericardial rub

Typical pericarditis ECG features - widespread concave ST depression + PR depression
 

Diagnosis Guidelines

Chest pain / discomfort is the main presenting feature of ACS, it can be mapped to the SOCRATES framework:[ref]
  • Site: central or retrosternal (typically non-specific)
  • Onset: sudden onset, usually at rest
  • Character: heavy / crushing / tightness
  • Radiation: classically to the left arm, neck, jaw 
  • Associated symptoms: dyspnoea, nausea, vomiting, diaphoresis
  • Timing: often does not resolve on its own
  • Exacerbating factors: often precipitated by exertion or emotional stress but may occur at rest (ACS symptoms is characteristically not relieved by rest and nitrate)
  • Severity: can be severe
 
 

The above-described are the typical features of ACS, one should also be aware of atypical features:

  • Epigastric pain 
  • No chest pain at all, with just associated symptoms

Atypical features are usually seen in:
  • Inferior MI (esp. if epigastric pain)
  • Female
  • Diabetes (due to autonomic neuropathy)

Reproducible chest pain on palpation points away from ACS, this is more suggestive of musculoskeletal causes of chest pain.

Other clues of musculoskeletal chest pain:

  • Pain on movement
  • Pain in a very specific location (cardiac chest pain is typically non-specific)

Perform ALL the following in suspected ACS cases:[ref]

  • Clinical history and examination
  • 1st line diagnostic tool: 12-lead ECG 
  • Serial high-sensitivity cardiac troponin
 
  • Other tests (non-ACS specific but routine in all chest pain cases)
    • Chest X-ray - to rule out chest pathology
    • Routine bloods

Diagnostic criteria of ACS:[ref]
 

ACS spectrum Diagnostic criteria
STEMI
  • Rise and/or fall of cardiac troponin (at least 1 value >99th percentile upper reference limit), and
  • Clinical evidence of myocardial ischaemia - ECG or ischaemic symptoms
NSTEMI
Unstable angina
  • Clinical evidence of myocardial ischaemia - ECG or ischaemic symptoms, and
  • Troponin level normal (<99th percentile upper reference limit + no dynamic pattern)

Rise and/or fall of cardiac troponin is indicative of myocardial infarction (STEMI and NSTEMI) (but not unstable angina, as there is no necrosis)[ref]
  • Troponin is a marker of myocardial injury, not specific to MI
  • Necrosis in STEMI and NSTEMI causes a dynamic release of troponin, thus the rise and/or fall pattern
  • A persistently raised troponin level is NOT indicative of ACS

Important non-ACS causes of elevated troponin:[ref]
 
Category Important causes
Cardiovascular causes
  • Myocarditis (NB pericarditis alone would not raise troponin but myopericarditis is common)
  • Tachyarrhythmias
  • Severe hypertension
  • Pulmonary embolism → right ventricular strain
  • Aortic dissection
Non-cardiac causes
  • Renal failure
  • Sepsis
  • Stroke
  • Subarachnoid haemorrhage
  • Multi-organ failure
 

Dynamic ECG changes seen in STEMI:[ref]
  • ST elevation in ≥2 contiguous leads
  • Reciprocal ST depression in opposite territory - presence strengthens diagnosis of STEMI as opposed to other causes of ST elevation
  • Hyperacute T waves, T wave inversion, pathological Q wave
 

Dynamic changes in ECG (and troponin levels) are characteristic of ACS.

ECG changes over time in STEMI:

  1. Hyperacute T waves
  2. ST elevation
  3. T wave inversion
  4. Q wave (pathological) formation - may persist indefinitely
 
ECG changes in various myocardial territories:[ref]
 
Territory Coronary artery involved Leads with ST elevation Leads with reciprocal ST depression Other notes
Anterior LADLeft anterior descending V1-V4 Inferior leads (II, III, aVF) Poor R wave progression is common
Lateral LCxLeft circumflex V5-V6, I, aVL Often occurs with anterior MI (anterolateral MI)
Inferior RCARight coronary artery II, III, aVF Lateral leads (I, aVL +/- V5-V6) AV block is common in inferior MI
Posterior PDAPosterior descending artery V7-V9 Anterior leads (V1-V4) Often occurs with inferior MI, always consider using posterior leads (V7-V9) in inferior MI to exclude posterior MI

Other important causes of ST elevation:
 
Cause Features
Pericarditis Widespread 'global' changes (not specific to myocardial territory):
  • Concave ('saddle-shaped') ST elevation
  • PR depression

No reciprocal ST depression, apart from in V1 and aVR

Clinical features are important in distinguishing from STEMI:
  • Viral prodrome
  • Pleuritic chest pain (worse with lying flat and relieved sitting forward)
  • Pericardial rub possible
Myocarditis Non-specific ECG changes, often widespread:
  • ST elevation (may mimic pericarditis or STEMI)
  • T wave inversion
  • Arrhythmias

Clinical features is important in distinguishing from STEMI:
  • Absence of cardiovascular risk factors
  • Younger patients (often female)
  • Viral prodrome
  • Central chest pain

Note that myocarditis commonly causes an elevated cardiac troponin too
Left bundle branch block ECG changes:
  • Wide QRS complex
  • Discordant ST elevation (ST elevation only in leads with -ve QRS)
  • Deep S wave in V1 and broad notched R wave in V6
Brugada syndrome ECG changes seen in V1-V3
  • Coved ST elevation
  • T wave inversion
Prinzmetal (vasospastic) angina Transient ST elevation during angina episodes

Classically caused by cocaine induced coronary vasospasm
Early repolarisation Seen in young, healthy adults
  • Widespread concave ST elevation - non-dynamic
  • J-point notching
 

Main changes include:[ref]
  • Normal ECG
  • ST depression (horizontal / down-sloping)
  • T wave inversion

Management Guidelines

MONA is a common acronym

  • M – Morphine (only if in severe pain)
  • O – Oxygen  (only if O2 saturation <94%)
  • N – Nitrate (should not be used in suspected right ventricular infarction) 
  • A – Aspirin 300mg

There are 2 management pathways - depending on whether it is STEMI or non-STEMI (i.e. NSTEMI and unstable angina):
  • STEMI pathway - 2 options
    • Reperfusion therapy (PCIPercutaneous coronary intervention / fibrinolysis)
    • Medical management
 
  • NSTEMI / unstable angina pathway - 2 options (depending on risk stratification)
    • PCIPercutaneous coronary intervention 
    • Medical management

To decide on the management pathways, use the STEMI criteria (NICE guidelines did not specify criteria for STEMI. Information from this section is as per ESC guidelines):

New ST elevation at J point in ≥2 contiguous leads:
  • ST elevation in V2-V3
    • Men <40 y/o: ≥2.5mm
    • Men ≥40 y/o: ≥2.0mm
    • Women of any age: ≥1.5mm
  • AND/OR
  • Other leads: ≥1mm in the absence of LVHLeft ventricular hypertrophy / LBBBLeft bundle branch block
 

Initial management: aspirin 300mg 


Definitive management depends on eligibility for reperfusion therapy, which is determined by time from symptom onset - cut off is 12 hours. 
 

There are 2 options for reperfusion therapy:
  • Angiography +/- percutaneous coronary intervention (PCI) 
  • Fibrinolysis (medical) 


The choice is determined by whether there is access to cath lab within 120 min (2 hours). 

 

NICE guidelines also made the following recommendations regarding PCI:

  • Offer if symptoms onset <12 hours with acute STEMI + cardiogenic shock
  • Consider if onset >12 hours with evidence of MI
  • Consider if onset >12 hours but develops cardiogenic shock

Recommendations regarding angiography +/- PCI:

  • Drug-eluting stent preferred over bare metal stent, if stenting indicated 
  • Radial access preferred over femoral access

Adjuvant drug therapy:
  • Dual antiplatelet therapy 
    • 1st line: aspirin + prasugrel 
    • If patient already takes oral anticoagulant: aspirin + clopidogrel
 
  • Anti-thrombin therapy during PCI
    • Radical access: UFHUnfractionated heparin (also known as just heparin) + bailout GpIIb/IIIa inhibitor
    • Femoral access: bivalirudin + bailout GpIIb/IIIa inhibitor
 
 

Choice of drug is often not that straightforward. Influenced by local guidelines and local availability.

NICE also recommend offering ticagrelor or clopidogrel as an alternative in people aged 75 and over, considering whether the risk of bleeding with prasugrel outweighs its benefit.

Offer all the following:

  • Fibrinolytic agent: tissue plasminogen activator (e.g. alteplase, streptokinase)
  • Anti-thrombin 
  • Dual antiplatelet therapy 
    • 1st line: aspirin + ticagrelor 
    • High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy 
 

Then, offer ECG 60-90 minutes after:

  • If ST elevation still present on ECG → immediate angiography +/- PCI if indicated
  • Do not repeat fibrinolytic therapy

Dual antiplatelet therapy 

  • 1st line: aspirin + ticagrelor 
  • High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy

Offer echocardiogram to assess left ventricular function in all patients who had a STEMI.

Initial management (both):
  • Aspirin 300mg 
  • Antithrombin therapy
    • 1st line: fondaparinux
    • If high bleeding risk / renal impairment (creatinine >265 mmol/L) / immediate angiography planned: UFHUnfractionated heparin (also known as heparin)

Definitive management depends on risk stratification with GRACE score (predicts 6-month mortality).

 

If the patient is clinically unstable → offer immediate PCI without taking GRACE score into account.

Offer all of the following:
  • Angiography +/- PCI within 72 hours
  • UFHUnfractionated heparin (also known as heparin), even if fondaparinux has been given
  • Dual antiplatelet therapy
    • 1st line: aspirin + prasugrel / ticargrelor
    • Already taking oral anticoagulant: aspirin + clopidogrel
 

Recommendations regarding angiography +/- PCI:

  • Drug-eluting stent, if stenting indicated 
  • Radial access, preferred over femoral access

Medical management with dual antiplatelet therapy:
  • 1st line: aspirin + ticagrelor 
  • High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy 
 

Only consider angiography +/- PCI if ischaemia testing is positive

  • Offer echocardiogram to assess left ventricular function
    • In all NSTEMI cases
    • Consider in unstable angina  
 
  • Consider ischaemia testing in those who have been medically managed without coronary angiography

No PCI (STEMI / NSTEMI / Unstable angina)

  • 1st line: aspirin + ticagrelor 
  • High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy 
 

STEMI with PCI

  • 1st line: aspirin + prasugrel 
  • If taking oral anticoagulant: aspirin + clopidogrel 
 

NSTEMI / Unstable angina with PCI

  • 1st line: aspirin + prasugrel / ticagrelor 
  • If taking oral anticoagulant: aspirin + clopidogrel

ACS Secondary Prevention Guidelines

  • Cardiac rehabilitation program
  • Lifestyle advice
    • Mediterranean-style diet
    • Regular physical activity
    • Smoking cessation
    • Advice on alcohol consumption
    • Weight management
    • Sexual activity can be resumed 4 weeks after 

NICE guideline recommendations regarding various supplements:
 

Omega-3 fatty acid 

Do not recommend

  • But if the person chooses to, there is no evidence of harm 

Beta-carotene 

Advise against 

Vitamin E/C/B9 (folic acid)

Do not recommend 

Offer ALL the following to ALL patients:
  • Dual antiplatelet therapy
    • Aspirin life-long (if aspirin not appropriate → clopidogrel)
    • 2nd antiplatelet agent for up to 12 months
  • High-intensity statin (e.g. atorvastatin 80mg) life-long
  • ACE inhibitor for life-long - start once hemodynamically stable
  • Beta blocker for 12 months if normal LVEF - start once hemodynamically stable

Add-on if presence of heart failure features and ↓ LVEF
  • Aldosterone antagonist (e.g. spironolactone) - initiate within 3-14 days of MI, preferably after starting ACE inhibitor

References

Author: Canada Edu 
Reviewer:
Last edited: 05/09/25