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Cardiovascular

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is acute myocardial ischaemia, usually from thrombosis on a disrupted coronary plaque, triaged by the first ECG into a reperfusion pathway or a troponin pathway.

Definition

Acute coronary syndrome is a clinical working diagnosis covering unstable angina and acute myocardial infarction caused by acute myocardial ischaemia. The initial ECG separates suspected STEMI from NSTE-ACS. High-sensitivity troponin and evidence of ischaemia then distinguish infarction, unstable angina and non-ischaemic myocardial injury.

Epidemiology

ACS is a common life-threatening cardiovascular emergency. Risk increases with age and with established atherosclerotic risk factors including smoking, hypertension, diabetes, dyslipidaemia, chronic kidney disease and family history. The absence of those factors does not exclude the diagnosis.

Pathophysiology

Type 1 ACS most often follows coronary plaque rupture or erosion with platelet activation and thrombosis. The resulting obstruction, distal embolisation and vasoconstriction cut myocardial oxygen delivery, but the presenting ECG phenotype does not reliably prove the degree of obstruction or the depth of infarction. Prolonged ischaemia causes irreversible myocyte injury and troponin release. Type 2 MI instead reflects oxygen supply-demand imbalance without acute atherothrombosis, while several cardiac and systemic illnesses cause non-ischaemic myocardial injury.

First principles

ACS is a syndrome, not one coronary anatomy

Type 1 ACS usually follows rupture or erosion of an atherosclerotic plaque, with platelet activation and coronary thrombosis. The clinical labels describe the presentation. They do not prove the depth of infarction or how completely the artery is blocked. When the findings do not fit, consider type 2 myocardial infarction (MI) from oxygen supply-demand mismatch, and non-ischaemic myocardial injury from sepsis, arrhythmia, renal disease or heart failure.1,2

The ECG decides the first emergency move

Persistent ST elevation reaching threshold in two contiguous leads means presumed coronary occlusion and immediate reperfusion. This is ST-elevation myocardial infarction (STEMI). The threshold is higher in leads V2 and V3, and differs by sex and age, because healthy hearts normally show some ST elevation there. That normal variation is greatest in younger men. A normal tracing does not prove a patent artery: posterior occlusion, bundle branch block and ventricular pacing all conceal the pattern.2,3

Troponin shows injury; ischaemia makes it infarction

Acute MI requires a rise and/or fall in cardiac troponin, with at least one value above the assay-specific 99th-percentile upper reference limit. It also requires evidence of acute ischaemia from symptoms, ECG, imaging or coronary thrombus. A raised or chronically stable troponin on its own is myocardial injury, not MI. Non-ST-elevation myocardial infarction (NSTEMI) meets both criteria; unstable angina (UA) is ischaemia without the troponin pattern.4,2

Time and instability decide who cannot wait

Occlusion destroys myocardium continuously, so a clear STEMI pathway never waits for troponin. In non-ST-elevation ACS (NSTE-ACS), shock, refractory or recurrent ischaemia, life-threatening arrhythmia or acute heart failure overrides any risk score and means angiography now. Once the patient is stable, predicted six-month mortality, bleeding risk, renal function and the planned invasive strategy set the timing and the drugs.3,2

Presentation

Suspect ACS with new chest discomfort or pressure, often lasting more than 15 minutes or occurring at rest. It is more suggestive when it radiates to either arm, the back, neck or jaw, or comes with breathlessness, sweating, nausea, vomiting or haemodynamic disturbance.1,3,2

Cardinal features

  • Central chest pressure, heaviness, tightness or discomfort
  • Discomfort radiating to one or both arms, the back, neck or jaw
  • Symptoms at rest, on minimal exertion, or a new or falling exertional threshold
  • Breathlessness, sweating, nausea or vomiting
  • A presentation without central chest pain, such as breathlessness, syncope or epigastric discomfort

Red flags

  • Persistent ST elevation or another pattern suggesting ongoing coronary occlusion: activate the reperfusion pathway now
  • Shock, hypotension, or pain continuing despite treatment: immediate senior cardiology and critical-care escalation
  • Acute heart failure or pulmonary oedema: urgent cardiology review and echocardiography, without delaying reperfusion
  • Ventricular arrhythmia, high-grade atrioventricular block or cardiac arrest: resuscitate and expedite coronary assessment
  • Sudden deterioration or a new murmur: suspect a mechanical complication and get emergency echocardiography

Investigations

Immediate 12-lead ECG

Obtain and interpret a 12-lead ECG within 10 minutes of first medical contact, and repeat it whenever symptoms recur or change. The ECG, not the troponin, selects the immediate reperfusion pathway. Do not let it delay emergency transfer.

Expected finding: Persistent regional ST elevation, ST depression, T-wave change, transient ST elevation, a conduction pattern that blocks interpretation, or no acute abnormality at all. A normal first ECG does not exclude ACS.

2,1

ST-elevation thresholds

STEMI is new ST elevation at the J point in two contiguous leads. In leads V2 to V3 the threshold is 2.5 mm or more in men under 40, and 2 mm or more in men aged 40 and over. In women of any age it is 1.5 mm or more. In every other lead it is 1 mm or more. These figures assume no left ventricular hypertrophy and no left bundle branch block (LBBB).

Expected finding: Regional ST elevation reaching threshold in a compatible presentation means a presumed occluded artery. These thresholds come from the Fourth Universal Definition of Myocardial Infarction as carried into the 2023 European Society of Cardiology (ESC) ACS guideline.

2

Posterior and right-sided leads

ST depression in V1 to V3 with tall R waves and an upright T wave suggests posterior occlusion, usually of the left circumflex artery. Record posterior leads V7 to V9. In a suspected inferior STEMI, record right-sided leads V3R and V4R.

Expected finding: ST elevation in V7 to V9 means a posterior STEMI: an occluded artery the standard 12-lead missed, so it earns primary percutaneous coronary intervention (PCI), not the NSTEMI pathway. ST elevation in V3R or V4R means right ventricular ischaemia, which is preload dependent, so nitrates and other preload-reducing drugs can cause severe hypotension.

2

Patterns that are not ST elevation but still mean occlusion

LBBB, right bundle branch block (RBBB) and ventricular pacing prevent accurate assessment of ST elevation. Do not wait for an old tracing to compare. Widespread ST depression is also read for its territory, not just its presence.

Expected finding: With signs or symptoms highly suspicious of ongoing ischaemia, LBBB, RBBB or a paced rhythm is managed like clear ST elevation, whether or not the block was already known. Sgarbossa and modified Sgarbossa (Smith) criteria are the tools used to identify occlusion behind these patterns. ST depression of 1 mm or more in six or more leads, with ST elevation in aVR or V1, suggests multivessel or left main disease.

2

High-sensitivity cardiac troponin

NICE recommends two early rule-out approaches. One is a single sample on presentation, using a threshold at or near the assay's limit of detection. The other is a multiple-sample strategy: an initial sample and a second at 30 minutes to 3 hours. The ESC 0 hour/1 hour algorithm is the preferred rapid protocol, with 0 hour/2 hour second best. Each sorts patients into rule-out, observe or rule-in.

Expected finding: A rise and/or fall with at least one value above the assay-specific 99th-percentile upper reference limit is acute myocardial injury. MI additionally requires evidence of acute ischaemia. Cut-offs are published per assay, which is a real published reason hospitals differ. Never delay reperfusion for troponin in a clear STEMI.

4,2

Baseline bloods and formal risk assessment

Check FBC, renal function, electrolytes, glucose and a full lipid profile. Once UA or NSTEMI is diagnosed, and aspirin and an antithrombin have been offered, formally assess risk with a score that predicts six-month mortality. GRACE (Global Registry of Acute Cardiac Events) is the example NICE gives. NICE does not mandate GRACE specifically.

Expected finding: The assessment must include a full history covering age, previous MI, and previous PCI or coronary artery bypass grafting. Add blood pressure, heart rate, a resting 12-lead ECG, and troponin, creatinine, glucose and haemoglobin. NICE bands predicted six-month mortality as 1.5% or below (lowest), above 1.5% to 3.0% (low), above 3.0% to 6.0% (intermediate), above 6.0% to 9.0% (high) and over 9.0% (highest).

3

Echocardiography and left ventricular assessment

Use urgent echocardiography for shock, heart failure, a new murmur or diagnostic uncertainty, when it will not delay reperfusion. Assess left ventricular function in every STEMI and NSTEMI, and consider it in unstable angina before discharge.

Expected finding: Regional wall-motion abnormality, impaired ejection fraction, right ventricular involvement, or a mechanical complication such as papillary-muscle rupture or ventricular septal rupture.

3,2

Glucose and post-ACS diabetes screening

Measure blood glucose on admission in every ACS. In people who are hyperglycaemic without known diabetes, check HbA1c before discharge. Also check a fasting blood glucose no earlier than 4 days after the onset of the ACS. Neither test should delay discharge.

Expected finding: Hyperglycaemia after ACS marks increased risk of type 2 diabetes and needs at least annual monitoring of HbA1c or fasting glucose in primary care. Do not routinely offer an oral glucose tolerance test if both results are normal.

3

Management

StepDetailSource
Immediate assessment, monitoring and aspirinUse ABCDE (airway, breathing, circulation, disability, exposure), get IV access, attach rhythm and saturation monitoring, ensure a defibrillator is present and record an ECG. Give aspirin 300 mg orally, chewed or dispersed, unless clearly allergic. Give oxygen only if saturation is below 94%: target 94% to 98%, or 88% to 92% at risk of hypercapnic respiratory failure.3,1,5,6NICE NG185 recommendations 1.1.4 and 1.2.2 for the aspirin loading dose; NICE CG95 recommendation 1.2.3.3 for the oxygen thresholds; Resuscitation Council UK, The ABCDE approach; BNF aspirin monograph
Relieve pain and ischaemiaGlyceryl trinitrate (GTN) sublingual: one tablet (500 or 600 micrograms) or one to two 400 microgram sprays, repeated at 5 minutes, maximum three doses. Avoid nitrates in suspected right ventricular infarction and after a phosphodiesterase-5 inhibitor. Severe pain: morphine 5 to 10 mg by slow IV injection at 1 to 2 mg/minute, or 2.5 to 5 mg if frail.7,8,5BNF glyceryl trinitrate and morphine monographs; Resuscitation Council UK, The ABCDE approach
STEMI: choose the reperfusion strategyActivate the STEMI network on the ECG alone, without waiting for troponin. Presenting within 12 hours of symptom onset, prefer coronary angiography with follow-on primary PCI. The condition is that it can be delivered within 120 minutes of the time when fibrinolysis could have been given. Otherwise offer fibrinolysis. Offer angiography for cardiogenic shock presenting within 12 hours.3NICE NG185 recommendations 1.1.3, 1.1.6, 1.1.7 and 1.1.19
STEMI beyond 12 hours, and after cardiac arrestBeyond 12 hours, consider angiography with follow-on PCI if there is evidence of continuing myocardial ischaemia, and consider angiography with a view to revascularisation for cardiogenic shock. Consider radial rather than femoral access. Do not use level of consciousness after cardiac arrest caused by suspected STEMI to decide whether someone is eligible for angiography.3NICE NG185 recommendations 1.1.2, 1.1.8, 1.1.9 and 1.1.10
STEMI having primary PCI: the second antiplateletOffer prasugrel with aspirin: 60 mg loading, then 10 mg once daily, or 5 mg daily if under 60 kg or aged 75 and over. At 75 and over, use ticagrelor or clopidogrel instead if bleeding risk outweighs effectiveness. If already anticoagulated, offer clopidogrel 300 mg or 600 mg loading (600 mg unlicensed), then 75 mg daily.3,9,10,6NICE NG185 recommendation 1.1.11; BNF prasugrel and clopidogrel monographs
STEMI having primary PCI: antithrombin, chosen by access routeWith radial access, offer unfractionated heparin with a bailout glycoprotein IIb/IIIa inhibitor alongside dual antiplatelet therapy (DAPT). When femoral access is needed, consider bivalirudin instead with the same bailout arrangement; in November 2020 its use with prasugrel and aspirin was off-label. Do not routinely give a glycoprotein IIb/IIIa inhibitor or a fibrinolytic before arrival at the catheter laboratory.3NICE NG185 recommendations 1.1.5, 1.1.12 and 1.1.13
STEMI: the fibrinolytic and its doseTenecteplase IV over 10 seconds, within 6 hours of symptom onset. Dose 30 mg under 60 kg, rising 5 mg per 10 kg band to 50 mg at 90 kg and above. The alteplase alternative is its accelerated myocardial infarction regimen: 15 mg IV bolus, then 0.75 mg/kg over 30 minutes, then 0.5 mg/kg over 60 minutes, maximum 100 mg.3,11,12NICE NG185 recommendation 1.1.19; BNF tenecteplase and alteplase monographs (alteplase accelerated myocardial infarction regimen, not the stroke or pulmonary embolism regimen)
STEMI: what follows fibrinolysisGive an antithrombin at the same time as the fibrinolytic. Repeat the ECG 60 to 90 minutes later. Residual ST elevation suggesting failed reperfusion means immediate coronary angiography with follow-on PCI if indicated, and fibrinolysis must not be repeated. Recurrent ischaemia needs immediate specialist cardiology advice. After successful lysis in a clinically stable patient, consider angiography during the same admission.3NICE NG185 recommendations 1.1.20, 1.1.21, 1.1.22 and 1.1.23
STEMI not treated with PCI: antiplateletsOffer ticagrelor with aspirin: 180 mg loading, then 90 mg twice daily, usually up to 12 months. If bleeding risk is high, consider clopidogrel with aspirin, or aspirin alone. Clopidogrel in STEMI is 300 mg then 75 mg daily for at least 4 weeks at ages 18 to 75. From 76 it is 75 mg daily with no loading dose.3,13,10NICE NG185 recommendations 1.1.24 and 1.1.25; BNF ticagrelor and clopidogrel monographs
UA and NSTEMI: aspirin and the initial antithrombinOffer aspirin 300 mg loading as soon as possible, then 75 mg once daily, continued indefinitely unless contraindicated by bleeding risk or hypersensitivity. Offer fondaparinux 2.5 mg subcutaneously once daily unless bleeding risk is high or immediate angiography is planned, for up to 8 days or until discharge. Avoid fondaparinux if creatinine clearance is under 20 mL/minute.3,6,14NICE NG185 recommendations 1.2.1, 1.2.2 and 1.2.3; BNF aspirin and fondaparinux sodium monographs
UA and NSTEMI: heparin instead, and heparin in the laboratoryWith significant renal impairment, meaning creatinine above 265 micromoles per litre, consider unfractionated heparin instead of fondaparinux. Give 5000 units IV loading (or 75 units/kg), then 18 units/kg/hour by infusion, adjusted by clotting monitoring. Offer unfractionated heparin in the catheter laboratory to anyone having PCI, whether or not fondaparinux was already given; in November 2020 this was off-label.3,15NICE NG185 recommendations 1.2.4, 1.2.5 and 1.2.16; BNF unfractionated heparin monograph
UA and NSTEMI: risk-stratify and time the angiographyDo not offer DAPT before UA or NSTEMI is diagnosed. Offer immediate coronary angiography if the clinical condition is unstable. Otherwise use predicted six-month mortality: above 3.0%, consider angiography with follow-on PCI within 72 hours of first admission if there is no contraindication. At 3.0% or less, consider conservative management, with angiography if ischaemia recurs or is demonstrated.3NICE NG185 recommendations 1.2.6, 1.2.12, 1.2.13, 1.2.14 and 1.2.20
UA and NSTEMI: selecting the second antiplateletHaving coronary angiography with no separate indication for anticoagulation: offer prasugrel or ticagrelor with aspirin, giving prasugrel only once coronary anatomy is defined and PCI is intended. With a separate indication for ongoing oral anticoagulation: clopidogrel with aspirin. When PCI is not indicated: ticagrelor with aspirin, or clopidogrel with aspirin or aspirin alone if bleeding risk is high.3,9,13,10NICE NG185 recommendations 1.2.17, 1.2.21 and 1.2.22
Hyperglycaemia and acute deteriorationKeep blood glucose below 11.0 mmol/litre while avoiding hypoglycaemia, in the first instance considering a dose-adjusted insulin infusion with regular monitoring. Do not routinely offer intensive insulin therapy, meaning an IV infusion of insulin and glucose with or without potassium. Treat cardiac arrest and ventricular arrhythmia through the resuscitation pathway while expediting reperfusion.3,5NICE NG185 recommendations 1.3.1 and 1.3.2; Resuscitation Council UK, The ABCDE approach
Escalate complications immediatelyShock, acute pulmonary oedema, recurrent ischaemia, sudden hypotension, a raised JVP or a new murmur require immediate senior cardiology and critical-care review with emergency echocardiography. Discuss surgery or intervention early when a mechanical complication is suspected.3,2NICE NG185 recommendation 1.2.12; 2023 ESC guidelines for the management of acute coronary syndromes
Secondary prevention: antiplatelets and the statinContinue aspirin 75 mg once daily indefinitely, and continue DAPT for up to 12 months after an MI unless contraindicated. Start atorvastatin 80 mg once daily without delay, aiming for LDL-cholesterol 2.0 mmol/litre or below, or non-HDL cholesterol 2.6 mmol/litre or below. Measure a full lipid profile on admission and again at 2 to 3 months.3,16,6,17NICE NG185 recommendations 1.4.14 and 1.4.15; NICE NG238 recommendations 1.7.1, 1.7.2 and 1.7.5; BNF aspirin and atorvastatin monographs
Secondary prevention: the ACE inhibitorOffer an angiotensin-converting enzyme (ACE) inhibitor once stable and continue indefinitely. NICE advises short-interval inpatient titration, but BNF schedules differ by indication. With clinical heart failure, ramipril starts 48 hours after infarction: 2.5 mg twice daily for 3 days, then 5 mg twice daily if tolerated. Use the cardiology formulary. Use an angiotensin receptor blocker if intolerant, never both.3,18NICE NG185 recommendations 1.4.6, 1.4.7, 1.4.8 and 1.4.9; BNF ramipril monograph
Secondary prevention: the beta-blockerOffer a beta-blocker after MI once haemodynamically stable. NICE names no preferred agent. With heart failure and reduced left ventricular ejection fraction, bisoprolol can start at 1.25 mg once daily and titrate stepwise to 10 mg, continuing indefinitely. Without reduced ejection fraction, consider 12 months and discuss stopping thereafter. Do not start beyond 12 months without another indication.3,19NICE NG185 recommendations 1.4.27, 1.4.29, 1.4.30, 1.4.31 and 1.4.33; BNF bisoprolol fumarate monograph
Secondary prevention: aldosterone antagonist, monitoring and what not to giveWith symptoms or signs of heart failure and reduced LVEF after MI, start an aldosterone antagonist licensed for post-MI treatment within 3 to 14 days, preferably after the ACE inhibitor. Halve the dose or stop it if hyperkalaemia is a problem. Check renal function, electrolytes and blood pressure before starting an ACE inhibitor and again within 1 to 2 weeks.3NICE NG185 recommendations 1.4.10, 1.4.38 and 1.4.41
Discharge, rehabilitation and activityDo not offer nicorandil, and do not routinely offer calcium channel blockers, to reduce cardiovascular risk after MI. Begin cardiac rehabilitation before discharge, with the first session within 10 days of discharge. Advise 20 to 30 minutes of daily activity to slight breathlessness, and that sexual activity is usually safe after about 4 weeks.3NICE NG185 recommendations 1.4.34, 1.4.37, 1.8.13, 1.8.33 and 1.9.11

Illustrations

Plaque disruption and coronary thrombosisDiagram of an atherosclerotic plaque with cap disruption, platelet activation and thrombus in the coronary lumen. This is a common type 1 ACS mechanism, not a diagram that determines the presenting ECG label or proves the degree of occlusion.PassFinals ยท original
Schematic troponin rise and fallA teaching schematic of troponin concentration over time after myocardial injury. It is not an assay rule-out algorithm: high-sensitivity assays use validated, assay-specific thresholds and intervals, and symptom timing and acute change must be interpreted with evidence of ischaemia.PassFinals ยท original

Differentials

Aortic dissection

Abrupt severe chest or back pain, pulse or neurological deficit, new aortic regurgitation or marked blood-pressure asymmetry. Exclude it urgently before fibrinolysis or antithrombotic escalation.

Pulmonary embolism

Acute breathlessness, pleuritic pain, hypoxaemia, venous thromboembolism risk factors or right-heart strain. Troponin can rise without coronary infarction.

Pericarditis or myocarditis

Pleuritic or positional pain, diffuse rather than territorial ECG change, recent inflammatory illness, or cardiac dysfunction disproportionate to the coronary findings. Myocarditis can raise troponin.

Pneumothorax

Sudden pleuritic pain with unilateral reduced air entry. Tension physiology causes hypotension and needs immediate decompression.

Oesophageal rupture

Severe chest pain after vomiting or instrumentation, with systemic toxicity, surgical emphysema or pleural contamination.

Non-ischaemic myocardial injury or type 2 MI

Troponin elevation in sepsis, tachyarrhythmia, anaemia, heart failure or renal disease. It needs evidence of acute ischaemia before being labelled MI, and does not automatically receive the type 1 ACS antithrombotic pathway.

Complications

  • Ventricular tachycardia, ventricular fibrillation, bradyarrhythmia and atrioventricular block
  • Acute left ventricular failure, pulmonary oedema and cardiogenic shock
  • Papillary-muscle rupture with acute mitral regurgitation, ventricular septal rupture or free-wall rupture
  • Recurrent ischaemia, reinfarction and stent thrombosis
  • Left ventricular thrombus, systemic embolism and ventricular aneurysm
  • Early pericarditis and later post-MI inflammatory pericarditis
  • Bleeding from antiplatelet, antithrombin and fibrinolytic treatment

Prognosis

Outcome depends on the presenting instability, infarct size and location, time to effective reperfusion, left ventricular function, comorbidity and recurrent ischaemia. Prompt pathway activation, evidence-based revascularisation, bleeding-aware antithrombotic treatment, lipid lowering, risk-factor control and post-MI rehabilitation all reduce recurrent events.

Guidelines

  • Acute coronary syndromes (NG185) (NICE, 2020)
  • Recent-onset chest pain of suspected cardiac origin (CG95) (NICE, 2010)
  • High-sensitivity troponin tests for early rule out of NSTEMI (HTG552) (NICE, 2020)
  • Cardiovascular disease: risk assessment and reduction, including lipid modification (NG238) (NICE, 2023)
  • 2023 ESC Guidelines for the management of acute coronary syndromes (European Society of Cardiology, 2023)
  • The ABCDE approach (Resuscitation Council UK, 2024)

References

  1. NICE, Recent-onset chest pain of suspected cardiac origin: assessment and diagnosis, recommendations (NICE-published full text) (CG95)Published 24 Mar 2010 | Updated 30 Nov 2016
  2. 2023 ESC Guidelines for the management of acute coronary syndromes, European Heart Journal 2023;44(38):3720-3826 (doi:10.1093/eurheartj/ehad191)Published 25 Aug 2023
  3. NICE, Acute coronary syndromes (NG185)Published 18 Nov 2020
  4. NICE HealthTech guidance, High-sensitivity troponin tests for the early rule out of NSTEMI, recommendations 1.2 and 1.3 (HTG552)Published 26 Aug 2020
  5. Resuscitation Council UK, The ABCDE approachPublished 1 Oct 2015 | Updated 1 Jul 2024
  6. BNF, Aspirin (BNF drug monograph)
  7. BNF, Glyceryl trinitrate (BNF drug monograph)
  8. BNF, Morphine (BNF drug monograph)
  9. BNF, Prasugrel (BNF drug monograph)
  10. BNF, Clopidogrel (BNF drug monograph)
  11. BNF, Tenecteplase (BNF drug monograph)
  12. BNF, Alteplase (BNF drug monograph)
  13. BNF, Ticagrelor (BNF drug monograph)
  14. BNF, Fondaparinux sodium (BNF drug monograph)
  15. BNF, Heparin (unfractionated) (BNF drug monograph)
  16. NICE, Cardiovascular disease: risk assessment and reduction, including lipid modification (NG238)Published 14 Dec 2023
  17. BNF, Atorvastatin (BNF drug monograph)
  18. BNF, Ramipril (BNF drug monograph)
  19. BNF, Bisoprolol fumarate (BNF drug monograph)

Evidence checked: 2026-08-08

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.