Skip to textbook content
Doctor’s PassportTextbook
TopicsAll topics

Loading topic navigation…

Textbook navigation
TopicsAll topics

Loading topic navigation…
← Cardiology indexOn this topic
Overview and mechanismClinical features and differentialInvestigationsImmediate managementSTEMI managementNSTEMI / UA managementSecondary preventionComplications and special situationsApplied casesQuestionsSources
Full textbook11 sections
Complete UK clinical chapter
Educational draft · awaiting clinical reviewThe full textbook develops clinical judgement but does not replace live national or local guidance, specialist advice, or current prescribing information.

Acute coronary syndrome

Cardiology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
!
Suspected ACS is time-critical.

Current or recurrent ischaemia, haemodynamic instability, pulmonary oedema, a serious arrhythmia or a STEMI-pattern ECG requires emergency escalation. Do not wait for troponin before activating a reperfusion pathway.

Overview, aetiology and pathophysiology

Acute coronary syndrome is an umbrella term covering STEMI, NSTEMI and unstable angina. In a typical type 1 event, disruption of an atherosclerotic plaque triggers platelet activation and thrombus formation. Coronary blood flow falls, the myocardium becomes ischaemic and sustained injury releases troponin.

Run stabilisation, diagnosis and transfer in parallel. The decisive branch is persistent ST elevation or an equivalent occlusion pattern versus non-ST-elevation ACS; instability overrides a leisurely risk-score sequence.

1Plaque disruption→
2Platelet activation→
3Thrombus→
4Coronary flow falls→
5Ischaemia→
6Injury + troponin
  1. 1
    Recognise and stabilise

    ABCDE, cardiac monitoring with defibrillator access, IV access, observations and focused examination. Treat shock, pulmonary oedema or life-threatening arrhythmia immediately.

  2. 2
    ECG now

    Obtain a 12-lead ECG as soon as possible without delaying transfer. Repeat during recurrent pain and use posterior/right-sided leads when the territory may be hidden.

  3. 3
    Give aspirin and control pain

    Aspirin 300 mg orally once unless aspirin hypersensitivity or another clear contraindication such as active major bleeding. Use GTN if haemodynamics allow; reserve a titrated IV opioid for severe persistent pain.

  4. 4
    Choose the branch

    STEMI: immediate reperfusion decision. NSTEMI/unstable angina: confirm the diagnosis, give antithrombin therapy when appropriate, calculate GRACE and choose angiography timing.

  5. 5
    Make every medicine traceable

    Record indication, loading dose, maintenance dose, contraindication check and stop/review date—especially when antiplatelet and anticoagulant drugs overlap.

Educational boundary

The doses below are adult UK guideline or licensed examples. Pregnancy, active bleeding, extreme body weight, organ failure, shock and procedures require immediate senior/pharmacy input and the current BNF or specialist protocol.

Clinical features, red flags and differential diagnosis

Typical central chest pressure is important, but ACS does not require a textbook presentation. Assess the whole pattern and actively consider other time-critical causes of chest pain.

Key symptoms

Current or recurrent pressure, prolonged pain, sweating, nausea, vomiting or breathlessness.

ECG

Regional ST elevation or dynamic ischaemic ST–T changes.

Instability

Shock, poor perfusion, pulmonary oedema, syncope or serious arrhythmia.

Alternatives

Look for aortic dissection, pulmonary embolism and other emergency diagnoses.

A raised troponin shows cardiomyocyte injury. Myocardial infarction additionally requires an acute rise or fall and clinical evidence of ischaemia. This avoids converting every troponin rise in sepsis, tachyarrhythmia, pulmonary embolism, myocarditis, renal disease or heart failure into “NSTEMI”.

Myocardial injury

Troponin above the assay's 99th percentile. This is a laboratory finding, not yet a diagnosis of infarction.

Look for a rise or fall, timing, chronic elevation and non-ischaemic causes.
Myocardial infarction

Acute myocardial injury plus clinical evidence of ischaemia, such as compatible symptoms, ECG change or new imaging evidence.

Do not label every troponin rise as ACS.
Type 1 MI

A primary coronary event, usually plaque disruption with thrombosis.

Use the ACS antithrombotic and revascularisation pathway.
Type 2 MI

Ischaemic injury caused by oxygen supply–demand imbalance without acute atherothrombosis.

Treat the precipitant and assess coronary disease; do not automatically copy a type 1 regimen.
MINOCA

A working label when MI criteria are met but angiography shows no obstructive lesion explaining the event.

Investigate the mechanism: plaque disruption, spasm, embolism, dissection, myocarditis and takotsubo syndrome lead to different plans.
Useful documentation

Investigations and diagnosis

No single gold-standard test

ACS is diagnosed from the clinical presentation, serial ECGs and high-sensitivity troponin together. Invasive angiography is definitive for coronary anatomy and can enable treatment, but it is not the universal first diagnostic test.

  1. 1
    First line: 12-lead ECG

    Obtain it as soon as possible without delaying emergency transfer or treatment.

  2. 2
    Serial high-sensitivity troponin

    Use the locally validated assay pathway and interpret change over time with symptom timing.

  3. 3
    Repeat and extend the ECG

    Repeat during recurrent pain; add posterior V7–V9 or right-sided leads when the territory may be hidden.

  4. 4
    Target uncertainty

    Use echocardiography, angiography or alternative imaging according to haemodynamics, the differential and the treatment decision.

Use ECG and high-sensitivity troponin as a sequence. A normal first ECG does not exclude ACS, and a normal early troponin may be too early. Interpret the assay result with symptom timing, change over time, ECG findings and the pre-test probability.

01

Ongoing pain, first ECG normal

Continue monitoring, repeat the tracing during symptoms and use the validated serial troponin algorithm. One normal snapshot cannot end the assessment.

02

ST depression V1–V3

Consider reciprocal posterior change. Repeat the ECG and add V7–V9 when the history and pattern fit.

03

Inferior STEMI + hypotension

Obtain right-sided leads, look for right-ventricular infarction and avoid uncritical preload-reducing treatment. Escalate urgently.

04

Troponin high, story discordant

Confirm the rise/fall and an ischaemic feature, then actively test alternatives such as PE, myocarditis, severe hypertension, arrhythmia or sepsis.

Assay boundary

Absolute troponin thresholds and delta values differ by assay. Use the current laboratory-validated 0/1-hour, 0/2-hour or other pathway; never transplant a numerical delta from another assay.

Immediate management

Antiplatelet

Aspirin

300 mg orally once

Give as soon as possible unless aspirin hypersensitivity or another clear contraindication such as active major bleeding. Document any pre-hospital dose; continue 75 mg once daily after MI unless contraindicated or a separate oral-anticoagulation plan changes the combination.

Pain: first option

GTN spray

400–800 micrograms SL

Repeat every 5 minutes to a maximum of 3 sprays (1.2 mg) in 15 minutes if symptoms and blood pressure permit. Avoid in shock, SBP below 90 mmHg, preload dependence or recent PDE5-inhibitor use.

Pain: escalation

IV opioid

Diamorphine 5 mg slow IV

A licensed MI example for severe persistent pain: give at 1 mg/min, then 2.5–5 mg more if needed. Reduce in older, frail, renal or hepatic impairment; monitor BP, respiratory rate, SpO₂ and consciousness.

Hypoxaemia only

Oxygen

Target 94–98%

Give only if SpO₂ is below 94% when there is no hypercapnic risk. If hypercapnic respiratory failure is possible, target 88–92% until blood gases guide treatment.

Do not let symptom relief delay reperfusion

GTN response does not diagnose ACS. Opioids are not routine for anxiety or mild pain and may delay absorption of oral P2Y12 inhibitors.

STEMI management

First-line / preferred reperfusion

Primary PCI

For symptoms under 12 hours, offer immediate angiography and PCI if it can be delivered within 120 minutes of when fibrinolysis could have been given. The 120 minutes is a maximum relative delay, not permission to wait.

Alternative when timely PCI is unavailable

Fibrinolysis + antithrombin

After a contraindication check, give fibrinolysis with an antithrombin. Repeat the ECG at 60–90 minutes. If residual ST elevation suggests failed reperfusion, offer immediate angiography with PCI if indicated and do not repeat fibrinolysis. If ischaemia recurs, obtain immediate specialist cardiology advice and offer angiography/PCI when appropriate. If reperfusion succeeds and the patient is stable, consider angiography during the same admission.

Escalation: shock or presentation after 12 hours

Angiography remains an active decision

For cardiogenic shock within 12 hours, offer immediate angiography with PCI if indicated. If shock persists or develops after 12 hours, consider angiography and revascularisation. When presentation is after 12 hours with continuing myocardial ischaemia, consider angiography with PCI if indicated.

If reperfusion is unsuitable

Medical management

Continue specialist ACS care, document why reperfusion is unsuitable and reassess if ischaemia, shock or the clinical picture changes.

P2Y12 inhibitor with aspirin for primary PCI

These are conditional options rather than an arbitrary potency ladder. Prasugrel is the NICE preference when proceeding to primary PCI without oral anticoagulation; bleeding risk, age, stroke history and anticoagulation determine the alternative.

DrugAdult regimenWhen it fits or fails
Prasugrel

60 mg oral load → 10 mg once daily

If body weight is below 60 kg, use 5 mg once daily. At age 75 or over it is generally not recommended; if selected after specialist benefit–risk assessment, use 5 mg once daily. Do not use after previous stroke/TIA. In NSTEMI, load only after anatomy is known and PCI is intended.

NSTEMI and unstable angina management

Do not start routine dual antiplatelet therapy before unstable angina or NSTEMI is established. Once diagnosed, give aspirin 300 mg, then select antithrombin therapy and angiography timing.

1 · First-line antithrombin when appropriate

Fondaparinux first when appropriate

2.5 mg SC once daily, started after diagnosis and continued for up to 8 days or earlier discharge, when bleeding risk is not high and immediate angiography is not planned. It is contraindicated when CrCl is below 20 mL/min; evidence is limited at CrCl 20–30 mL/min, so weigh benefit and bleeding risk.

If immediate angiography is planned, use UFH. Separately, NICE says to consider monitored UFH when serum creatinine is above 265 micromol/L. A general licensed UA regimen is 5,000 units IV loading, then 1,000–2,000 units/hour, titrated to APTT 1.5–2.5 times control; this is not the PCI bolus. If PCI follows fondaparinux, give cath-lab UFH.

2 · Angiography timing

Stability and GRACE set the clock

  • Unstable: immediate angiography.
  • Predicted 6-month mortality above 3%: consider angiography with PCI if indicated within 72 hours.
  • 3% or below: conservative management is reasonable; reconsider for recurrent or demonstrable ischaemia.
3 · P2Y12 choice

Match the drug to the strategy

  • PCI, no oral anticoagulant: prasugrel or ticagrelor with aspirin; give prasugrel only after anatomy is known and PCI is intended.
  • PCI plus long-term anticoagulant: clopidogrel with the anticoagulant; explicitly document combination duration and stop dates.
  • No PCI: ticagrelor plus aspirin unless bleeding risk is high; then consider clopidogrel plus aspirin or aspirin alone.
Renal distinction

NICE's creatinine threshold and the fondaparinux SmPC's CrCl cut-off answer different practical questions. The SmPC contraindicates fondaparinux when CrCl is below 20 mL/min; renal function, weight and trajectory still require medication review.

Acute antithrombotic checklist

Record current body weight before weight-based tenecteplase, enoxaparin, bivalirudin or UFH. Before selection, document haemoglobin, platelet count, renal function and trajectory, active bleeding and concurrent antithrombotics. For a UFH infusion, begin APTT monitoring 4–6 hours after initiation and repeat after dose changes; during bivalirudin, monitor access and non-access bleeding and use ACT through the cath-lab pathway. Recheck haemoglobin, platelets and renal function promptly if bleeding, thrombocytopenia or renal deterioration occurs.

Secondary prevention and follow-up

Antiplatelet

Aspirin 75 mg once daily is generally continued indefinitely after MI unless contraindicated or there is a separate oral-anticoagulation plan. Continue the selected second antiplatelet for the documented duration—commonly up to 12 months—then review rather than allowing an accidental indefinite combination.

Lipid lowering

Start atorvastatin 80 mg once daily without delay unless interactions, high adverse-effect risk or preference justify less. In CKD, NICE starts atorvastatin 20 mg; increase if response is inadequate and eGFR is at least 30, and agree higher doses with a renal specialist when eGFR is below 30. Recheck full lipids and liver transaminases at 2–3 months, and transaminases again at 12 months. If LDL is above 2.0 mmol/L or non-HDL is above 2.6 mmol/L, confirm adherence and maximum tolerated statin, then discuss additional lipid lowering. Separately, consider ezetimibe 10 mg once daily for further risk reduction even when target is met; if target remains unmet or statins are not tolerated, assess NICE eligibility for inclisiran, bempedoic acid/ezetimibe or a PCSK9 inhibitor.

ACE inhibitor

Start an ACE inhibitor as soon as the person is haemodynamically stable and continue it indefinitely; NICE does not require a 48-hour delay. Titrate at short intervals before discharge towards the maximum tolerated or target dose, completing titration within 4–6 weeks of discharge when necessary. The cited ramipril SmPC gives a licensed post-MI example specifically for people with clinical heart-failure signs: start after 48 hours at 2.5 mg twice daily, or 1.25 mg twice daily if 2.5 mg is not tolerated, then double at 1–3-day intervals towards 5 mg twice daily. Check blood pressure, creatinine/eGFR and potassium before treatment, within 1–2 weeks and during titration, then at least annually once stable.

Beta-blocker

Start once stable when there is no shock, acute decompensated heart failure, significant bradycardia, hypotension or high-grade AV block. A practical bisoprolol example is 5 mg once daily, usually 10 mg once daily if needed and tolerated; this dose is licensed for hypertension/stable angina rather than specifically for post-MI secondary prevention. If HFrEF is present, use the licensed slower heart-failure titration from 1.25 mg once daily towards 10 mg. Continue for about 12 months when EF is preserved and indefinitely when EF is reduced.

Mineralocorticoid antagonist

Complications and special situations

Chronic kidney disease

Expect more chronically elevated troponin and higher bleeding risk, but do not dismiss a rise/fall or ischaemic presentation. Renal function changes fondaparinux/enoxaparin use, contrast planning, ACE-inhibitor monitoring and lipid dosing. NICE starts atorvastatin 20 mg in CKD; increase if response is inadequate and eGFR is at least 30, and agree higher doses with a renal specialist when eGFR is below 30.

Ask: acute change, ischaemic evidence, CrCl/eGFR, weight, bleeding risk?

Already anticoagulated

Atrial fibrillation or another indication changes the P2Y12 choice and usually shortens combination therapy. After PCI, clopidogrel is generally used rather than prasugrel or ticagrelor with the anticoagulant.

Ask: why anticoagulated, PCI/stent, exact stop dates?

Older age, low weight or previous bleeding

Review haemoglobin, renal function, intracranial/GI bleeding, frailty and the necessity of each agent. Prasugrel and fibrinolysis carry specific age/weight cautions.

Ask: what benefit is expected, and what harm is plausible?

MINOCA

MINOCA is a working diagnosis, not the mechanism. Review imaging and use targeted testing to distinguish plaque disruption, spasm, dissection, embolism, myocarditis and takotsubo syndrome.

Ask: which mechanism remains unproven?
Minutes to hours

Ventricular arrhythmia, bradyarrhythmia, acute heart failure, recurrent ischaemia and cardiogenic shock.

Continuous monitoring, repeat ECG, haemodynamic assessment and immediate escalation.
Hours to days

Sudden pulmonary oedema, shock or a new murmur can signal a mechanical complication.

Re-examine and obtain urgent echocardiography; do not attribute abrupt deterioration to routine post-MI recovery.
Before discharge

Assess LV function, reconcile antithrombotic stop dates, start secondary prevention and refer to cardiac rehabilitation.

Give written return precautions and the follow-up route.

Applied cases

MLA

Safe first action

Recognise the emergency, choose the immediate investigation or treatment and avoid a harmful delay.

Trap: waiting for troponin before escalating a STEMI-pattern presentation.
MSRA

Best next step

Rank plausible options using setting, timing, stability and information already available.

Trap: treating one abnormal number instead of the whole presentation.
Foundation+

Ward-level application

Prescribe safely, monitor response and recognise when senior or specialist escalation is needed.

Trap: copying a standard antithrombotic bundle into CKD or anticoagulation.
Applied case 1Chest pain, dynamic troponin, no obstructive lesion

Question: What is the most accurate working diagnosis immediately after angiography?

Answer: MINOCA, provided MI criteria are met. It is a working diagnosis, not a mechanism. Review the angiogram and use targeted testing—often echocardiography and cardiac MRI—to distinguish infarction from myocarditis, takotsubo syndrome and other causes.

Why the tempting answer fails: “NSTEMI, discharge on standard therapy” closes the diagnostic process before the cause is known.

Applied case 2NSTEMI in a patient taking apixaban for atrial fibrillation

Question: What must be settled before copying the usual dual-antiplatelet pathway?

Answer: The reason for anticoagulation, whether PCI/stenting occurs, bleeding risk and the duration of combined therapy. NICE generally uses clopidogrel with the anticoagulant after PCI rather than prasugrel or ticagrelor.

Why the tempting answer fails: Adding two antiplatelets indefinitely ignores the increased bleeding burden and the need for explicit stop dates.

Practice

Two practice questions

Your practice draft is saved in this browser.

Question 1 of 2
0 correct
CardiologyOriginal SBA

A normal initial ECG

A 52-year-old woman reports 25 minutes of central chest pressure with nausea and marked sweating. She is now pain-free and her first ECG is normal. Which statement is most accurate?

Choose one answer, then submit
← Rapid synopsisBack to overviewAll Cardiology topics →
Sources and review status20 sources · checked 27 August 2026 · clinical review pending+
Sources and governance

National pathway, licensed dose examples, visible limits

NICE NG185 remains the UK management anchor and was last reviewed on 29 July 2026. Diagnostic context uses NICE CG95 and the Fourth Universal Definition of MI. Exact medicine examples use current UK SmPCs; source check completed 27 August 2026. Clinical approval remains outstanding.

  • NICE NG185: Acute coronary syndromes — recommendations
  • NICE CG95: Recent-onset chest pain — recommendations
  • NICE NG238: Lipid modification — secondary prevention
  • BNF: Acute coronary syndromes treatment summary
  • ESC: typical PCI anticoagulant dosing
  • Fourth Universal Definition of Myocardial Infarction
  • GTN spray — UK SmPC
  • Diamorphine injection — UK SmPC
  • Prasugrel — UK SmPC
  • Ticagrelor — UK SmPC
  • Clopidogrel — UK SmPC
  • Fondaparinux — UK SmPC
  • Unfractionated heparin — UK SmPC
  • Bivalirudin — UK SmPC
  • Tenecteplase — UK SmPC
  • Enoxaparin — UK SmPC
  • Ramipril — UK SmPC
  • Bisoprolol — UK SmPC
  • Ezetimibe — UK SmPC
  • Eplerenone — UK SmPC
Authoring stateComplete draftClinical stateAwaiting review

State the level of certainty: “acute myocardial injury with dynamic ST depression; type 1 NSTEMI likely” carries more information than treating the troponin as the diagnosis.

Ticagrelor

180 mg oral load → 90 mg twice daily

Use with aspirin 75–150 mg daily. Typical ACS duration is 12 months unless bleeding, surgery, intolerance or a revised cardiology plan changes it. Avoid after intracranial haemorrhage and with strong CYP3A4 inhibitors.

Clopidogrel

Strategy- and age-specific loading → 75 mg once daily

Selected SmPC regimen: NSTE-ACS with PCI intended—300 mg, or consider 600 mg only if under 75; primary PCI or PCI more than 24 hours after fibrinolysis—600 mg, with individual bleeding assessment at age 75 or over; PCI within 24 hours after fibrinolysis—300 mg. Medically treated fibrinolytic STEMI—300 mg then 75 mg daily, but if over 75 start 75 mg without a load. The public BNF describes a 600 mg pre-PCI load as unlicensed while this product SmPC licenses it in defined settings; document the source and strategy.

Procedural anticoagulant route

For radial primary PCI, NICE uses UFH with a GP IIb/IIIa inhibitor only as bailout. A common ACT-guided cath-lab regimen is UFH 70–100 units/kg IV, reduced to about 50–70 units/kg if a GP IIb/IIIa inhibitor is planned. For femoral PCI, NICE says to consider bivalirudin plus bailout GPI: 0.75 mg/kg IV bolus followed immediately by 1.75 mg/kg/hour for the procedure; reduce the infusion to 1.4 mg/kg/hour when GFR is 30–59 mL/min and do not use below GFR 30. The cited bivalirudin product is licensed with aspirin and clopidogrel; bivalirudin with prasugrel plus aspirin is off-label, as NICE notes. Make that specialist decision explicit and use the live cath-lab protocol.

When fibrinolysis is used

Licensed tenecteplase example

Give as a single IV bolus over about 10 seconds.

Below 60 kg30 mg
60 to below 70 kg35 mg
70 to below 80 kg40 mg
80 to below 90 kg45 mg
90 kg or more50 mg
The UK MI licence states treatment within 6 hours, whereas NICE permits a fibrinolysis strategy within 12 hours when timely PCI is unavailable. The specialist network must resolve that 6–12-hour mismatch. The current UK SmPC advises caution at age 75 or over; it does not mandate a universal half-dose.
Common enoxaparin antithrombin

Under 75: 30 mg IV bolus, immediately followed by 1 mg/kg SC, then 1 mg/kg SC every 12 hours; cap each of the first two SC doses at 100 mg.

Age 75 or over: omit the IV bolus; give 0.75 mg/kg SC every 12 hours, capped at 75 mg for each of the first two doses.

CrCl 15–30 mL/min: use every-24-hour dosing; under 75 still receives the 30 mg IV bolus, while over 75 receives no bolus and 1 mg/kg SC every 24 hours. Avoid below CrCl 15 mL/min outside haemodialysis.

Give enoxaparin between 15 minutes before and 30 minutes after fibrinolysis begins; continue up to 8 days or discharge. This is a licensed common option, not a NICE-mandated choice.
Open the fibrinolysis safety screen

Do not give tenecteplase with a significant bleeding disorder now or in the preceding 6 months; effective oral anticoagulant activity; hypersensitivity to tenecteplase, an excipient or gentamicin; any previous haemorrhagic or unknown-origin stroke; ischaemic stroke/TIA within 6 months; any history of central-nervous-system damage including CNS neoplasm, aneurysm, intracranial surgery or spinal surgery; severe uncontrolled hypertension; major surgery or significant trauma within 2 months; recent head trauma; bacterial endocarditis/pericarditis; acute pancreatitis; severe hepatic disease; active ulcerative GI disease; bleeding-risk neoplasm; arterial aneurysm/AV malformation; or dementia.

Additional high-risk features include SBP above 160 mmHg, recent GI/GU bleeding, recent IM injection or non-compressible vessel puncture, traumatic/prolonged CPR, age 75 or over and weight below 50 kg. Use the live thrombolysis checklist.

If there is clinical heart failure with LVEF 40% or less, start eplerenone 25 mg once daily 3–14 days after MI, usually after ACE inhibition, and titrate to 50 mg once daily within 4 weeks. With CrCl 30–60 mL/min, start 25 mg on alternate days; severe renal impairment/eGFR below 30 mL/min/1.73 m² is contraindicated. Experience after MI is limited below CrCl 50 and doses above 25 mg daily have not been studied there. Do not start if potassium is above 5.0 mmol/L; check potassium and renal function at baseline, 1 week, 1 month and after dose changes.

Recovery

Document LV function, medicines and stop dates; refer to cardiac rehabilitation before discharge; address smoking, activity, diet, weight, blood pressure and diabetes; explain when recurrent pain or breathlessness requires urgent help.

Monitoring matters

Before discharge, check haemoglobin, renal function, potassium, blood pressure and heart rate against the proposed regimen. Give the patient a plain-language list stating what each medicine does, how long it is intended for and who will review it.

JurisdictionUnited Kingdom