01Overview, aetiology and pathophysiologyDefinition, plaque disruption, thrombosis and the complete initial pathway.
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.
- 1Recognise and stabilise
ABCDE, cardiac monitoring with defibrillator access, IV access, observations and focused examination. Treat shock, pulmonary oedema or life-threatening arrhythmia immediately.
- 2ECG 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.
- 3Give 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.
- 4Choose the branch
STEMI: immediate reperfusion decision. NSTEMI/unstable angina: confirm the diagnosis, give antithrombin therapy when appropriate, calculate GRACE and choose angiography timing.
- 5Make every medicine traceable
Record indication, loading dose, maintenance dose, contraindication check and stop/review date—especially when antiplatelet and anticoagulant drugs overlap.
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.
02Clinical features, red flags and differential diagnosisSymptoms, instability, myocardial injury, infarction subtypes and time-critical alternatives.
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.
Current or recurrent pressure, prolonged pain, sweating, nausea, vomiting or breathlessness.
Regional ST elevation or dynamic ischaemic ST–T changes.
Shock, poor perfusion, pulmonary oedema, syncope or serious arrhythmia.
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”.
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.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.A primary coronary event, usually plaque disruption with thrombosis.
Use the ACS antithrombotic and revascularisation pathway.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.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.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.
03Investigations and diagnosisThe ordered ECG and troponin pathway, followed by targeted tests for uncertainty.
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.
- 1First line: 12-lead ECG
Obtain it as soon as possible without delaying emergency transfer or treatment.
- 2Serial high-sensitivity troponin
Use the locally validated assay pathway and interpret change over time with symptom timing.
- 3Repeat and extend the ECG
Repeat during recurrent pain; add posterior V7–V9 or right-sided leads when the territory may be hidden.
- 4Target 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.
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.
ST depression V1–V3
Consider reciprocal posterior change. Repeat the ECG and add V7–V9 when the history and pattern fit.
Inferior STEMI + hypotension
Obtain right-sided leads, look for right-ventricular infarction and avoid uncritical preload-reducing treatment. Escalate urgently.
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.
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.
04Immediate managementThe first ten minutes, including aspirin, pain relief, oxygen and safety checks.
Aspirin
300 mg orally onceGive 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.
GTN spray
400–800 micrograms SLRepeat 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.
IV opioid
Diamorphine 5 mg slow IVA 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.
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.
GTN response does not diagnose ACS. Opioids are not routine for anxiety or mild pain and may delay absorption of oral P2Y12 inhibitors.
05STEMI managementReperfusion strategy, antiplatelets, procedural anticoagulation and fibrinolysis.
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.
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.
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.
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.
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.
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.
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.
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
Give as a single IV bolus over about 10 seconds.
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.
06NSTEMI and unstable angina managementAntithrombin therapy, risk stratification, angiography and antiplatelet selection.
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.
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.
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.
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.
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.
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.
07Secondary prevention and follow-upDischarge medicines, monitoring targets, rehabilitation and review.
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.
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.
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.
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.
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.
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.
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.
08Complications and special situationsEarly complications and modifications for renal disease, anticoagulation, age and MINOCA.
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?Ventricular arrhythmia, bradyarrhythmia, acute heart failure, recurrent ischaemia and cardiogenic shock.
Continuous monitoring, repeat ECG, haemodynamic assessment and immediate escalation.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.Assess LV function, reconcile antithrombotic stop dates, start secondary prevention and refer to cardiac rehabilitation.
Give written return precautions and the follow-up route.09Applied casesExamples that test safe first actions and management choices.
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.Best next step
Rank plausible options using setting, timing, stability and information already available.
Trap: treating one abnormal number instead of the whole presentation.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.