ST-elevation myocardial infarction

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

STEMI usually reflects acute coronary occlusion, but the ECG must be interpreted in its clinical context. Posterior infarction, paced rhythm and bundle-branch block can obscure standard criteria; reciprocal change and serial traces help.

Reperfusion choice is time-dependent. Primary PCI is preferred when the NICE 120-minute threshold is achievable; fibrinolysis is an active alternative for eligible early presenters when it is not, followed by planned transfer to a PCI centre.

Treatment does not end with an open artery. Monitor for no-reflow, reinfarction, heart failure, shock, arrhythmia, pericarditis and mechanical complications, then implement prevention, rehabilitation and follow-up.

Key points

Obtain and interpret a 12-lead ECG promptly; repeat it and add posterior or right-sided leads when the first trace is non-diagnostic but suspicion remains.
Give aspirin 300 mg as soon as possible unless there is clear allergy or active contraindication.
Offer primary PCI within 12 hours of symptom onset when it can be delivered within 120 minutes of the time fibrinolysis could have been given.
If timely primary PCI is not possible within 12 hours and there is no contraindication, offer fibrinolysis rather than accepting prolonged delay.
Before fibrinolysis, check the chosen product's full SmPC; major exclusions include previous haemorrhagic stroke or stroke of unknown origin, ischaemic stroke or TIA within 6 months, significant active or recent bleeding, effective oral anticoagulation, intracranial disease, recent major surgery or trauma, severe uncontrolled hypertension and suspected aortic dissection.
After fibrinolysis, repeat ECG at 60–90 minutes; residual ST elevation suggesting failed reperfusion requires immediate rescue angiography and PCI, not repeat lysis.
Give oxygen only when needed to achieve 94–98% saturation, or 88–92% for people at risk of hypercapnic respiratory failure; do not routinely give oxygen to a normoxic patient.
Inferior STEMI with hypotension warrants right-sided leads and caution with nitrates because right-ventricular preload may be critical.
Start secondary prevention and cardiac rehabilitation before discharge, with an explicit antiplatelet plan and LV-function assessment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Acute atherothrombosis

Rupture or erosion of an atherosclerotic coronary plaque exposes thrombogenic material, causing platelet-rich thrombus that can abruptly occlude an epicardial artery.

Atherosclerotic risk burden

Smoking, diabetes, hypertension, dyslipidaemia, kidney disease and established vascular disease promote plaque formation, inflammation and instability, increasing the likelihood of an occlusive event.

Non-atherosclerotic coronary occlusion

Spontaneous coronary dissection, embolism or intense coronary spasm can cause acute severe flow limitation or occlusion and a STEMI presentation, particularly when angiography shows little conventional plaque.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Coronary plaque is disrupted
In the usual atherothrombotic mechanism, a vulnerable plaque ruptures or erodes, exposing thrombogenic material to circulating blood and initiating local platelet adhesion and activation.
2
Occlusive thrombus forms
Activated platelets aggregate while coagulation generates fibrin, enlarging thrombus until coronary flow becomes critically reduced or completely interrupted within the culprit artery.
3
An acute transmural injury pattern develops
Severe downstream ischaemia impairs relaxation and contraction, while regional electrical injury currents can produce characteristic ST-segment elevation. This ECG pattern does not mean that full-thickness necrosis is already complete.
4
Myocytes undergo necrosis
Persistent ischaemia causes irreversible cell death that progresses across the myocardial wall and releases cardiac troponin, with infarct size increasing as occlusion continues.
5
Reperfusion modifies injury
Timely restoration of flow salvages threatened myocardium, but microvascular obstruction, reperfusion arrhythmia or tissue fragility may persist despite opening the epicardial artery.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Diagnostic STEMI patternRed flag

Persistent ST elevation in anatomically contiguous leads with a compatible acute presentation; apply sex-, age- and lead-specific ECG criteria and compare with prior traces.

Posterior occlusionRed flag

Horizontal ST depression with tall R waves in V1–V3 can be reciprocal posterior change; confirm with V7–V9 without delaying reperfusion when the pattern is convincing.

Right-ventricular infarctionRed flag

Inferior STEMI with hypotension, raised JVP and clear lungs suggests RV involvement; record right-sided leads and avoid preload reduction.

Cardiogenic shockRed flag

Hypotension with cool peripheries, altered mentation, oliguria, raised lactate or pulmonary congestion requires immediate critical-care and interventional escalation.

Mechanical complicationRed flag

New murmur, abrupt pulmonary oedema, recurrent shock or electromechanical dissociation after MI suggests papillary-muscle rupture, septal rupture or free-wall rupture.

Reperfusion failureRed flag

Persistent pain and less-than-expected ST resolution 60–90 minutes after fibrinolysis suggest failed reperfusion and indicate rescue PCI.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial 12-lead ECG with posterior or right-sided leadsFirst step
Why
Localise occlusion, detect evolution and identify complications.
Interpretation and limitations
Act on a diagnostic tracing immediately; use extra leads and repeats when standard leads are equivocal.
02
High-sensitivity cardiac troponin
Why
Confirm myocardial injury and support later diagnosis or prognosis.
Interpretation and limitations
A first value may be normal early and must never delay reperfusion for diagnostic STEMI.
03
Urgent coronary angiography
Why
Identify and open the culprit artery and define other coronary disease.
Interpretation and limitations
Assess flow, thrombus and complications; non-obstructive arteries require a structured alternative-mechanism assessment.
04
Transthoracic echocardiography
Why
Assess LV and RV function, regional motion, thrombus and mechanical complications.
Interpretation and limitations
Use urgently for unexplained shock or a new murmur, but do not delay transfer to the catheter laboratory.
05
Baseline blood tests
Why
Assess full blood count, renal function, electrolytes, glucose, coagulation and lipid profile while preparing treatment.
Interpretation and limitations
Correct dangerous abnormalities and modify drug or contrast choices without delaying reperfusion.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute pericarditis

Positional pleuritic pain, a pericardial rub and widespread concave ST elevation with PR change favour pericarditis over territorial coronary occlusion.

Early repolarisation or conduction abnormality

Stable prior ST elevation, left-ventricular hypertrophy or bundle-branch block can mimic infarction; symptoms, reciprocal change and serial ECG evolution guide urgent interpretation.

Aortic dissection

Abrupt tearing chest or back pain, pulse deficit or aortic regurgitation suggests dissection; coronary involvement can also create true infarction, making antithrombotic or fibrinolytic treatment hazardous.

Pulmonary embolism

Pleuritic pain, hypoxaemia, venous thrombosis signs and right-heart strain favour embolism; embolism can still cause troponin release and non-specific ECG abnormalities.

Myocarditis or takotsubo syndrome

A non-ischaemic injury pattern on cardiac magnetic resonance or ventricular dysfunction beyond one arterial territory supports myocarditis or takotsubo when angiography lacks an occlusive culprit.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Preferred routePrimary PCIFirst stepPreferredSTEMI within 12 hours and PCI deliverable within 120 minutes of when fibrinolysis could be given

1Activate the regional PPCI service from the diagnostic ECG; give aspirin and the catheter-laboratory antithrombotic regimen.
2Transfer directly with continuous monitoring and defibrillation capability.
3Perform immediate angiography and culprit-vessel PCI; assess non-culprit disease after stabilisation.
4Monitor in a coronary-care setting and document reperfusion time, flow and complications.

02AlternativeFibrinolysis and pharmaco-invasive careAlternativePresentation within 12 hours when PPCI cannot meet the NICE 120-minute threshold

1Exclude the chosen product's absolute and relative contraindications, then give a fibrinolytic licensed for the presentation with an antithrombin at the same time; use its weight-, age- and renal-specific SmPC regimen.
2Transfer immediately to a PCI-capable centre rather than waiting locally for deterioration.
3Repeat ECG at 60–90 minutes and assess pain and haemodynamics.
4Perform immediate rescue angiography for failed reperfusion; otherwise arrange early angiography under the regional pathway and never repeat fibrinolysis for failure.

03EscalationLate presentation or shockEscalationSymptoms beyond 12 hours, ongoing ischaemia or cardiogenic shock

1Offer PPCI for continuing clinical or ECG evidence of ischaemia and for eligible patients with cardiogenic shock.
2Consider angiography and PCI between 12 and 72 hours even without ongoing symptoms after senior assessment.
3Use urgent echo and invasive assessment for shock or suspected mechanical complication.
4Engage critical care and cardiothoracic surgery early when mechanical support or surgery may be required.

04Ongoing careBefore dischargeAfter reperfusion and clinical stabilisation

1Assess LV function, rhythm, renal function, haemoglobin, glucose and lipid profile.
2Confirm DAPT agent and intended duration, high-intensity lipid lowering and other indicated post-MI medicines with contraindications recorded.
3Refer to cardiac rehabilitation and address smoking, driving, work, sexual activity and emergency nitrate advice.
4Arrange timely follow-up and clear safety-netting for recurrent pain, dyspnoea, syncope or bleeding.

Key medicines and prescribing safety7 treatments · regimens, roles and cautions

Immediate platelet inhibition and long-term secondary prevention.

Aspirin

300 mg orally as a single loading dose as soon as possible, then typically 75 mg once daily long term.

Active major bleeding, true aspirin hypersensitivity and severe aspirin-exacerbated respiratory disease; give even if already taking low-dose aspirin unless contraindicated.

P2Y12 inhibition with aspirin when fibrinolysis is used; later antiplatelet choice and duration depend on angiography, PCI and bleeding risk.

Clopidogrel

With fibrinolysis for STEMI: 300 mg orally as a loading dose in people aged 75 or younger, then 75 mg once daily; in people over 75, start 75 mg once daily without a loading dose.

Active pathological bleeding, hepatic impairment, interacting medicines and combined antithrombotic bleeding risk; do not substitute the PCI loading regimen for the age-specific fibrinolysis regimen.

P2Y12 inhibition as part of DAPT for STEMI treated with PCI.

Prasugrel

For PCI: 60 mg oral loading dose, then 10 mg once daily with aspirin; use 5 mg once daily after the load if body weight is under 60 kg, and only after individual benefit-risk review in people aged 75 or over.

Contraindicated with previous stroke or TIA, active bleeding or severe hepatic impairment; generally avoid age 75 or over unless benefit outweighs bleeding risk. Verify the PCI pathway and SmPC.

Alternative P2Y12 inhibition, including when STEMI is managed without PCI or prasugrel is unsuitable.

Ticagrelor

180 mg orally once, then 90 mg twice daily with aspirin 75–150 mg daily, usually for 12 months after ACS unless duration is modified.

Active bleeding, previous intracranial haemorrhage, strong CYP3A interactions, severe hepatic impairment, dyspnoea and bradyarrhythmia; individualise with oral anticoagulation.

Relief of ischaemic pain when blood pressure and physiology permit; it does not restore coronary patency.

Glyceryl trinitrate sublingual spray

400–800 micrograms under the tongue for pain; if needed repeat at 5-minute intervals, to a maximum total of 3 sprays while urgent help is in progress.

Avoid in hypotension, suspected right-ventricular infarction, severe aortic stenosis or with riociguat. Do not give within at least 24 hours of sildenafil or vardenafil or 48 hours of tadalafil.

Analgesia for severe persistent pain despite nitrates; not a routine reperfusion treatment.

Morphine sulfate injection

Titrate 2.5–5 mg by IV injection over at least 5 minutes to effect; the SmPC adult IV range is 2.5–10 mg, using the minimum effective dose.

Respiratory depression, hypotension, reduced consciousness, renal or hepatic impairment and nausea; monitor closely and recognise delayed absorption of oral P2Y12 drugs.

High-intensity lipid lowering after MI irrespective of baseline cholesterol.

Atorvastatin

80 mg orally once daily for secondary prevention, unless interactions, adverse-effect risk or patient preference require a lower dose or alternative.

Review liver disease, myopathy symptoms, pregnancy, interacting medicines and previous intolerance; measure lipids and liver transaminases per NICE NG238.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Malignant arrhythmia

Acute ischaemia and reperfusion create electrical instability, causing ventricular tachycardia, ventricular fibrillation or conduction block and making early monitored defibrillation capability essential.

Heart failure and cardiogenic shock

Loss of contracting myocardium reduces stroke volume and raises filling pressure. Large infarction, right-ventricular involvement or recurrent ischaemia may progress to pulmonary oedema and shock.

Mechanical rupture

Necrotic tissue may fail, causing papillary-muscle rupture with acute mitral regurgitation, ventricular septal rupture or free-wall rupture with tamponade and sudden collapse.

Pericarditis

Inflammation overlying injured myocardium can cause early post-infarction pericarditic pain, while a later immune-mediated syndrome may include recurrent inflammation and effusion.

Ventricular remodelling and thromboembolism

A large akinetic infarct can remodel into chronic ventricular dysfunction or aneurysm and promote mural thrombus, creating later heart-failure and systemic embolic risk.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuous ECG and frequent blood pressure, oxygen saturation, pain and perfusion assessment during acute care.
After fibrinolysis, document ECG and clinical reperfusion assessment at 60–90 minutes and trigger rescue PCI when indicated.
Monitor access site, haemoglobin, renal function and contrast exposure after PCI.
Use urgent echocardiography for shock, a new murmur, recurrent pulmonary oedema or suspected mechanical complication.
Before discharge document LV ejection fraction, DAPT plan, lipid treatment and cardiac-rehabilitation referral.
Review lipids and treatment tolerance at 2–3 months under NICE secondary-prevention guidance, earlier when clinically indicated.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Time zero is clinical

A diagnostic ECG starts the reperfusion pathway; laboratory confirmation is retrospective support, not permission to act.

Posterior STEMI can hide

Anterior ST depression may be the reciprocal face of posterior transmural injury rather than 'NSTEMI'.

Right ventricle needs preload

Nitrates or aggressive diuresis can precipitate hypotension in RV infarction.

Lysis needs a destination

Fibrinolysis is not the end-point; transfer, reperfusion assessment and rescue or early angiography are integral.

New murmur is a siren

After MI, a new murmur with instability means mechanical complication until urgent imaging proves otherwise.

Normoxic oxygen adds no routine benefit

Target saturation rather than automatically prescribing oxygen to every patient with MI.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for troponin before activating primary PCI.
02
Transferring for PPCI despite a delay beyond the NICE threshold without considering eligible fibrinolysis.
03
Repeating fibrinolysis after failed reperfusion instead of arranging rescue PCI.
04
Giving nitrates in hypotensive right-ventricular infarction, with riociguat, within 24 hours of sildenafil or vardenafil or within 48 hours of tadalafil.
05
Omitting a clearly documented DAPT duration and secondary-prevention plan at discharge.