Myocardial Infarction

Myocardial infarction is acute myocardial injury (a rise and fall of cardiac troponin with at least one value above the 99th percentile) together with clinical evidence of acute ischaemia. It is the dominant presentation of acute coronary syndrome, with annual incidence of roughly 1 to 3 per 1,000 adults in high-income settings, and it rises steeply with age.

Universal classification

• Type 1: atherothrombotic, from plaque rupture or erosion with occlusive or non-occlusive thrombus. This is the typical infarct.
• Type 2: supply and demand mismatch without acute plaque event, from severe anaemia, tachyarrhythmia, hypotension, hypertensive crisis, hypoxaemia, coronary spasm, embolism or spontaneous coronary artery dissection.
• Type 3: cardiac death with symptoms and presumed new ischaemic ECG changes before troponin could be sampled.
• Types 4 and 5: infarction associated with PCI (4a), stent thrombosis (4b), restenosis (4c), and with bypass surgery (5).
• MINOCA: infarction with non-obstructive coronary arteries (stenosis under 50%). It accounts for 5 to 10% and includes plaque disruption, dissection, vasospasm, embolism and Takotsubo syndrome.

ECG-based subtypes

• STEMI: persistent ST elevation from acute total or near-total occlusion, which needs immediate reperfusion.
• NSTEMI: troponin rise without persistent ST elevation, usually from subtotal occlusion or distal embolisation.

Pathophysiology

• Plaque rupture or erosion exposes thrombogenic material, platelets aggregate, and fibrin-rich thrombus forms.
• Myocardial necrosis begins within 20 to 30 minutes of complete occlusion and spreads from endocardium to epicardium (wavefront phenomenon). Salvage falls steeply after about 3 to 4 hours, so time to reperfusion drives outcome.
• Ventricular remodelling follows, with infarct expansion, dilatation and neurohormonal activation.

Risk factors are as for coronary disease: smoking, dyslipidaemia, hypertension, diabetes, obesity, family history, chronic kidney disease. Cocaine, amphetamines and cannabis are important triggers in younger patients.

Infarct location by culprit artery

• Anterior (LAD): ST elevation V1 to V4 or V6.
• Inferior (right coronary in 80%, circumflex in 20%): II, III, aVF.
• Lateral (circumflex or diagonal): I, aVL, V5, V6.
• Posterior (circumflex or right coronary): ST depression V1 to V3 with tall R waves, confirmed by V7 to V9 elevation.
• Right ventricular: V4R elevation, with inferior infarction.

Typical presentation is retrosternal pressure or crushing pain, lasting over 20 minutes, radiating to the left arm, jaw, neck or back, with sweating, nausea, dyspnoea and a sense of impending doom. It does not settle with rest or nitrates.

Atypical presentations are frequent in

• Women, older adults and patients with diabetes, who present with dyspnoea, fatigue, epigastric pain, nausea or syncope.
• Silent infarction, found in roughly a quarter of cases on later ECG.

Examination

• Pallor, diaphoresis, tachycardia or bradycardia (more common in inferior infarction), hypotension.
• Fourth heart sound, soft first sound, new mitral regurgitant murmur, pulmonary crackles, raised jugular venous pressure.
• Killip classification: I no failure, II crackles or S3, III pulmonary oedema, IV cardiogenic shock.

Complications to recognise early

• Arrhythmia: ventricular fibrillation (highest in the first hours), sinus bradycardia, AV block (inferior infarcts have narrow QRS escape, anterior infarcts have wide QRS and worse prognosis), atrial fibrillation.
• Heart failure and cardiogenic shock: systolic pressure under 90 mmHg with hypoperfusion despite adequate filling, in 5 to 8% of STEMI.
• Right ventricular infarction: hypotension, clear lungs and raised jugular venous pressure, with preload dependence.
• Mechanical complications (days 3 to 7, up to 2 weeks):
• Papillary muscle rupture: sudden pulmonary oedema with a soft murmur, since the regurgitant jet equalises pressures quickly.
• Ventricular septal rupture: new loud pansystolic murmur with thrill and shock.
• Free wall rupture: sudden collapse with pulseless electrical activity, or subacute tamponade.
• Pericarditis: early (days 1 to 3) or Dressler syndrome (weeks later).
• Left ventricular thrombus and aneurysm, with persistent ST elevation.

Differential diagnosis: aortic dissection (check before any antithrombotic), pulmonary embolism, pericarditis, myocarditis, Takotsubo syndrome, oesophageal rupture, pneumothorax, acute cholecystitis and pancreatitis.

ECG within 10 minutes of first contact

• STEMI criteria: new ST elevation at the J point in two contiguous leads of at least 1 mm (0.1 mV), except V2 and V3 where the threshold is 2 mm in men aged 40 years or over, 2.5 mm in men under 40, and 1.5 mm in women.
• STEMI equivalents needing reperfusion: new left bundle branch block with Sgarbossa criteria, posterior infarction (ST depression V1 to V3), de Winter T waves (upsloping ST depression with tall symmetrical T waves, suggesting proximal LAD occlusion), Wellens pattern (critical LAD stenosis), and diffuse ST depression with ST elevation in aVR suggesting left main or multivessel ischaemia.
• Repeat ECGs every 15 to 30 minutes if symptoms continue with a non-diagnostic tracing, and record right-sided and posterior leads.

Cardiac troponin

• High sensitivity troponin T or I, drawn on arrival and repeated at 1 to 3 hours (0/1 hour or 0/2 hour algorithms), with a third sample at 3 hours when uncertain. A rise or fall of 20% or more (when baseline is elevated) supports an acute process.
• Do not wait for troponin in STEMI.
• Non-ischaemic causes of troponin elevation: myocarditis, pulmonary embolism, sepsis, renal failure, heart failure, Takotsubo syndrome, tachyarrhythmia, stroke, aortic dissection and strenuous exercise.
• CK-MB is useful only for timing reinfarction.

Imaging and further tests

• Bedside echocardiography for wall motion abnormality, ventricular function, mechanical complications, right ventricular involvement and effusion. It is also used to exclude dissection and tamponade.
• Chest radiograph for pulmonary oedema and mediastinal widening.
• Laboratory tests: CBC, creatinine, electrolytes, glucose, lipids, HbA1c, liver tests, coagulation.
• Coronary angiography is the gold standard for culprit identification. Coronary CT angiography can exclude obstructive disease in low-risk NSTEMI-type presentations.
• Cardiac MRI in MINOCA or diagnostic uncertainty identifies infarct pattern (subendocardial late enhancement) versus myocarditis (subepicardial) and Takotsubo syndrome.
• Risk stratification: GRACE score (above 140 is high risk) and TIMI score.

Initial measures

• Continuous ECG monitoring, defibrillator at hand, IV access.
• Aspirin 300 mg chewed (150 to 300 mg), unless allergic.
• Oxygen only if saturation is under 90%.
• Nitroglycerin 0.4 mg sublingually every 5 minutes up to three doses, or IV infusion starting at 5 to 10 micrograms/min for ongoing pain, hypertension or pulmonary oedema. Avoid in right ventricular infarction, hypotension (systolic under 90 mmHg), recent phosphodiesterase-5 inhibitor use (24 hours for sildenafil, 48 hours for tadalafil) and bradycardia.
• Morphine 2 to 5 mg IV, repeated, for severe pain only, since it delays oral antiplatelet absorption. Metoclopramide 10 mg or ondansetron 4 mg for nausea.

STEMI reperfusion

• Primary PCI is preferred if achievable within 120 minutes of first medical contact (door to balloon target under 90 minutes). Radial access, drug-eluting stents, and thrombus aspiration are not routine.
• P2Y12 inhibitor loading: ticagrelor 180 mg (preferred) then 90 mg twice daily, or prasugrel 60 mg then 10 mg daily (5 mg if under 60 kg or age 75 and over, and avoid with prior stroke or TIA), or clopidogrel 600 mg then 75 mg daily when others are unavailable or contraindicated.
• Anticoagulation during PCI: unfractionated heparin 70 to 100 units/kg IV bolus, with ACT 250 to 300 seconds. Enoxaparin 0.5 mg/kg IV is an alternative. Bivalirudin 0.75 mg/kg bolus then 1.75 mg/kg/h during PCI is an option with high bleeding risk.
• Culprit-only intervention in cardiogenic shock. In stable multivessel disease, complete revascularisation of significant non-culprit lesions (during the index admission or within about 45 days) lowers recurrent events.
• Fibrinolysis when PCI cannot be delivered within 120 minutes, ideally within 30 minutes of arrival and within 12 hours of onset:
• Tenecteplase single IV bolus by weight: 30 mg (under 60 kg), 35 mg (60 to under 70), 40 mg (70 to under 80), 45 mg (80 to under 90), 50 mg (90 kg and over). Use half the dose in patients aged 75 and over.
• Alteplase accelerated regimen: 15 mg bolus, then 0.75 mg/kg over 30 minutes (maximum 50 mg), then 0.5 mg/kg over 60 minutes (maximum 35 mg).
• Reteplase 10 units IV, repeated after 30 minutes.
• Adjuncts: aspirin 300 mg, clopidogrel 300 mg (75 mg if aged 75 or over) then 75 mg daily, and enoxaparin 30 mg IV bolus then 1 mg/kg SC every 12 hours (first dose 15 minutes after the bolus; no bolus and 0.75 mg/kg if aged 75 and over; reduce if creatinine clearance under 30 mL/min), continued up to 8 days or to discharge. Alternatively use unfractionated heparin 60 units/kg bolus (maximum 4,000 units) then 12 units/kg/h (maximum 1,000 units/h).
• Absolute contraindications: prior intracranial haemorrhage, ischaemic stroke within 6 months, central nervous system tumour or vascular lesion, major trauma, surgery or head injury within 3 weeks, gastrointestinal bleeding within a month, known bleeding disorder, aortic dissection, and non-compressible punctures within 24 hours. Severe uncontrolled hypertension (above 180/110 mmHg) is a relative contraindication.
• Success is judged at 60 to 90 minutes by 50% or greater ST resolution and pain relief. Rescue PCI for failure, and routine angiography within 2 to 24 hours for all successful lysis cases.
• Patients presenting after 12 hours with ongoing ischaemia, heart failure or instability are still taken for primary PCI. Late presenters who are stable and pain free are assessed for inducible ischaemia or revascularised electively.

NSTEMI management

• Antithrombotic therapy: aspirin plus ticagrelor 180 mg then 90 mg twice daily, or prasugrel (if proceeding to PCI after anatomy is defined), and parenteral anticoagulation with fondaparinux 2.5 mg SC daily (lowest bleeding), enoxaparin 1 mg/kg SC twice daily, or unfractionated heparin.
• Invasive strategy timing:
• Immediate (under 2 hours): refractory angina, haemodynamic instability, life-threatening arrhythmia, mechanical complications, acute heart failure with refractory angina.
• Early (under 24 hours): GRACE score above 140, dynamic ST-T changes, troponin rise consistent with NSTEMI.
• Within 72 hours: diabetes, renal impairment, reduced ejection fraction, early post-infarct angina, prior PCI or bypass, or GRACE above 109.
• Low-risk patients with no recurrent pain can have non-invasive testing before discharge.

Cardiogenic shock and complications

• Emergency revascularisation of the culprit artery. Norepinephrine 0.05 to 0.5 micrograms/kg/min first-line pressor, dobutamine 2.5 to 10 micrograms/kg/min for low output, and temporary mechanical circulatory support (Impella, VA-ECMO) in selected patients. Intra-aortic balloon pump gives no routine mortality benefit.
• Right ventricular infarction: IV saline 250 to 500 mL boluses to restore preload, avoid nitrates and diuretics, inotropes if needed, temporary pacing for AV block.
• Pulmonary oedema: furosemide 40 to 80 mg IV, nitrates if blood pressure permits, non-invasive ventilation.
• Ventricular fibrillation or pulseless ventricular tachycardia: defibrillation, amiodarone 300 mg IV then 150 mg, correction of potassium (4.0 to 5.0 mmol/L) and magnesium (above 2 mmol/L). Beta blocker for electrical storm.
• Symptomatic bradycardia: atropine 0.5 to 1 mg IV, temporary transvenous pacing for high-grade block.
• Mechanical complications: urgent echocardiography, vasodilators with intra-aortic balloon pump support, and surgical repair, which is usually required early.
• Pericarditis: aspirin 500 to 1,000 mg every 8 hours for 1 to 2 weeks with colchicine 0.5 mg twice daily. Avoid NSAIDs and steroids in the early weeks because they impair scar formation.
• Left ventricular thrombus: anticoagulation with warfarin (INR 2 to 3) or a direct oral anticoagulant for 3 to 6 months, repeating imaging.

Medical therapy before discharge and long term

• Dual antiplatelet therapy (aspirin 75 to 100 mg plus ticagrelor 90 mg twice daily, prasugrel 10 mg daily or clopidogrel 75 mg daily) for 12 months. Shorten to 1 to 3 months followed by P2Y12 monotherapy in high bleeding risk, and continue aspirin lifelong afterwards. Add a proton pump inhibitor such as pantoprazole 40 mg daily. In patients needing oral anticoagulation, use a DOAC with clopidogrel for up to 12 months and drop aspirin after the peri-PCI period.
• Atorvastatin 80 mg (or rosuvastatin 20 to 40 mg) started immediately. Target LDL cholesterol below 55 mg/dL (1.4 mmol/L), adding ezetimibe 10 mg at 4 to 6 weeks if not at target, and a PCSK9 inhibitor if still above target.
• Beta blocker (metoprolol succinate 25 to 200 mg daily, bisoprolol 1.25 to 10 mg daily, carvedilol 3.125 to 25 mg twice daily) when ejection fraction is 40% or less or in heart failure. Avoid early IV beta blockers with signs of heart failure, shock or heart block. Benefit is uncertain with preserved ejection fraction beyond 1 year.
• ACE inhibitor started within 24 hours in anterior infarction, heart failure, ejection fraction of 40% or less, hypertension or diabetes: ramipril 2.5 mg twice daily titrated to 5 mg twice daily, or lisinopril 5 to 10 mg daily. Use an ARB such as valsartan 40 to 160 mg twice daily if intolerant, or sacubitril/valsartan in heart failure with reduced ejection fraction.
• Mineralocorticoid receptor antagonist: eplerenone 25 mg daily titrated to 50 mg, in ejection fraction 40% or less with heart failure or diabetes, if potassium is below 5.0 mmol/L and creatinine clearance above 30 mL/min.
• SGLT2 inhibitor (empagliflozin 10 mg or dapagliflozin 10 mg daily) in heart failure, diabetes or chronic kidney disease. Colchicine 0.5 mg daily may reduce recurrent events.
• Blood pressure below 130/80 mmHg, HbA1c individualised.
• Influenza vaccination annually.

Rehabilitation and secondary prevention

• Cardiac rehabilitation starting before discharge (moderate exercise 150 minutes weekly), smoking cessation with varenicline or nicotine replacement, weight loss, Mediterranean diet, limited alcohol, depression screening.
• Driving: private driving after 1 week if revascularised and stable, and after 4 weeks otherwise.
• Return to sexual activity when able to climb two flights of stairs.
• Device therapy: reassess ejection fraction at 6 to 12 weeks (at least 40 days after infarction and 90 days after revascularisation). ICD for ejection fraction of 35% or less with NYHA II to III, or 30% or less with NYHA I, on optimal therapy. Wearable defibrillator is an interim option in selected cases.
• Follow-up with clinic review at 2 to 6 weeks, then at 3, 6 and 12 months.

MINOCA and Takotsubo syndrome

• MINOCA: determine mechanism with cardiac MRI, intracoronary imaging and spasm testing. Standard secondary prevention applies (antiplatelet, statin, ACE inhibitor, beta blocker). Calcium channel blocker for vasospasm.
• Spontaneous coronary artery dissection: conservative therapy when stable, beta blocker, avoid thrombolysis, and test for fibromuscular dysplasia.
• Takotsubo syndrome: supportive care, ACE inhibitor and beta blocker, and anticoagulation for apical thrombus.