3.1 Myocardial Infarction (MI) – Coronary Artery Thrombosis

📘 Cross-reference: [See Section 2 – Acute Coronary Syndromes (ACS)] https://passmap.co.uk/cardiology-1-acute-coronoary-syndromes/ for full clinical approach, ECG patterns, biomarkers, and guideline-driven management.

📄 Definition

Myocardial infarction (MI) is myocardial necrosis due to acute thrombotic occlusion of a coronary artery. It is a clinical manifestation of arterial thrombosis and a common cause of sudden cardiac death.

🧠 PASSMAP Integration

This condition is the archetype of arterial thrombosis and integrates with systemic atherosclerosis. Recognising shared risk factors with PAD, stroke, and acute limb ischaemia is high-yield for PARA success.

🔬 Pathophysiology

  • Triggered by rupture of an atherosclerotic plaque in a coronary artery.

  • Results in platelet aggregation and formation of a white thrombus in high-pressure arterial flow.

  • Thrombus partially or completely occludes the coronary artery:

    • Partial occlusion → NSTEMI

    • Complete occlusion → STEMI

  • Leads to ischaemia, hypoxia, and myocyte death.

⚠️ Risk Factors – Mnemonic: THROMBUS

  • Tobacco use

  • Hypertension

  • Raised lipids

  • Obesity

  • Male sex / Metabolic syndrome

  • Blood glucose (diabetes mellitus)

  • Unhealthy diet / sedentary lifestyle

  • Stress / psychosocial factors

🩺 Red Flag Signs (pre-hospital recognition)

  • Crushing central chest pain ± radiation to arm/jaw

  • Sweating, nausea, breathlessness

  • Syncope or hypotension

  • Sudden collapse or cardiac arrest

🧪 Investigations

✅ Full workup found in Section 2 (ACS), but key mechanistic markers include:

  • Troponin T or I – indicates myocardial necrosis

  • ECG – ST elevation (STEMI) or T wave changes/ST depression (NSTEMI)

  • Coronary angiography – to confirm thrombotic occlusion

💡 Did You Know? Type 1 vs. Type 2 MI

While both present with a rise and/or fall in Troponin and symptoms of ischaemia, the “Type” refers to the underlying mechanism, which fundamentally changes the management plan.

Type 1 MI: The “Clot” Problem

This is the “classic” heart attack where the problem is a physical blockage in the blood vessels of the heart.

A – Acute: Rapid onset of symptoms.

C – Clot: Formation of a Thrombus (blood clot).

D – Disruption: Rupture or erosion of an Atherosclerotic Plaque (fatty buildup in the artery wall).

C – Coronary: Specifically involving the Coronary Arteries (the vessels that supply the heart muscle).

  • Mechanism: Acute atherothrombosis. A plaque ruptures, a thrombus forms, and the artery is blocked.

  • Key Feature: This is your classic Acute Coronary Syndrome (ACS).

  • Management: Reperfusion (PCI), DAPT, and aggressive secondary prevention (The 6 As).

Type 2 MI: The “Supply vs. Demand” Problem

  • Mechanism: Ischaemia occurs without acute atherothrombosis. It is a mismatch between how much oxygen the heart needs and how much it gets.

  • Common Triggers: * Reduced Supply: Severe anaemia, hypotension, hypoxaemia, or coronary artery spasm.

    • Increased Demand: Severe tachycardia (e.g., AF with RVR), sepsis, or hypertensive crisis.

  • Management: Treat the underlying cause first (e.g., give a blood transfusion for anaemia, or slow the heart rate in AF). You do not usually give DAPT or offer urgent PCI unless there is evidence of concurrent obstructive CAD.

🎯 EXAM ANCHOR – Comparison Table

FeatureType 1 MIType 2 MI
Primary CausePlaque rupture + ThrombosisSupply/Demand imbalance
TroponinElevated (Dynamic)Elevated (Dynamic)
ECG ChangesCommon (ST elevation or depression)Common (often ST depression/T-wave inversion)
AngiographyShows thrombus/occlusionOften shows stable CAD or normal arteries
Mnemonic“The ACDC MI” (ACS-type)“The Can’t Cope MI” (Heart can’t cope with demand)

Mechanism-Based Management Highlights

🧠 Refer to ACS section for comprehensive protocol, but note:

  • Antiplatelet therapy (Aspirin + P2Y12 inhibitor) targets arterial thrombosis

  • Anticoagulation (e.g. fondaparinux) in NSTEMI

  • Thrombolysis if PCI not available within 120 minutes (STEMI)

  • PCI (Percutaneous Coronary Intervention) – definitive treatment

  • Statins + ACE-i/ARB + Beta-blockers post-event

Long-Term Considerations

  • Lifestyle modification

  • Cardiac rehabilitation

  • Antiplatelets and statins long-term

  • Risk factor optimisation (BP, glucose, lipids)

Last updated in line with:

  • NICE NG185 (2025/26 Consolidated Update): Replacing separate CG167 (STEMI) and NG185 (NSTEMI) targets with a unified ACS “Invasive-First” framework.

  • ESC ACS Guidelines (2025 Focused Update): Addressing the shift towards P2Y12 inhibitor monotherapy after 1–3 months in high-bleeding-risk patients.

  • UDMI-5 (2026): The 5th Universal Definition of Myocardial Infarction, emphasizing the Type 1 vs. Type 2 distinction.

  • PARA/MLA-aligned: Fully reviewed February 2026 for current exam blueprints.

🔒 PASSMAP Assurance: This content is peer-reviewed, NICE-compliant, and optimised for the GMC Medical Licensing Assessment (MLA) and PA National Exam (PARA).

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Educational platform. Not medical advice.

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