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PA26.6 | Ischaemic Heart Disease & Acute Coronary Syndromes — Summary & Reflection
REFLECT
Return to the opening case: the 55-year-old man with chest pain for 40 minutes, troponin I = 18 ng/mL, and ST elevation in II, III, aVF.
- Which coronary artery is most likely occluded, and what territory does it supply?
- At the moment of his cardiac arrest, what pathological process had already started in his myocardium? What would you see under the microscope if he had not survived and autopsy was performed 18 hours later?
- If he is successfully resuscitated and reperfused, what additional pathological process will occur in his myocardium, and what microscopic finding would you see?
- If he survives to day 5 but deteriorates with sudden hypotension and a new loud holosystolic murmur, what complication has occurred, and which pathological phase of MI explains its timing?
Document your answers and bring them to your next tutorial.
KEY TAKEAWAYS
IHD is the leading cause of death globally, driven by coronary atherosclerosis. The pivotal event converting chronic IHD to emergency is acute plaque change (rupture or erosion) → coronary thrombosis.
ACS spectrum: Unstable Angina (no necrosis) → NSTEMI (subendocardial, partial occlusion) → STEMI (transmural, complete occlusion).
MI evolution timeline (examination-critical): wavy fibres (0–12h) → coagulative necrosis + contraction bands (12–24h) → neutrophil infiltrate (1–3d) → macrophage phagocytosis (3–7d) → granulation tissue (1–2wk) → collagen scar (>2wk).
Reperfusion injury produces contraction band necrosis via calcium overload.
Biomarkers: Troponin I/T — most sensitive and specific; CK-MB — useful for reinfarction; Myoglobin — earliest, least specific.
Complications: arrhythmia (most common, early), free wall rupture (days 3–7), papillary muscle rupture (posteromedial > anterolateral), VSD (days 3–7), mural thrombus (anterior MI), Dressler's syndrome (weeks later), ventricular aneurysm (late).
PA26.6 clinical interpretation: serial troponins + ECG + echo = ACS workup; delta troponin distinguishes acute MI from chronic injury.