Acute myocardial infarction

1. Definition

• Acute myocardial infarction (AMI) = ischemic necrosis of myocardium from an imbalance between coronary perfusion and myocardial O₂ demand.
• Ischemia = coronary obstruction (atherosclerosis); infarction = the resulting necrotic area.

2. Pathogenesis

• Fixed component: pre-existing atherosclerotic plaque; critical stenosis at ~70–75% occlusion.
• Dynamic component: most AMIs are acute coronary thrombosis on a disrupted plaque.
  1. Plaque rupture/erosion exposes thrombogenic collagen + necrotic core.
  2. Platelets adhere/aggregate, release TXA₂, ADP, serotonin → more aggregation + vasospasm.
  3. Tissue-factor (extrinsic) pathway adds fibrin.
  4. Within minutes → complete luminal occlusion.
• Coronary spasm causes ~10%.

3. Myocardial Response & Wavefront

• Seconds: aerobic glycolysis stops, ↓ATP, lactic acid, loss of contractility (reversible: myofibril relaxation, glycogen loss, mitochondrial swelling).
• Irreversible injury after 20–40 min; reperfusion before this preserves viability.
• Wavefront phenomenon: necrosis begins subendocardially (last perfused, highest pressure/demand) → spreads transmurally over 3–6 h.

4. Coronary Territories

Artery	% of AMI	Region infarcted
LAD	40–50%	Anterior LV wall, anterior 2/3 septum, apex
RCA	30–40%	Posterior wall, posterior 1/3 septum
LCx	25–30%	Lateral/posterior LV

5. Time Course (Morphology & Complications)

Time	Morphology	Complication
0–1.5 h	Reversible; no changes (diaphorase ↓)	Arrhythmia, cardiogenic shock
4–24 h	Dark discoloration; coagulative necrosis, pyknosis, eosinophilia	Arrhythmia
1–3 d	Yellow pallor + hyperemic border; neutrophils	Fibrinous pericarditis
3–7 d	Clay-yellow; macrophages, soft tissue	Rupture → tamponade, VSD, papillary muscle (→ acute MR)
1–2 wk	Red border; granulation tissue	—
Months	Grey-white scar (collagen)	Aneurysm, mural thrombus, Dressler syndrome

• Diaphorase (TTC) reaction: living tissue stains; necrotic (no dehydrogenase) stays pale — detects early infarct.

6. Clinical & Diagnosis

• Symptoms: crushing substernal pain >20 min, radiating to jaw/left arm, not relieved by rest/nitroglycerin; dyspnea; “silent MI” in elderly/diabetics.
• ECG: STEMI (ST-elevation, pathological Q waves, T-wave changes) vs NSTEMI.
• Biomarkers: troponin I/T (most specific), CK-MB (reinfarction), LDH.

7. Complications (summary)

• Contractile dysfunction → LV failure/pulmonary edema, cardiogenic shock
• Arrhythmias (most common cause of early death)
• Myocardial rupture (days 3–7): tamponade / L→R shunt / papillary muscle
• Ventricular aneurysm (→ mural thrombus), mural thrombosis, pericarditis, progressive CIHD, reinfarction

💡 High-yield: Subendocardial → transmural wavefront over 3–6 h; rupture risk peaks at days 3–7 (macrophage softening, no collagen yet). Troponin = most specific marker; LAD = most common occluded artery.