Myocardial infarction, sudden cardiac death

1. Concept

Acute myocardial infarction (AMI) = necrosis of myocardium from ischemia — an imbalance between coronary supply and myocardial O₂ demand. Usually caused by acute coronary thrombosis on a disrupted atherosclerotic plaque (fixed stenosis + dynamic plaque change).

2. Pathogenesis

Fixed AS plaque (critical stenosis ~70–75%) + dynamic event: plaque rupture/fissure exposes thrombogenic collagen/lipid core → platelet adhesion/aggregation (TXA₂, ADP, serotonin) + extrinsic coagulation → thrombus occludes lumen within minutes.

3. Cellular response & timing

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

4. Coronary territories

• LAD (40–50%) → anterior LV, anterior 2/3 septum, apex.
• RCA (30–40%) → posterior wall, posterior 1/3 septum.
• LCX (15–30%) → lateral/posterior LV.

5. Morphology over time & complications

Time	Change	Complication
0–4 h	None visible (diaphorase/TTC stain)	Arrhythmia, cardiogenic shock
4–24 h	Coagulative necrosis, pyknosis	Arrhythmia
1–3 d	Neutrophil infiltrate	Fibrinous pericarditis
3–7 d	Macrophages, soft tissue	Rupture (free wall → tamponade; septum → shunt; papillary → mitral regurg)
1–3 wk	Granulation tissue	—
Months	Grey-white scar	Aneurysm, mural thrombus, Dressler syndrome

• Diagnosis: ECG (STEMI = ST elevation, pathological Q waves; vs NSTEMI); troponin I/T (most specific), CK-MB, LDH.
• Reperfusion (PCI/stent, thrombolysis, bypass) — may cause reperfusion injury (ROS, contraction-band necrosis).

6. Sudden cardiac death (SCD)

• Unexpected cardiac death within 1–24 h of symptoms; usually from lethal ventricular arrhythmia (VF).
• Most common cause = coronary artery disease; in the young — hypertrophy, conduction abnormalities, myocarditis, mitral valve prolapse, cardiomyopathy.
• Prevention: implantable cardioverter-defibrillator (ICD).

💡 High-yield: AMI = plaque rupture → thrombosis; necrosis irreversible after 20–40 min, subendocardial → transmural wavefront. LAD most common (anterior). Markers: troponin (most specific). Complications by time: arrhythmia → pericarditis → rupture (3–7 d) → aneurysm/Dressler. SCD = VF, usually from CAD; treat risk with ICD.