Coagulative necrosis, then neutrophils, macrophages, granulation tissue and scar
Mnemonic
The histological sequence, which underlies both complications and their timing:
- 0 to 4 hours - no visible change; only electron microscopy
- 4 to 12 hours - early coagulative necrosis, oedema, haemorrhage
- 12 to 24 hours - contraction band necrosis, early neutrophils. Risk of arrhythmia
- 1 to 3 days - dense neutrophil infiltrate. Risk of fibrinous pericarditis
- 3 to 7 days - macrophages clear debris. The wall is at its weakest, so this is when free wall rupture, papillary muscle rupture and ventricular septal defect occur
- 1 to 3 weeks - granulation tissue, neovascularisation
- Weeks to months - collagenous scar. Risk of ventricular aneurysm and Dressler’s syndrome
“Neutrophils first, macrophages next, then granulation, then scar”, the same sequence as any healing wound.
The 3 to 7 day window is the dangerous one for rupture, because macrophages have removed the necrotic muscle but collagen has not yet replaced it.
Expansion
| Time | Histology | Complication risk |
|---|---|---|
| 0 to 4 h | No change visible | Arrhythmia, sudden death |
| 4 to 12 h | Early coagulative necrosis, wavy fibres | Arrhythmia |
| 12 to 24 h | Coagulative necrosis, contraction bands | Arrhythmia |
| 1 to 3 days | Neutrophil infiltrate | Fibrinous pericarditis |
| 3 to 7 days | Macrophages removing debris; wall is weakest | Free wall rupture, papillary muscle rupture, septal rupture |
| 1 to 3 weeks | Granulation tissue, neovascularisation | |
| Over 1 month | Collagenous scar | Ventricular aneurysm, mural thrombus, Dressler syndrome |
The rupture window at 3 to 7 days is the crucial concept: necrotic muscle has been digested by macrophages but new collagen has not yet been laid down, so the wall is at its mechanically weakest.
Dressler syndrome is an autoimmune pericarditis occurring weeks after infarction, distinct from the early fibrinous pericarditis of days 1 to 3.
Reperfusion alters the picture: it salvages myocardium but produces contraction band necrosis and haemorrhage into the infarct.
Infarction spreads as a wavefront from subendocardium to epicardium, which is why early reperfusion salvages the outer layers.