TIME
GROSS
MICROSCOPIC
MAIN RISK IN THIS WINDOW
No visible change
None, or wavy fibers at the border
Arrhythmia (VF) → sudden death; cardiogenic shock, acute HF
Dark mottling; pale on TTC stain
Early coagulative necrosis: eosinophilic fibers, edema, hemorrhage; contraction bands if reperfused
Arrhythmia
Hyperemia at margins
Coagulative necrosis with loss of nuclei and striations; neutrophils flood in
Fibrinous pericarditis (transmural infarcts)
Yellow-brown, soft center with red border
Macrophages clear dead myocytes; wall at its weakest
Papillary muscle, septal and free-wall rupture; pseudoaneurysm
Red-gray depressed border
Granulation tissue (new vessels, fibroblasts) grows in from the margin
Free-wall rupture still possible
Gray-white scar
Collagen scar, mostly complete by ~2 months
True ventricular aneurysm, mural thrombus, Dressler syndrome, HF
Reperfusion
any time it occurs
Hemorrhagic (red) infarct
Contraction band necrosis (Ca²⁺ influx), free-radical injury
Troponin may keep rising after successful PCI
Subendocardium
Highest wall stress, farthest from epicardial supply
Irreversible injury from ~20–30 min; wavefront reaches epicardium by 3–6 h