Timeline of myocardial infarction pathology

This table gives an overview of the pathology seen in myocardial infarction by time after obstruction.

For the first ~30 minutes no change at all can be seen by gross examination or by light microscopy in histopathology. However, in electron microscopy relaxed myofibrils, as well as glycogen loss and mitochondrial swelling can be seen.

Time	Gross examination	Histopathology (light microscopy)
0 - 0.5 hours	None	None
0.5 – 4 hours	None*	Glycogen Depletion, as seen with a PAS Stain Possibly waviness of fibers at border
4 – 12 hours	Sometimes dark mottling	Initiation of coagulation necrosis Edema Hemorrhage
12 – 24 hours	Dark mottling	Ongoing coagulation necrosis Karyopyknosis Hypereosinophilia of myocytes Contraction band necrosis in margins Beginning of neutrophil infiltration
1 – 3 days	Infarct center becomes yellow-tan	Continued coagulation necrosis Loss of nuclei and striations Increased infiltration of neutrophils to interstitium
3 – 7 days	Hyperemia at border Softening yellow-tan center	Beginning of disintegration of dead muscle fibers Necrosis of neutrophils Beginning of macrophage removal of dead cells at border
7 – 10 days	Maximally soft and yellow-tan Red-tan margins	Increased phagocytosis of dead cells at border Beginning of granulation tissue formation at margins
10 – 14 days	Red-gray and depressed borders	Mature granulation tissue with type I collagen[1]
2 – 8 weeks	Gray-white granulation tissue	Increased collagen deposition Decreased cellularity
More than 2 months	Completed scarring	Dense collagenous scar formed
If not else specified in boxes, then reference is nr [2]

Once scarring is completed, there is yet no common method of telling the actual age of the infarct, since e.g. a scar that is four months old looks identical to a scar that is ten years old.

• *It is often possible, however, to highlight the area of necrosis that first becomes apparent after 2 to 3 hours by immersion of tissue slices in a solution of triphenyltetrazolium chloride. This dye imparts a brick-red color to intact, noninfarcted myocardium where the dehydrogenase activity is preserved. Because dehydrogenases are depleted in the area of ischemic necrosis (i.e., they leak out through the damaged cell membranes), an infarcted area is revealed as an unstained pale zone.

Instead of a triphenyltetrazolium chloride dye, a LDH (lactate dehydrogenase) dye can also be used to visualize an area of necrosis.

References

1. Bishop JE, Greenbaum R, Gibson DG, Yacoub M, Laurent GJ. Enhanced deposition of predominantly type I collagen in myocardial disease. J Mol Cell Cardiol. 1990;22:1157–1165
2. Table 11-2 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.