Table 2 Histological/immunohistochemical and Western blotting age determination of MI

Cell death

Up to 30 minutes – 1 hour

Cytoplasm and mitochondrial swelling and dissolution of the cristae mitochondriales (electron microscopy); loss of contraction with stretching of the myocardium in flaccid paralysis, resulting in a very early elongation of sarcomeres and nuclei; mild myofiber eosinophilia. Foci of contraction band necrosis. At immunohistochemistry loss of cellular antigen (myoglobin and cardiac troponin) is detectable earlier than the accumulation of plasma markers (C5b-9 complex, fibronectin).

Inflammatory phase

4-6 hours

Mild positivity of immunoreaction (tryptase, CD15, IL-1β, IL-6, IL-8, TNF-α) and stronger reactivity for IL-15, MCP-1 in areas where depletion of cellular antigens (myoglobin and cardiac troponin) is detectable within 30 – 40 minutes from ischemia.

6-8 hours

Necrosis of the infarcted area becomes more evident; a crowd of polymorphonuclear leukocyte infiltration from the periphery is evident. General and intense eosinophilia of myofibers. Interstitial oedema. Immunopositivity to the antibodies anti tryptase, CD15, IL-1β, IL-6, IL-8, IL-15, TNF-α becomes stronger and ubiquitously widespread. MCP-1 decrease as intensity in respect to the first hours.

Pronounced necrosis of the infarcted areas; strong evidence of PMN margination with further leukocyte penetration of the infarct area. Strong immunopositivity to anti CD15 antibodies was observed.