Time

Gross findings

Histopathology

Clinical correlations

1½- 4 hours

None for 1^st 12 hours by direct examination.

None or wavy fibers. Wavy fibers as early as 1-3 hours. Contraction bands, when present, can occur early (as early as after 2 minutes of reperfusion in animal experiments). .

Mural thrombi can form early and embolize at any time

4-12 hours

Special staining shows lack of dehydrogenase as early as 2-3 hours.

Early coagulation necrosis, edema, hemorrhage, Earliest sign is hypereosinophilia of myocytes.

CK and CK-MB elevated 4-48 hours. Troponin I

8-72 hours.

12-24 hours

Pallor or red-blue hue. Occasionally, hemorrhage, especially when thrombolysis was administered.

Coagulation necrosis, hypereosinophilia, pyknosis as early as 5 hours, loss of striations later, contraction band necrosis, polys as early as 6-8 hours 

Serious arrhythmias can occur at any time. Primary ventricular fibrillation – usually in 1^st 12 hours.

1-3 days

Coagulation necrosis, loss of nuclei 24-48 hours, more loss of striations, polys peak at 48 hours 

Pericardial friction rub, due to fibrinous pericarditis, most common on days 2-3

3-7 days

As macrophages and necrotic tissue predominate, tissue is soft and appears yellow with red border due to hyperemia. Prone to rupture.

Early disintegration of dead muscle, dying polys. Macrophages appearing and increasing.

Rupture of free wall, ventricular septum, or papillary muscle at 3-6 days

7-10 days

Macros with phagocytosis, early granulation tissue. Proliferation of blood vessels as early as 3 days.

Fibroblasts as early as 4 days.

10-14 days

Granulation tissue recognized as early as 7-10 days. Collagen fibers as early as 9 days.

Dressler syndrome, an autoimmune-based pericarditis, at 1-8 weeks

2-8 weeks

Appearance evolves to that of a white, fibrous scar.

Increased collagen and decreased cellularity. Peak granulation tissue at 2-4 weeks. Dense scar as early as 6 weeks.

Ventricular aneurysms are a late complication.