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1½- 4 hour
Gross: None for 1st 12 hours by direct examination.
Micro: None or wavy fibers. Contraction bands, when present, can occur early (as early as after 2 minutes of reperfusion in animal experiments). .
Clinical: Mural thrombi
can form early and embolize at any time

4-12 Hour
Gross: Special staining shows lack of dehydrogenase, dark mottling
Micro: Early coagulation necrosis
, edema, hemorrhage, Earliest sign is hypereosinophilia of myocytes.
Clinical: CK and CK-MB elevated 4-48 hours. Troponin I 3-12 hrs

12-24 Hour

Gross: Coagulation necrosis
.
Micro: Pyknosis, neutrophils begin to enter area of infarction.

Clinical: Serious arrhythmias can occur at any time. Primary ventricular fibrillation - usually in 1st 12 hours.

1-3 Days
Gross: Pallor of infracted tissue
Micro: loss of nuclei, loss of striations, neutrophils are abundant & lyse dead myocardial cells.
Clinical: Pericardial friction rub, due to fibrinous pericarditis, most common on days 2-3

3-7 days
Gross: macrophages and necrotic tissue predominate, tissue becomes soft
appears yellow with red border due to hyperemia.
Micro: Macrophages begin to remove necrotic debris
Clinical: Rupture of free wall, ventricular septum, or papillary muscle at 3-6 days

7-10 Days
Gross: Classic appearance of bright yellow infarct area surrounded by red granulation tissue
Micro: Necrotic area is bright yellow Granulation tissue & Collagen fibers are well developed
Clinical: Dressler syndrome
, an autoimmune-based pericarditis, at 1-8 weeks

2 Months
Gross: Appearance evolves to that of a white, fibrous, non contractile scar.
Miroc: Increased collagen and decreased cellularity.
Clinical: Ventricular aneurysms
are a late complication.
 
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