Sandbox:Hamid

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2], Usama Talib, BSc, MD [3]

Pathophysiology

Life cycle

Type 1

• 1
  • 1.1 Fever
  • 1.2 Pain
  • 1.3 Jaundice
• 2
• 3
• 4

Type 2

1	2	3	4
a
b
c

Coagulation necrosis, characterized by hypereosinophilia and nuclear pyknosis followed by karyorrhexis, karyolysis, total loss of nuclei, and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction. Necrotic myocytes may retain their striations for a long time. Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours, but generally closer to 12 hours. The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages who phagocytose or eat the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue: Which will replace the infarct with a fibrous or collagenous scar (which are typical steps in wound healing). The interstitial space or the space between cells, outside of blood vessels, may be infiltrated with red blood cells. Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts, and capillaries begins around the periphery at 3-10 days. Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an Infarct or with reperfusion, for example with thrombolytic therapy.