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ekgcircle3.gif (1164 bytes) Lecture Outlines: Diseases/Syndromes
Atherogenesis

Note: A video through Real Player may be helpful in your understanding of the rold of inflammation and Atherogenesis

I.  PATHOPHYSIOLOGY
Hypothesis of Atherogenesis
Elevated plasma LDL leads to infiltration of native LDL-C particles through endothelium into intimal layer of arterial wall
  1. LDL-C particles are then oxidized (leads to release of various chemotactic factors,cytokines etc.)
  2. Macrophages in the intima ingest oxidized LDL-C-à "foam cells"
  3. Formation of advanced lesions>>fissures>>platelet aggregation>>thrombin generation>>fibrin formation>>thrombus and OCCLUSION (eg. Acute Coronary Syndrome)

    4. -foam cells are the early atherosclerotic lesion

    • endothelial cells express glycoproteins allowing monocyte adhesion to endothelial surface
    • oxidized LDL-C stimulates endothelial cells to produce chemotactic factor and the cytokines -à more monocytes enter the intima and differentiate into macrophages.
    • Macrophages produce growth factor-à smooth muscle cell proliferation à fatty streak
 

 

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