Atherosclerosis

Summary: fatty streaks --> proliferative intima plaque --> complex atheromas --> plaque rupture --> atherotrombosis

Proces: - endothelial dysfunction resulting in disturbed regulation between blood and vascular wall.

    a large number of factors contribute to this process, including:
      oxidated LDL
      shear-stress (chronic pressureload on vessel-wall)                   
      infectious microbes
      toxines (e.g. nicotine)
      hyperglycemia

- foam cells and fatty streaks

   - macrophages enter the subendothelial space, degrade oxidized LDL and result in the formation of foam cells. Apoptosis of macrophages 
     causes further damage the endothelial lining of the vessel wall.
   - thrombocytes attach to the endothelium, causing the release of factors promoting growth and proliferation of smooth muscle cells.
   - this results in the formation of fatty streaks, a combination of degenerated foam cells, smooth muscle cells and connective tissue

- progression of fatty streaks to atheromas

   - this process gradually progresses, resulting in increased endothelial dysfunction, decreased elasticity of the vessel wall, build-up of 
     fatty streaks and formation of a fibrous plaque. Eventually the fibrous plaque also expands into the lumen of the vessel, resulting in a 
     atheromatous stenosis.

- plaque rupture and atherothrombosis

   - the intravascular plaque-structure will continue to increase in size, eventually resulting in occlusion or plaque rupture, depending on the structure and stability of the plaqye. Usually the "shoulder" of the plaque is most susceptable for rupture. When this happens, a atherothrombus is formed causing occlusion of the epicardial vessel "downstream"

--145.117.105.140 10:44, 11 January 2011 (CET)