Atherosclerosis: Difference between revisions

    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

    - 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

    - 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.

    - 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"