• Endothelial cell damage
    •  to elastic arteries and large and medium-sized muscular arteries 
    • resulting in fibrous plaques and atheromas formed in the intima
  • Epidemiology
    • Risk factors
      • blood chemistry abnormalities (↑ LDL, ↑ homocysteine)
      • hypertension, smoking, diabetes
      • genetic
  • Pathophysiology
    • endothelial cell dysfunction as a result of injurious stimuli 
    • macrophages and LDL adhere to damage
      • macrophages may phagocytose LDL and become lipid-laden foam cells 
      • now a fatty streak
    • macrophages/endothelial cells/platelets stimulate smooth muscle hyperplasia via cytokine release (PDGF and TGF-β
    • smooth muscle cells of vessel wall migrate into intima 
    • ↑ extracellular matrix (fibrous cap) produced as result of cytokines released by smooth muscle cells
      • has a necrotic center with cholesterol crystals and foam cells
    • stable plaques have a thick fibrous cap, unstable plaques have a thin fibrous cap
      • ↑ expression of matrix metalloproteinases may result in cap degradation and rupture
      • slow forming plaques allow for formation of collateral circulation
        • less likely to result in MI if plaque ruptures 
  • Symptoms
    • angina
      • if >75% obstruction 
    • claudication
    • can be asymptomatic
  • Location
    • abdominal aorta > coronary artery > popliteal artery > internal carotid artery
  • Labs
    • ↑ in C-reactive protein
      • strong predictor of disrupted plaques
  • Result of sudden ↓ in perfusion
    • presenting as ischemia/infarction
    • thrombus
      • rupture of fibrous cap resulting in immediate clot formation at site of rupture
    • emboli
      • ↓ in lumen size plugged by embolus from another source in body
      • may give rise to emboli that propagate forward
  • Result of chronic ↓ in perfusion
    • peripheral vascular disease
      • ↑ risk of gangrene
    • atrophy
      • cerebral atrophy when cerebral vessels are involved

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