• Atherosclerosis

    by  • 21/09/2013 • Cardiology


    1. Artery wall thickens as the result of a build-up of fatty materials such as cholesterol, causing a chronic oxidation / inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low-density lipoproteins (LDL) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL) = FOAM CELLS.


    1. Most artery flow disrupting events occur at locations with less than 50% lumen narrowing – that is to say the ‘mature’ plaques are more stable even if they are causing higher stenosis. New young plaques most likely to rupture.




    Anatomy of vessel wall:

    1. Intima: collagen, elastin, SMCs, valves, vWf
    2. Media: many SMCs, increased elastic
    3. Adventitia: vasa vasorun, nervi vascularis, structure.


    Presenting complaint

    1. Occlusive:
      1. o PVD
      2. o CV disease
      3. o Angina
    2. Ruptured:
      1. o MI
      2. o sudden cardiac death


    Diagnostic tools/investigations

    1. ETT and cardiac stress testing (MPI/DSE)
    2. Perfusion MRI/perfusion echo
    3. Angiographyangioplasty (balloon/stent)




    1. Having diabetes or Impaired glucose tolerance (IGT)
      1. o Dyslipoproteinemia
      2. o High serum concentration of LDL or VLDL
      3. o Low serum concentration of HDL
      4. o An LDL:HDL ratio greater than 3:1
    2. Tobacco smoking, increases risk by 200% after several pack years
    3. Having hypertension increases risk by 60%
    4. Elevated serum CRP concentrations



    1. Advanced age
    2. Male gender
    3. Having close relatives who have had some complication of atherosclerosis (CHD / CVA)
    4. Genetic abnormalities, e.g. familial hypercholesterolemia



    Accumulation of lipids endothelial cells are activated decreased NO (increase anti-atherogenic activity, increase SMC proliferation, erduce macrophage apoptosis, promoye monocyte adhesion) ApoB in LDL binds PGmonocytes in intima become macrophages and ingest oxidised LDLsfoam cells created = release PDGF and smooth muscle cells migrate chemoattractant for inflammatory cells smooth muscle cells and further monocytes are recruited proliferation and martix synthesis fatty streak formationfibrous cap formation plaque erosion over time rupture platelet aggregation thrombosis & MI

    Plaque can be stabalised by: inc SMC, antioxidants, thick cap

    Destabalised by: high LDL, few SMC, thin cap, cytokines

    Vessels can remodel to accommodate plaque (concentric and eccentric)

    Hereditary? Infective? How does it spread?

    Treatment and management (conservative/medical/surgical)

    1. Dietary changes and weight loss
    2. exercise
    3. Smoking cessation
    4. Statins (anti-thrombogenic, anti-inflammatroy, anti-oxidant, anti-chol)…
    5. Fibrates (increase HDL and lower TG. Have little effect on LDL)!
    6. Aspirin / clopidogrel… anti-coags
    7. Niacin (vit B3) in therapeutic doses increases HDL
    8. homocysteine
    9. Angioplasty with stenting


    Plaque rupture complications:

    1. Rupture and fissuring = showers of emboli
    2. Aneurysmal dilatation
    3. MI
    4. Gangrene of lower limbs
    5. Renal infarction
    6. Aortic dissection = dual flow and rupture
    7. Cerebral haemorrhage/ischaemia


    Chronology of atherosclerosis:

    1. 1st decade: foam cells, fatty streaks, lipid accumulation
    2. 3rd: intermediate lesion and atheroma
    3. 4th: fibrous plaque and risk of rupture


    After one rupture, 1-5 more follow (average 2). 

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