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  • Atherosclerosis

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    The document classifies human atherosclerotic lesions into 6 types based on histology and clinical correlation. Type I and II lesions are clinically silent and occur in the first two decades, consisting of isolated macrophage foam cells or fatty streaks. Type III and IV lesions occur from the third decade onward and involve extracellular lipid accumulation and growth through further lipid and connective tissue buildup. Type VI lesions involve surface defects such as thrombosis that can lead to clinical symptoms and occur from the fourth decade of life onward.

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    The document classifies human atherosclerotic lesions into 6 types based on histology and clinical correlation. Type I and II lesions are clinically silent and occur in the first two decades, consisting of isolated macrophage foam cells or fatty streaks. Type III and IV lesions occur from the third decade onward and involve extracellular lipid accumulation and growth through further lipid and connective tissue buildup. Type VI lesions involve surface defects such as thrombosis that can lead to clinical symptoms and occur from the fourth decade of life onward.

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    31 views1 page

    Atherosclerosis

    Uploaded by

    hemakumar1029
    The document classifies human atherosclerotic lesions into 6 types based on histology and clinical correlation. Type I and II lesions are clinically silent and occur in the first two decades, consisting of isolated macrophage foam cells or fatty streaks. Type III and IV lesions occur from the third decade onward and involve extracellular lipid accumulation and growth through further lipid and connective tissue buildup. Type VI lesions involve surface defects such as thrombosis that can lead to clinical symptoms and occur from the fourth decade of life onward.

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    AHA Classification of human atherosclerotic lesions

    Nomenclature Type I (initial, fatty dot) lesion Type II (fatty streak) lesion Type III (intermediate) lesion Type IV (atheroma) lesion Type VI (fibroatheroma) lesion

    Main histology Isolated macrophage foam cells Mainly intracellular lipid accumulation Type II changes and small extracellular lipid pools Type II changes and core of extracellular lipid Lipid core and fibrotic layer, or multiple lipid cores and fibrotic layers or mainly calcific or mainly fibrotic Surface defect, hematoma hemorrhage, thrombus

    Mechanism

    Earliest onset From first decade

    Clinical correlation Clinically silent

    Growth mainly by lipid accumulation

    From third decade

    Accelerated smooth muscle and collagen increase Thrombosis, hematoma

    From fourth decade

    Clinically silent or overt

    Type VI (complicated) lesion

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