THE CONTEXT
Atherosclerotic plaque evolution involves inflammatory-cell recruitment, lipid accumulation and a smooth muscle repair response.
Inflammatory cells and lipid accumulation
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Monocytes and other inflammatory cells bind to receptors on endothelial cells and then migrate into the intima.
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These cells phagocytose oxidised low-density lipoprotein (LDL) particles and become lipid-laden macrophages, also called foam cells.
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When foam cells die and release their contents, extracellular lipid pools develop in the intima.
Smooth muscle response and plaque stability
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Cytokines and growth factors from activated macrophages stimulate smooth muscle cells to migrate from the arterial media into the intima.
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The smooth muscle cells change from a contractile to a fibroblastic phenotype, which can stabilise the lesion.
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Successful repair covers the lipid core with smooth muscle cells and matrix. The resulting stable plaque remains asymptomatic until it becomes large enough to obstruct arterial flow.
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Clinical manifestations often do not appear until the sixth, seventh or eighth decade of life.