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Atherosclerotic plaques form in artery walls due to a chronic inflammatoryresponse driven by lipid accumulation. A key component of the inflammatoryresponse is the interaction between monocyte-derived macrophages andextracellular lipid. Although concentrations of low-density lipoprotein (LDL)and high-density lipoprotein (HDL) particles in the blood are known to affectplaque progression, their impact on the lipid load of plaque macrophagesremains unexplored. In this paper, we develop a lipid-structured mathematicalmodel to investigate the impact of blood LDL/HDL levels on plaque composition,and lipid distribution in plaque macrophages. A reduced subsystem, derived bysumming the equations of the full model, describes the dynamics of biophysicalquantities relating to plaque composition (e.g. total number of macrophages,total amount of intracellular lipid). We also derive a continuum approximationof the model to facilitate analysis of the macrophage lipid distribution. Theresults, which include time-dependent numerical solutions and asymptoticanalysis of the unique steady state solution, indicate that plaque lipidcontent is sensitive to the influx of LDL relative to HDL capacity. Themacrophage lipid distribution evolves in a wave-like manner towards anequilibrium profile which may be monotone decreasing, quasi-uniform orunimodal, attaining its maximum value at a non-zero lipid level. Our model alsoreveals that macrophage uptake may be severely impaired by lipid accumulation.We conclude that lipid accumulation in plaque macrophages may serve as apartial explanation for the defective uptake of apoptotic cells (efferocytosis)often reported in atherosclerotic plaques.

A new lipid-structured model to investigate the opposing effects of LDL and HDL on atherosclerotic plaque macrophages