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Atherosclerotic plaques are accumulations of cholesterol-engorged macrophagesin the artery wall. Plaque growth is initiated and sustained by the depositionof low density lipoproteins (LDL) in the artery wall. High density lipoproteins(HDL) counterbalance the effects of LDL by accepting cholesterol frommacrophages and removing it from the plaque. In this paper, we develop a freeboundary multiphase model to investigate the effects of LDL and HDL on earlyplaque development. We examine how the rates of LDL and HDL deposition affectcholesterol accumulation in macrophages, and how this impacts cell death ratesand emigration. We identify a region of LDL-HDL parameter space where plaquegrowth stabilises for low LDL and high HDL influxes, due to macrophageemigration and HDL clearance that counterbalances the influx of new cells andcholesterol. We explore how the efferocytic uptake of dead cells and therecruitment of new macrophages affect plaque development for a range of LDL andHDL levels. Finally, we consider how changes in the LDL-HDL profile can changethe course of plaque development. We show that changes towards lower LDL andhigher HDL can slow plaque growth and even induce regression. We find thatthese changes have less effect on larger, more established plaques, and thattemporary changes will only slow plaque growth in the short term.

HDL and plaque regression in a multiphase model of early atherosclerosis