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Atherosclerosis is a chronic inflammatory cardiovascular disease in whichfatty plaque is built inside an artery wall. Early atherosclerotic plaquedevelopment is typically characterized by inflammatory tissues primarilyconsisting of foam cells and macrophages. We present a biphasic model thatexplores early plaque growth to emphasize the role of cytokines (particularly,Monocyte Chemoattractant Protein-1) and oxidized low-density lipoprotein(oxLDL) in monocyte recruitment and foam cell production, respectively. Theplaque boundary is assumed to move at the same speed as the inflammatorytissues close to the periphery. This study discusses the oxLDL cholesterolsrecruitment inside intima and their internalization by the inflammatory cells.Excessive intracellular cholesterol accumulation becomes toxic to macrophagefoam cells, leading to cell death beyond a threshold. Our findings reveal thatinitially, the plaque evolves rapidly, and the growth rate eventually reducesbecause of the cholesterol-induced toxicity. The present study manifests thathigher oxLDL cholesterol flux reduces plaque growth rate, while elevatedcytokines flux promotes the corresponding plaque growth behaviour. BetweenoxLDL cholesterol and intracellular cholesterol, the second one is much moreeffective towards the growth of inflammatory tissue. The cholesterol-basedtoxicity-induced cell death parameters are crucial in flattening the plaquegrowth profile. A detailed analysis of the model presented in this articleprovides critical insights into the various biochemical and cellular mechanismsbehind early plaque development.

A Two-Phase Model of Early Atherosclerotic Plaque Development with LDL Toxicity Effects