Pattern Formation in Atherosclerotic Plaques

Abstract

Atherosclerosis is a disease of the cardiovascular system of humans that can lead to myocardial infarction and stroke. It begins in the arterial walls (intima) as an inflammatory response to dysfunction of the endothelium and access of the intima by oxidized low-density lipoproteins (oxLDLs). In response to this, white blood cells, specifically monocytes, are recruited from the bloodstream. Trapped in the intima, the monocytes differentiate into macrophages which, after engulfing oxLDLs, become foam cells, leading to the production of inflammatory cytokines and further recruitment of white blood cells. This self-accelerating process results in an increase of the thickness of arteries, in the formation of atherosclerotic plaques and, possibly, in their rupture. We suggest a one-dimensional mathematical model of the initial events of atherosclerosis. This model consists of a reaction–diffusion system with Neumann boundary conditions, and describes the recruitment of monocytes as a function of the concentration of inflammatory cytokines.