  Atherosclerosis, hardening of the arteries, originates from small plaque in
the arteries; it is a major cause of disability and premature death in the
United States and worldwide. In this paper, we study the bifurcation of a
highly nonlinear and highly coupled PDE model describing the growth of arterial
plaque in the early stage of atherosclerosis. The model involves LDL and HDL
cholesterols, macrophage cells as well as foam cells, with the interface
separating the plaque and blood flow regions being a free boundary. We
establish finite branches of symmetry-breaking stationary solutions which
bifurcate from the radially symmetric solution. Since plaque in reality is
unlikely to be strictly radially symmetric, our result would be useful to
explain the asymmetric shapes of plaque.
