Atherosclerosis is a common disease characterized by the localized build-up of plaque within the intimal layer of an artery. The vulnerable atherosclerotic plaque fractures and subsequent thrombosis and distal embolization are caused. We have developed the model of arterial disease using the artificial substitute. We examine the biomechanical interaction between blood flow and arterial disease by in vitro experiment and numerical computation to investigate the mechanical factor for plaque fracture for plaque vulnerability assessment.

(Figure: model of arterial disease and stress distribution by numerical computation)