The cardiovascular system is an internal flow loop with multiple branches c
irculating a complex liquid. The hallmarks of blood flow in arteries are pu
lsatility and branches, which cause wail stresses to be cyclical and nonuni
form. Normal arterial flow is laminar, with secondary flows generated at cu
rves and branches. Arteries can adapt to and modify hemodynamic conditions,
and unusual hemodynamic conditions may cause an abnormal biological respon
se. Velocity profile skewing can create pockets in which the wall shear str
ess is low and oscillates in direction. Atherosclerosis tends to localize t
o these sites and creates a narrowing of the artery lumen-a stenosis. Plaqu
e rupture or endothelial injury can stimulate thrombosis, which can block b
lood flow to heart or brain tissues, causing a heart attack or stroke. The
small lumen and elevated shear rate in a stenosis create conditions that ac
celerate platelet accumulation and occlusion. The relationship between thro
mbosis and fluid mechanics is complex, especially in the post-stenotic flow
field. New convection models have been developed to predict clinical occlu
sion from platelet thrombosis in diseased arteries. Future hemodynamic stud
ies should address the complex mechanics of flow-induced, large-scale wall
motion and convection of semisolid particles and cells in flowing blood.