The long saphenous vein is the most commonly used conduit in
cardiac surgery; however, its use is complicated by high failure
rates due to the development of vascular inflammation, intimal
hyperplasia (IH) and accelerated atherosclerosis leading to grafts
stenosis and occlusion. Changes in vascular smooth muscle cell
(SMC) phenotype leading to SMC proliferation and migration to the
luminal area of vessels (intima) are critical events in the
development of IH and atherosclerosis. Blood flow in vessels can
exert a force on EC known as shear stress. Veins are usually
subjected to low blood flow and shear stress in the body; however,
when grafted into arterial circulation with high flow, they
suddenly become exposed to high levels of shear stress. The impact
of such acute changes in shear stress on endothelial cells (ECs)
and its role in the development of IH is not understood. Vascular
EC can act as mechano-transducers which respond to flow changes by
secreting factors which have autocrine effects to promote vascular
inflammation and may have paracrine effects on SMC and thereby IH.
This cross talk between activated ECs and SMCs in vein grafts is
poorly understood. It has been shown that shear stress can induce
vascular inflammation via signalling intermediaries and augment
different growth factors which can influence the development of IH
by stimulating SMC growth through different pathways. A greater
understanding of the mechanisms underlying vein graft failure may
reveal new therapies which may have major impact on patient's
outcomes and health economics.
