Hemodynamics of a Femoral Graft-Artery Connector Mitigating Restenosis

Thrombosis or restenosis, i.e., blood clot formation or neo-intimal hyperplasia plus atheroma, are too frequently the causes of graft failure post-operatively within hours (cf. thrombosis) or within a few years (cf. restenosis). It is hypothesized that among the many factors triggering these abnormal biological events in curved and branching arteries, non-uniform hemodynamics, well characterized by large wall shear stress gradients (WSSG), is a leading cause in a cascade of intricate physico-biochemical processes. Local sustained WSSG’s have been implicated in “injury” to the endothelium leading to high cell turnover, leaky cell junctions, individual cell bond rupture, as well as DNA changes causing excessive release of growth factors, smooth muscle cell proliferation and platelet aggregation. In turn, a significant reduction of the WSSG may be achieved with (optimal) geometric designs of specific branching blood vessels, which implies that non-uniform hemodynamics can be minimized and hence restenosis may be measurably reduced.