Molecular and cellular changes in vein grafts

Adaptation of saphenous vein, with its intrinsic myogenic tone, from the low-pressure, minimally pulsatile flow of the venous system to the pulsatile flow of the arterial circulation is a minor miracle. Changes in gene expression caused by the pulsatile circumferential deformation (cyclic strain) initiate changes in gene expression, which lead to both vein graft adaptation and pathology. Removal of circumferential deformation by external stenting attenuates the early changes in gene expression and the later development of intimal hyperplasia. Pathways for the transduction of cyclic strain into cellular events have been elucidated in cultured vascular cells. The important second messengers include calcium and reactive oxygen species.