Inhibition of anastomotic intimal hyperplasia by a synthetic nonsulphated heparin-mimicking compound.

Despite extensive research in the design of endovascular catheters and advanced surgical techniques, stenosis recurs in a large percentage of patients undergoing angioplasty or anastomosis. Hence, neointimal hyperplasia, caused by migration and proliferation of vascular smooth muscle cells (SMC), remains a significant limitation to the relief of obstructive-occlusive vascular disease. It has been previously demonstrated that heparin displaces active basic fibroblast growth factor (bFGF) from the lumenal surface of blood vessels.