Antiplatelet therapy reduces serious vascular events and vascular death in patients with PVD. For infrainguinal arterial surgery or balloon angioplasty the benefit remains unproven, but the number of trials to date is small. There is also evidence to support the use of antiplatelet drugs other than aspirin for the prevention of vascular events in those with PVD.

this study provides further evidence that platelet hyperactivity is present in patients with PAD despite the use of antiplatelet therapy. Further antiplatelet strategies may be indicated to protect these patients.

Significant platelet activation and aggregation occurs during CEA despite the current use of antiplatelet treatment. Dextran 40 had an antiplatelet effect after CEA providing further evidence that it may contribute to reducing thromboembolic complications.

Dextran 40 has been used to prevent post-operative thrombosis. However, its antithrombotic and antiplatelet effects in peripheral arterial disease (PAD) are poorly understood. We studied the in vitro effects of Dextran 40 on platelet function in control subjects and PAD patients using whole blood methods. Platelet function was assessed in 20 control subjects and 20 PAD patients. Spontaneous platelet aggregation (SPA) and agonist-induced platelet aggregation in response to increasing concentrations of Dextran 40 in vitro were measured by whole blood aggregometry. Flow cytometric measurements of platelet P-selectin, GpIIb/IIIa, GpIb and PAC-1 binding were also performed. There was no difference in SPA or ADP-induced aggregation in control patients with Dextran 40 in vitro. However, Dextran 40 inhibited collagen-induced aggregation in control patients (P < 0.05, Friedman test). In PAD patients, SPA and ADP (1 microM)-induced aggregation were significantly reduced by Dextran 40 in vitro (P < 0.001, Friedman test). In PAD patients, collagen-induced platelet aggregation (1 and 5 microg/ml) was significantly reduced by Dextran 40 in vitro (P < 0.01, Friedman test). GpIIb/IIIa, PAC-1 and P-selectin expression were significantly reduced in whole blood samples from PAD patients following incubation with Dextran 40 (P < 0.05, Wilcoxon rank test) but not in samples from control patients. Dextran 40 reduces spontaneous and agonist-induced platelet aggregation as well as the surface expression of markers of platelet activation in PAD patients. This antiplatelet effect may be of benefit to patients undergoing vascular surgical procedures where thrombosis is a significant risk.