In peripheral arterial disease (PAD) risk of thrombosis is high and sy
stemic haemostatic derangement thought contributory. We investigated p
latelet and coagulatory activity in patients with PAD and sought to fi
nd the best disease indicator. Stagnation point flow adhesio-aggregome
try (SPAA) enables real-time quantitative assessment of platelet adhes
ion and aggregation under well-defined flow conditions. SPAA and agoni
st-induced aggregometry (Born method) were performed and concentration
s of fibrinogen, fibrin monomer (FM), D-dimer, and thrombin-antithromb
in complex (TAT) measured in 92 PAD patients and 70 healthy volunteers
. Agonist-induced aggregometry detected no differences between patient
s and controls. SPAA-measured platelet adhesion and spontaneous aggreg
ation (p < 0.001), and concentrations of fibrinogen (p < 0.001), FM (p
< 0.001), TAT (p < 0.02) and D-dimer (p < 0.001) were all significant
ly increased in patients. Neither platelet function nor coagulatory ac
tivity was altered in patients receiving aspirin. Sensitivity and spec
ificity in detecting PAD were as follows: SPAA (95%,93%), fibrinogen (
36%,91%), FM (48%,84%), TAT (36%,78%), D-dimer (73%,80%). Our findings
support the concept of ongoing thrombogenesis as being contributory t
o the progression and possibly to the initiation of PAD. Aspirin alone
did not prevent haemostatic hyperreactivity in these patients and flo
w-mediated platelet function was the most sensitive and specific indic
ator of advanced disease. This technique thus appears to be valuable,
not only for evaluating therapeutic strategies to prevent platelet act
ivation, but also in elaborating platelet-related mechanisms involved
in thrombogenesis and atheroma formation.