Summary
Hemostatic variables and platelet function were assessed as a part of a genetic study
in 15 patients with symptomatic peripheral arterial occlusive disease (PAOD) and 15
healthy siblings from ten families. D-dimer, a degradation product of cross-linked
fibrin, was increased in the PAOD group (mean ± SD) (448 ± 177 vs. 333 ± 121 ng/ml,
p <0.05). Ristocetin-induced maximal platelet aggregation (RIPA) was reduced in the
PAOD group in response to both a higher (0.75 mg/ml) (67 ± 28 vs. 87 ± 14%, p = 0.02)
and a lower (0.55 or 0.60 mg/ml) (33 ± 21 vs. 59 ± 32%, p = 0.02) concentration of
ristocetin. Accordingly, the rate of primary aggregation was smaller, and a larger
threshold concentration of ristocetin was needed to cause aggregation. However, ristocetin
cofactor activity, von Willebrand factor (vWF) antigen and its multimer distribution,
plasma glycocalicin, platelet glycoprotein lb content and the binding of vWF to frozen
and thawed washed platelets were equal in both groups. Thus, the observed reduced
RIPA in patients with PAOD is likely to reflect a down-regulation or blunted binding
affinity in the platelet surface glycoprotein Ib.
