Thromb Haemost 1990; 64(01): 087-090
DOI: 10.1055/s-0038-1647258
Original Article
Schattauer GmbH Stuttgart

Ridogrel, a Combined Thromboxane Synthase Inhibitor and Receptor Blocker, Decreases Elevated Plasma β-Thromboglobulin Levels in Patients with Documented Peripheral Arterial Disease[*]

Authors

  • B Hoet

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
  • J Arnout

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
  • C Van Geet

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
  • H Deckmyn

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
  • R Verhaeghe

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
  • J Vermylen

    The Center for Thrombosis and Vascular Research, K. U. Leuven, Leuven, Belgium
Further Information

Publication History

Received 05 January 1990

Accepted after revision 01 May 1990

Publication Date:
25 July 2018 (online)

Summary

The combination of thromboxane synthase inhibition with thromboxane receptor antagonism has been shown to result in a strong inhibition of platelet aggregation and a prolongation of the bleeding time (Gresele et al., J. Clin Invest 1987;80: 1435–45).

Ridogrel is a single molecule that efficiently achieves both inhibitions in human volunteers. The present study was performed in patients with obstructive peripheral arterial disease and elevated plasma β-thromboglobulin levels. Patients were treated with either 2 × 300 mg ridogrel or 2 × 300 mg placebo per day for 2½ days, according to a double blind randomised parallel design. Plasma β-thromboglobulin decreased significantly throughout active treatment starting within 2 h after administration; serum and urinary immunoreactive TxB2 levels and urinary 11-dehydro- TxB2 excretion were significantly lower and serum PGE2 and 6-keto-PcF levels significantly higher with ridogrel; no changes were observed in the placebo-treated group.

In conclusion this study demonstrates a reduction of platelet activation in vivo by ridogrel.

Dedicated to Professor M. Verstraete on the occasion of his 65th birthday.