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Effects of the Oral Direct Thrombin Inhibitor Ximelagatran on P-Selectin Expression and Thrombin Generation in Atrial FibrillationWolzt M.a · Boström S.L.b · Svensson M.b · Wåhlander K.b,c · Grind M.d · Sarich T.C.e
aDepartment of Clinical Pharmacology, University of Vienna, Vienna, Austria; bAstraZeneca R&D, Mölndal, cDepartment of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg, Sweden; dAstraZenca R&D Charnwood, Loughborough, UK; eAstraZeneca LP, Wilmington, Del., USA Corresponding Author
Troy C. Sarich, PhD
Experimental Medicine, AstraZeneca LP
PO Box 15347, C4C-123
Wilmington, DE 19850 (USA)
Tel. +1 302 885 8979, Fax +1 302 886 3386, E-Mail firstname.lastname@example.org
This study investigated the pharmacodynamic effects of the oral direct thrombin inhibitor ximelagatran on platelet activation and thrombin generation in patients with nonvalvular atrial fibrillation. Using an open, group-matched study design, the effects of ximelagatran (36 mg twice daily for 5 days) were studied in 12 patients with permanent nonvalvular atrial fibrillation and in 12 healthy controls. After ximelagatran for 5 days, elevated platelet P-selectin expression in atrial fibrillation patients was lowered to that during coumarin treatment or in controls but had no effect in control subjects. Using the endogenous thrombin potential as a marker, ximelagatran decreased and delayed thrombin generation in both groups. In conclusion, direct thrombin inhibition with ximelagatran reduced elevated platelet P-selectin expression and inhibited thrombin generation.
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