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A pilot study was performed to compare the thromboprophylactic effect of danaparoid, enoxaparin and dalteparin in patients with hip fracture. The study was a prospective, randomised assessor-blind, four-centre trial. Prophylaxis was given for 9–11 days, whereafter bilateral phlebography was performed. A total of 197 patients were randomised. There were no statistically significant differences in the frequency of deep vein thrombosis, in blood loss or bleeding complications between the three prophylaxis groups. In conclusion, this moderately sized study revealed no statistically significant difference in efficacy or safety between danaparoid, enoxaparin and dalteparin in patients undergoing hip fracture surgery.

Background Congestive heart failure (CHF) is associated with a hypercoagulable state. Patients and Methods A single-center, randomized, double-blind, placebo-controlled trial was performed to test the hypothesis that a prophylactic dose of low molecular weight heparin (bemiparin sodium 3500 IU/daily subcutaneously) will modify a hypercoagulable state in CHF. This study included 100 patients with CHF (New York Heart Association classification II to IV). All patients underwent 3 blood tests, at baseline (before randomization), 24 hours after randomization, and before hospital discharge or within 10 days from randomization. Results In comparison of baseline bemiparin sodium 3500 IU/daily subcutaneously with after 24 hours, there was a significant decrease in plasma levels of D-dimer (−13.8 ng/mL; P = .01) and prothrombin fragments 1 and 2 (−0.11 nmol/L; P = .01), whereas protein C was significantly increased (+3.5%; P = .03). In comparison of baseline bemiparin sodium 3500 IU/daily subcutaneously with after 4 to 10 days of therapy, there were significantly decreased plasma levels for factor VII:c (−3.0%; P = .01), D-dimer (−44.0 ng/mL; P = .002), and thrombin-antithrombin complex (−0.7 μg/L; P = .0001), whereas protein C was significantly increased (+16.0%; P = .03). On the other hand, in the group of patients treated with placebo after 24 hours, a significant decrease was observed of protein C (−4.0%; P = .04). After 24 hours, the changes from baseline were significantly different for some of the hemostatic factors in comparison of bemiparin sodium 3500 IU/daily and placebo (factor VII:c: −1.7 versus 0.0%; P = .04; D-dimer: −14 versus +24.3 ng/mL; P = .009; prothrombin fragments 1 and 2: −0.11 versus +0.11 nmol/L; P = .01; protein C: +3.5 versus −4.0%; P = .01). Also at discharge, the changes from baseline were different for some of the markers in comparison of bemiparin sodium with placebo (D-dimer: −44 versus 3.8 ng/mL; P = .002; thrombin-antithrombin complex: −0.70 versus +0.14 μg/L; P = .002; protein C: +16.0 versus +0.5%; P = .02). Conclusion Our findings suggest that a hypercoagulable state in heart failure can be modified with bemiparin sodium therapy. (Am Heart J 2002;143:e3.)