Fig. 1.  A Thromboelastometry (ROTEM®; Pentapharm, Munich, Germany) tracings during bivalirudin anticoagulation. Native whole blood samples (300 μl) were triggered with 20 μl of the commercial tissue factor reagent EXTEM (Pentapham). FibTEM® assays were performed similarly with the addition of cytochalasin D to exclude platelet interactions with polymerized fibrin. It is notable that blood clotting (  i.e. , fibrin polymerization) occurs even after the bolus bivalirudin injection after a delay.  B Thromboelastometry (ROTEM®) tracings in pooled plasma spiked with argatroban or bivalirudin. Plasma samples (300 μl) were triggered with 20 μl of EXTEM reagent and CaCl2. The onset of fibrin polymerization was more delayed with argatroban at 10 μg/ml than bivalirudin at 20 μg/ml due to lesser molar concentration of the latter (20 μm  vs. 10 μm). The maximal clot formation reaches the same level over time. 

Fig. 1.  A Thromboelastometry (ROTEM®; Pentapharm, Munich, Germany) tracings during bivalirudin anticoagulation. Native whole blood samples (300 μl) were triggered with 20 μl of the commercial tissue factor reagent EXTEM (Pentapham). FibTEM® assays were performed similarly with the addition of cytochalasin D to exclude platelet interactions with polymerized fibrin. It is notable that blood clotting (  i.e. , fibrin polymerization) occurs even after the bolus bivalirudin injection after a delay.  B Thromboelastometry (ROTEM®) tracings in pooled plasma spiked with argatroban or bivalirudin. Plasma samples (300 μl) were triggered with 20 μl of EXTEM reagent and CaCl2. The onset of fibrin polymerization was more delayed with argatroban at 10 μg/ml than bivalirudin at 20 μg/ml due to lesser molar concentration of the latter (20 μm  vs. 10 μm). The maximal clot formation reaches the same level over time. 

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