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Influence of Direct Oral Anticoagulants on Anti-Factor Xa Measurements Utilized for Monitoring Heparin.
Annals of Pharmacotherapy 2018 Februrary
BACKGROUND: Unanticipated drug-laboratory interactions may occur between direct oral anticoagulants (DOACs) and anti-factor Xa (AXA) levels used to monitor parenteral heparin infusions. Characterization of the extent and duration of DOAC effect on AXA levels may reduce complications with transition to heparin infusions.
OBJECTIVE: To evaluate the impact of oral factor Xa inhibitors on AXA levels with and without concurrent heparin.
METHODS: This retrospective descriptive study was approved by institutional review board waiver and included patients with AXA levels drawn on a heparin calibrated assay who had received a factor Xa inhibitor. Participants were divided on the basis of whether AXA levels were drawn with concurrent parenteral heparin. If transitioned to heparin, number of AXA draws required until AXA level was within therapeutic range was recorded.
RESULTS: A total of 50 patients (60% rivaroxaban, 40% apixaban) met inclusion criteria. When AXA levels were drawn within 12 hours of apixaban without concurrent heparin (n = 7), 71% were greater than 1 IU/mL, and 29% were below suggested trough levels (0.7-1.1 IU/mL). For AXA levels drawn within 24 hours of rivaroxaban without concurrent heparin (n = 11), 55% were greater than 1 IU/mL, 9% were within suggested trough (0.6-1 IU/mL), and 36% were below 0.6 IU/mL. In patients (n = 28) who were initiated on heparin infusion prior to AXA monitoring, administration of the DOAC within the prior 72 hours resulted in supratherapeutic initial AXA levels 69% of the time.
CONCLUSION: DOACs may cause elevations in heparin-calibrated AXA assays; this creates problematic challenges in using the AXA level to optimize heparin management.
OBJECTIVE: To evaluate the impact of oral factor Xa inhibitors on AXA levels with and without concurrent heparin.
METHODS: This retrospective descriptive study was approved by institutional review board waiver and included patients with AXA levels drawn on a heparin calibrated assay who had received a factor Xa inhibitor. Participants were divided on the basis of whether AXA levels were drawn with concurrent parenteral heparin. If transitioned to heparin, number of AXA draws required until AXA level was within therapeutic range was recorded.
RESULTS: A total of 50 patients (60% rivaroxaban, 40% apixaban) met inclusion criteria. When AXA levels were drawn within 12 hours of apixaban without concurrent heparin (n = 7), 71% were greater than 1 IU/mL, and 29% were below suggested trough levels (0.7-1.1 IU/mL). For AXA levels drawn within 24 hours of rivaroxaban without concurrent heparin (n = 11), 55% were greater than 1 IU/mL, 9% were within suggested trough (0.6-1 IU/mL), and 36% were below 0.6 IU/mL. In patients (n = 28) who were initiated on heparin infusion prior to AXA monitoring, administration of the DOAC within the prior 72 hours resulted in supratherapeutic initial AXA levels 69% of the time.
CONCLUSION: DOACs may cause elevations in heparin-calibrated AXA assays; this creates problematic challenges in using the AXA level to optimize heparin management.
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