In this episode, I’ll discuss how the use of drug-specific factor Xa inhibitor levels can reduce major bleeding.
Factor Xa inhibitors such as rivaroxaban and apixaban gained popularity over warfarin in part because of the lack of monitoring needed to provide reliable therapeutic anticoagulation. Because routine monitoring is not routinely needed, rapid turnaround laboratory testing for apixaban or rivaroxaban levels is relatively uncommon in hospitals. Without the ability to get a level in a clinically reasonable timeframe, making the transition to parenteral anticoagulants in hospitalized patients must be done blindly using only average half life and reported time of last dose as a guide.
Researchers who did have the availability for in-house testing of drug-specific anti-Xa concentrations recently published an observational, single-center, retrospective cohort study of hospitalized patients who were converted from apixaban or rivaroxaban to therapeutic parenteral anticoagulation with or without drug-specific anti-Xa concentration guidance.
The primary outcome compared between groups was major bleeding. 388 patients had concentration-guided transition to parenteral anticoagulation and 457 patients did not.
Major bleeding rates were about 80% less in the concentration-guided group at 2.2% vs 11.3% without concentration-guided transitions. This difference was statistically significant.
Other safety outcomes measured such as incidence of thromboembolic complications were similar between groups. This is important because it suggests that even when starting parenteral anticoagulation is delayed due to elevated oral anticoagulant levels, it does not result in failure of the anticoagulation strategies used to prevent a thromboembolism.
Based on the data collected the authors make the following recommendations for using anti-Xa levels to guide the transition to parenteral anticoagulants:
An anti-Xa concentration below 100 ng/mL appears to be a reasonably safe cutoff for when the transition can be made.
An anti-Xa concentration between 100 and 200 ng/mL should cause a patient-specific re-evaluation of the risks vs benefits of proceeding with the transition or waiting another 6-12 hours before proceeding.
An anti-Xa concentration above 200 ng/mL is cause for most patients to wait another 12-24 hours before re-checking their anti-Xa level.
The authors emphasize that these results and recommendations may not have external validity to other hospitals, and that more data is needed to develop a standardized approach.
Hopefully this and future studies can be used to justify the addition of drug-specific anti-Xa testing capability to more hospital laboratories.
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