Correspondence between Lawrence “Lance” Williams III, MD, University of Alabama at Birmingham (UAB) Hospital Special Coagulation Director and Michael Laposata, MD, University of Texas Medical Branch (UTMB) in Galveston Pathology Director:
Dr. Laposata, I am curious if you might have some insight on an issue we are having at UAB. We have noticed an increase in patients coming into the hospital on DOACs such as rivaroxiban, and apixiban. This is a problem when the patient comes in with a new thrombus or myocardial infarction because the clinicians prefer to start the patient on heparin (UFH), which we monitor with the chromogenic anti-Xa heparin assay.
In these situations our currently policy is to use the anti-Xa (calibrated for UFH) as a qualitative measure of these other Xa inhibitors and monitor it until it is < 0.3 units/mL before starting UFH therapy. We are doing this to avoid over-anticoagulating the patient. However, I worry that such a policy may risk patients forming additional clots or suffering damage due to inadequate anticoagulation. By using the anti-Xa calibrated for UFH, we do not have an accurate measure of how much rivaroxaban or apixaban the patient has in their system. I am considering moving the above target to < 0.5 units/mL, but I’m not sure this is good enough. Any sage advice from UTMB?
From Dr. Laposata, Lance, we had a long discussion about the issue you raised in the email about the anti-Xa target level in patients presenting with a presumed myocardial infarction who are already on a DOAC with anti-Xa activity. With four attendings in the room, and a search of the literature, as far as we can tell there are no guidelines that help us figure out what to do. We also realize this is likely to be an extremely common situation. We did have a lot of discussion about the fact that patients with a lupus anticoagulant and a prolonged PTT cannot be monitored with a “modified target range” for the PTT. The proposal of having a modified target range for anti-Xa to < 0.5 units/mL does this same thing and makes a presumption that elevating what we think is therapeutic when there is an interfering substance allows us to anticoagulate the patient with a reduced risk for the complications of bleeding and thrombosis. Having said that, however, no one else as far as we can tell has a better plan than this. Therefore, we concluded that in the absence of evidence, shooting for at least 0.5 units/ mL of anti-Xa activity in a patient on rivaroxban, apixaban, or edoxaban is something we should adopt just like you for the time being and keep a close eye on the literature. Hope this helps.
Added by George Fritsma: in this instance the patient assumas the risk of rethrombosis or hemorrhage while laboratory scientists await a decision from the US Food and Drug Admnistration Devices Division allowing us to employ the chromogenic anti-Xa with the respective calibrator and controls to monitor the anti-Xa DOACs rivaroxaban, apixaban, and edoxaban. This decision that has been pending for over a year despite the demonstrated validity of the assay. Both UAB’s and UTMB’s institutional policies ban the use of non-FDA approved assays, howeve others have moved ahead with the anti-Xa assays for DOACs, appending the standard Research Use Only (RUO) statement and Advance Beneficiary Notice (ABN). This topic came up in a May 11 discussion originating from Dahl Chase Associates in Maine, and in a January 12 entry, and we’ve seen no clear resolution. The two previous entries attracted several comments, so it is unlikely we will see any further comments.
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