Check AT Before Starting Heparin?

George,would it be better to check the patient’s antithrombin III (AT III, antithrombin, AT) level before starting unfractionated heparin (UFH)? Regards, Frances Weekes.

Hi, Frances, thanks for the question, and while I’d be happy to invite other opinions from our participants, I would not recommend screening for AT levels on everyone starting unfractionated heparin for the following reasons:

• The false positive rate for AT deficiency would undoubtedly exceed the true positive rate, consequently the laboratory scientist would end up fruitlessly tracking down a number of positive results at considerable expense and time.
• A cardiologist is unlikely to choose to delay starting UFH for the purpose of collecting specimens for AT. This argument could be moot, given that the cardiologist may want a baseline PTT and other laboratory assays and could simply add the AT.
• While knowing the baseline AT level may help the laboratory identify AT deficiency later, providing a reason for “heparin resistance,” it may not actually influence the patient’s therapy.

One could argue in response that knowing the baseline AT, the laboratory director could order a switch to an alternative assay that is not sensitive to the AT level, such as Stago’s Stachrom Heparin, which provides AT in the reagent; as opposed to the partial thromboplastin time (PTT) or Stago’s Sta Rotachrom Heparin, which does not provide AT, and therefore is sensitive to plasma AT levels. Additionally, the pathologist could recommend AT therapy (Thrombate III) to ensure heparin efficacy. Nevertheless, testing in response to suspicion of heparin resistance is likely to provide better efficacy than screening all UFH candidates without exposing the patient to the risk of UFH overdose.

To explain further, heparin resistance is the jargon applied to the circumstance in which the PTT becomes insensitive to UFH dosage increases, often because of AT deficiency. Heparin resistance may also be the result of raised coagulation factor VIII or fibrinogen levels in inflammation that render the PTT less sensitive to the anticoagulant.