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Ann Thorac Surg 2003;75:284-285
© 2003 The Society of Thoracic Surgeons
a Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences, General Site, 237 Barton St East, Hamilton, ON L8L 2X2, Canada
e-mail: twarken{at}mcmaster.ca
An interesting feature of the case report by Nair and Colleagues describing successful heart transplantation for a rare congenital anomaly was the uneventful reexposure to heparin sodium to permit use of cardiopulmonary bypass during the transplantation performed only 2 weeks after an apparent episode of immune heparin-induced thrombocytopenia (HIT). This benign course might seem bizarre, as one could have expected pathogenic platelet factor 4 (PF4)–reactive immunoglobulin G antibodies to cause recurrent thrombocytopenia—possibly with life- or limb-threatening thrombotic complications–on heparin reexposure [1]. However, there are at least three ways that this unremarkable clinical course can be explained.
First, it is now known that the levels of pathogenic HIT antibodies usually decline fairly quickly after an episode of clinical HIT: the median time to nondetectability of antibodies is 50 to 80 days (depending on the assay performed) [1]. Indeed, about 20% of patients who initially have a positive platelet-activation assay for HIT show negative test results about 2 weeks after their episode of HIT [1]. Because the platelet activation assay correlates strongly with risk of thrombocytopenia [2], this suggests there is a real possibility (perhaps also about 20%) that the HIT antibodies may have declined sufficiently by 2 weeks to permit safe reexposure to heparin for a cardiac surgical procedure. (Conversely, no one would be surprised if such a reexposure led instead to clinically overt HIT.)
Second, it is possible that the patient seen by Nair and co-workers never had HIT, but rather had a positive assay indicating subclinical seroconversion of PF4–reactive antibodies [2, 3]. Formation of clinically insignificant antibodies is very common in patients who have received heparin for 5 or more days, especially when the testing is performed using one of the enzyme immunoassays that detect PF4–reactive antibodies. In this case, the thrombocytopenia would actually have been the result of other clinical factors (not HIT related), such as cardiac failure, intraaortic balloon pump, or drugs (e.g, milrinone lactate).
Third, there is the possibility of a false-positive assay that does not reflect the presence of any kind of HIT antibody. This is suggested by the finding that 20% to 30% of healthy controls can test (generally weakly) positive for these antibodies using one of the commercially available assays [4, 5]. It has been suggested that this might reflect an inappropriate cutoff between positive and negative values selected by the manufacturer [5]. Most laboratories do not provide the quantitative results of HIT antibody testing, even though there is evidence that the stronger the reaction, the greater the clinical likelihood of HIT [2].
In summary, there are several reasons why a patient might do well with reexposure to heparin despite even a recent "positive test for HIT." The practical lesson for the cardiac surgeon is that in the absence of a readily available and biologically correlative test, sometimes a "judgment call" (to use the authors’ words)—and perhaps a bit of luck—can lead to a happy conclusion.
References
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