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Ann Thorac Surg 2007;84:1423-1424
© 2007 The Society of Thoracic Surgeons
Deutsches Herzzentrum Berlin, Department of Anesthesia, Augustenburger Platz 1, Berlin, 13353 Germany
(Email: koster{at}dhzb.de).
Lappa and colleagues [1] commented on what they believe to be potentially misleading aspects of our article reporting on heparin-induced thrombocytopenia (HIT) in patients on ventricular assist device (VAD) support [2]. Some of these comments deserve discussion.
It was pointed out that the laboratory of Lappa and colleagues’ [1] institution observed cross-reactivity of certain proteins (ie, thyroglobulin, peroxidase) with the particle gel assay (PGIA) for anti-heparin/platelet factor 4 antibodies, potentially leading to false positive test results and consequential over-diagnosis of HIT in our study.
This is an interesting observation and we look forward to seeing these data published. It is well known that the current HIT antibody assays are sensitive but have limited specificity, although in this regard the PGIA seems to be superior to the ELISA. Indeed, the stronger the PGIA test result (e.g., result of 3 to 4* [a cutoff we employed]), the more specific the result for HIT [3]. Moreover, in view of these well-recognized limitations (and as outlined in the article), in all of our patients we also performed a "functional" HIT test, the heparin-induced platelet activation assay (HIPAA) (ie, a washed platelet assay for HIT that is comparable with the gold standard serotonin release assay [SRA]). The HIPAA was positive in 27 of 28 of our patients, indicating a high likelihood of clinically relevant, biologically active antibodies being present. However, as outlined by Warkentin and Crowther’s [4] editorial, the predominant criterion for evaluating a patient as having clinical HIT, besides strong positive test results (especially with the functional assay), is a typical course of time of onset or exacerbation of thrombocytopenia, or the development of thrombosis, in parallel with the development of these antibodies. Of our 28 patients diagnosed with clinical HIT, 22 showed the typical course of platelet count changes indicating HIT, and most of these patients also exhibited an increase in the platelet count after the initiation of lepirudin anticoagulation, which provides further clinical evidence supporting the diagnosis of HIT. Of the remaining 6 patients, 4 were diagnosed in a referral hospital and 2 showed a pattern of persistent thrombocytopenia, a condition in which the platelet count remains low after surgery; the physician can only base the diagnosis of HIT and its therapeutic implications on the results of the HIT assays. Considering these patterns of strong positive PGAI and HIPA test results, together with the typical platelet count profiles in most of our patients, we believe a strong case can be made that all of our patients indeed had clinical HIT. We understand the skepticism when the frequency of a disease in a special patient population seems unusually high, and particularly the concerns when therapeutic-dose anticoagulation is fundamental for management, as in the VAD patient where a balance is always needed to prevent both hemorrhagic complications and thromboembolism. However, in this regard, it should also be considered that this observation is not a single-center experience but it has also been made at another institution with a large VAD program that cooperates with a reference institution laboratory for HIT diagnosis [5].
As outlined by Warkentin and Crowther [4] in their editorial, the debate about HIT or non-HIT may become academic to a certain extent. The important decision for the treating physician is whether to stop heparin and start alternative anticoagulation. This decision has to balance the potential risks when the potent nonreversible alternative drugs are used, particularly when experience with the alternative agents is limited or high-dose anticoagulation is required, and the potentially catastrophic consequences that may occur when HIT develops into thromboembolism.
Lappa and colleagues [1] pointed out that according to the American College of Chest Physicians (ACCP) guidelines the intraoperative anticoagulation procedures used are second-choice strategies. This statement is correct for 5 of the 15 patients diagnosed for HIT before surgery without presenting active HIT antibodies at the time of surgery. In this constellation, according to the ACCP guidelines, the sole use of heparin for anticoagulation during the short period of CPB would have been the strategy of choice [6]. During the observational period of this study, our hospital standards differed in this regard, as the ACCP guidelines were published at the end of 2004 whereas our investigation included the time from 2000 to 2005. However, current hospital standards are adjusted to the ACCP suggestions.
In addition, the question was raised why lepirudin had not been used for anticoagulation during cardiopulmonary bypass (CPB) and why lepirudin anticoagulation was started immediately after surgery. Lepirudin is exclusively eliminated through the kidneys; the relative long half-life of 60 to 80 minutes is dramatically prolonged in the case of impairment of renal function and no antidote is available. Apart from the fact that the implantation of a VAD is a complex surgical procedure and is frequently associated with bleeding problems, most of the patients at the time of surgery also have renal failure. In this situation, the use of lepirudin as an anticoagulant during CPB would result in uncontrollable bleeding complications. Therefore, despite our prior experience in using lepirudin for anticoagulation during CPB, we stopped its use in this setting and established the described protocols [7]. As with these alternative protocols, heparin is given and the HIT reaction is only attenuated by concomitant administration of a powerful short-acting antiplatelet agent, and we initiate lepirudin anticoagulation (ie, target activated partial thromboplastin time 40 to 60 seconds, see article [2]) immediately after surgery to reduce the risk of thromboembolism.
In the interim, protocols for intraoperative use of bivalirudin have been developed and assessed in the high-risk group of HIT patients [8]. After gaining considerable experience with this agent for anticoagulation during CPB in a variety of surgical procedures, we now consider this a further option for patients in whom HIT is strongly suspected or confirmed. We agree with Lappa and colleagues [1] that further study is required to better define the diagnostic and management strategies for this challenging patient population.
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