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Ann Thorac Surg 2007;84:1422-1423
© 2007 The Society of Thoracic Surgeons
Department of Cardiovascular Anaesthesia, S. Camillo-Forlanini Hospital, Via Portuense 332, Rome, 00149 Italy
(Email: ppicozzi{at}scamilloforlanini.rm.it).
We read with great interest the contribution by Koster and colleagues [1]. Unfortunately we found several aspects of the analysis to be rather misleading.
Currently an increased incidence of clinical cases of heparin-induced thrombocytopenia (HIT) has been observed; however the actual incidence has not been documented. There are considerable differences in diagnostic specificity among various laboratory assays to detect HIT antibodies. In their editorial, Warkentin and Crowther [2] criticized Koster and colleagues [1] for their usage of particle gel immunoassay (PaGIA) due to its intermediate specificity (ie, potential over-diagnosis) compared with serotonin-release assay (ie, the gold standard).
The magnitude of the positive tests has not been described; we know a weak result is less likely to cause a clinically evident HIT. Moreover, in this study the patients who are positive for HIT antibodies have not been further studied to detect antibodies against thyroglobulin and peroxidase enzyme. Our laboratory has observed a cross-reaction between these antibodies and PF (Platelet Fraction)4/heparin complexes, producing false positive results (unpublished observations).
We doubt whether the reported incidence of HIT (ie, 7.8% during ventricular assist device [VAD] implantation) is verified or not. Were all the patients affected by HIT?
Once diagnosis of HIT has been confirmed, it is mandatory to suspend all heparin administrations.
Three months after HIT diagnosis and after negative test results, heparin may be readministered in 1 single dose during the bypass pump time.
Koster and co-workers [1] used two different protocols for cardiopulmonary bypass (ie, heparin plus tirofiban and heparin plus prostaglandin for patients affected by pulmonary hypertension). Both protocols are considered to be second choice according to the evidence-based guidelines for HIT management [3].
Moreover the time span between HIT diagnosis and surgery has never been specified. The authors used lepirudin with both the preoperative and postoperative times. However it is not clear why the same lepirudin has not been used intraoperatively.
The type of monitoring and dosage of the drug have never been described. Therefore their protocol is difficult to be followed.
Finally, we do not understand why they started lepirudin anticoagulation immediately after transferring the patient to the intensive care unit. Although we have limited experience about patients affected by HIT, we are aware that it is essential to conduct tight quantitative control of hourly bleeding and coagulation patterns before beginning any anticoagulant drug.
We know that the anticoagulation protocols during postoperative time change according to the different implanted VADs. Because there are many different types of VADs we believe it is not correct to focus on so many various conditions (ie, BiVAD and left VAD, intracorporeal and extracorporeal, emergency and elective patients) in the same study.
Heparin-induced thrombocytopenia is a frequent complication in cardiac surgical patients, especially VAD patients. It can impair outcome because of hemorrhagic life-threatening events. A solution to this problem still needs to be found. The alternative anticoagulant drugs suggested for HIT patients are unmanageable, without antidotes, and require tight monitoring. We think that further studies are needed to find out common appropriate management strategies for this disease.
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A. Koster Reply Ann. Thorac. Surg., October 1, 2007; 84(4): 1423 - 1424. [Full Text] [PDF] |
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