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a Departments of Cardiovascular, Anesthesia, and Intensive Care, ASO Santa Croce e Carle, Via Michele Coppino n. 26, Cuneo, 12100 Italy
b Department of Cardiothoracic and Vascular Anesthesia, and Intensive Care, IRCCS Policlinico S. Donato, Via R. Morandi n. 30, San Donato Milanese, 20097 Italy
(Email: barzaghi.n{at}ospedale.cuneo.it; cardioanestesia{at}virgilio.it).
In a recent article, Koster and colleagues [1] reported a higher than expected frequency of heparin-induced thrombocytopenia (HIT) in patients with ventricular assist devices (VADs) who were receiving anticoagulation with unfractionated heparin. Furthermore, mortality in patients who experienced HIT after VAD implantation was considerably higher, suggesting a strong relationship between HIT occurrence and outcome. HIT was diagnosed as thrombocytopenia associated with detection of antibodies against the heparin-PF4 complexes.
"When is HIT really HIT?" is an editorial by Warkentin and Crowther [2] who question the true incidence of HIT in VAD patients, indicating that it may be over diagnosed. Therefore, they state that it is time "to develop and to evaluate appropriate management strategies for this problem," focusing especially on the laboratory features of HIT.
There is no doubt that the cause of a low platelet count after cardiac surgery is multifactorial, and that to ascribe each episode of thrombocytopenia to HIT is at best simplistic. Therefore, we understand the authors’ reasons for deeming a more sophisticated and specific diagnosis of HIT than currently obtainable with serology alone. However, it is a fact that, to date, the functional assay that measures 14C-serotonin release from platelets exposed to heparin is not routinely performed by most laboratories.
In patients who are on VAD, anticoagulation is mandatory, warfarin absorption may be impaired for a long time after VAD implantation, and clinical conditions potentially causing critical thrombocytopenia often coexist. Therefore, in presence of a thrombocytopenia that could be suggestive for HIT, and while waiting for a laboratory confirmation, we believe that alternative anticoagulant strategies not causing HIT could be considered. Presently, there are different drugs that could meet these requirements. Danaparoid could be considered, but we must consider of course that renal function may be impaired in these patients. Lepirudin suffers from the same limitations, and may even cause worse bleeding problems. Conversely, bivalirudin is largely cleared by proteolysis and secondarily by the kidney; this drug offers the advantage of a short half-life. Therefore, bivalirudin could be precious in allowing the performance of all potentially necessary invasive maneuvers with relatively short notice. Neither lepirudin, argatroban, nor danaparoid and fondaparinux share the flexibility of bivalirudin; however, these drugs may represent very valuable alternatives to bivalirudin for patients in more stable clinical conditions [3]. Of course, we are aware that presently the approved drugs for the treatment of HIT are lepirudin, danaparoid, and argatroban, but in the specific scenario of the HIT prevention in VAD patients, bivalirudin could find a role as first choice treatment whenever HIT is suspected and while waiting for adequate laboratory tests.
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  T. E. Warkentin, M. A. Crowther, and A. Koster Reply Ann. Thorac. Surg., January 1, 2008; 85(1): 361 - 361. [Full Text] [PDF]
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