K HIT and Heparin Coated Devices

Heparin can be bonded to artificial surfaces (Larsson et al., 1987), either through ionic attachment, as used for pulmonary artery catheters (Eldh and Jacobsson, 1974), or by end-linked covalent bonding (e.g., Carmeda BioActive Surface [CBAS]) (Larm et al., 1983). CBAS has been used for CPB circuits and filters (Borowiec et al., 1992a,b, 1993), extracorporeal membrane oxygenation (ECMO) devices (Koul et al., 1992), and coronary stents (Serruys et al., 1996). During use in patients, ionically attached heparin is displaced by albumin from the catheter surface, where it could contribute to HIT (discussed subsequently). End-linked heparin is an effective and longer-lasting anticoagulant, as the immobilized, but flexible, heparin chains are able to interact with fluid-phase antithrombin and thrombin (Elgue et al., 1993). Nevertheless, the end-linked, but relatively unconstrained, heparin is capable of interacting with PF4 (Suh et al., 1998). Therefore, it is theoretically possible that covalent heparin-bonded devices could result in formation of HIT antibodies or could cause HIT in a patient who has formed antibodies. Alternatively, even covalently bonded heparin might "leach" into blood by proteolytic mechanisms, thereby contributing in a more conventional way to the pathogenesis of HIT (Almeida et al., 1998a). Use of heparin-coated pulmonary catheters in contributing to HIT has been implicated by Laster and Silver (1988). These workers reported 10 patients with HIT whose platelet counts did not rise until the removal of their heparin-coated pulmonary catheters, despite discontinuing all other sources of heparin. Incubation of the heparin-coated catheters with platelets in the presence of patient sera resulted in catheter-induced platelet aggregation. Based on the identification of four such cases, during which time 1112 heparin-coated catheters had been used, they estimated the frequency of catheter-associated HIT to be 0.4%.

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