In Reply:—

We agree with Drs. Lewis and Collard that measurement of anti-Xa activity and platelet function would have provided important information. Nevertheless, in the presence of normal ACT, no detectable heparin by heparin concentration assay (Hepcon, Medtronic Blood Management, Parker, CO), no identifiable surgical source, and a borderline platelet count, possible explanations for this patients’ excessive and protracted chest tube output that was unresponsive to hemostatic blood product transfusion, include either the persistent anticoagulant properties of low molecular weight heparin i.e., anti-Xa activity, or a platelet function abnormality that may be related to either of these agents, or a possible interaction between low molecular weight heparins and tirofiban. Previous anecdotal reports of increased bleeding when patients had received either low molecular weight heparin preparations 1,2or platelet inhibitors 3–5support our findings.

Furthermore, we are uncertain of the potential beneficial effects of hemofiltration, because we have previously shown that hemofiltration (using one specific filter) during cardiopulmonary bypass failed to remove the lower molecular weight fraction of unfractionated heparin (no anti-Xa activity in ultrafiltrate). 6Factors related to the low molecular weight heparin molecule, such as, its linear shape, electrostatic charge, or binding to antithrombin III may account for these findings. Therefore, we would recommend that in patients receiving either enoxaparin or tirofiban, postponement of elective cardiac surgery should be considered for a period of time well over the five half-lives of either medication. Another alternative would be to switch patients from low molecular weight heparin to unfractionated heparin as soon as an operation is proposed. Further studies are needed to evaluate the efficacy of hemofiltration or plasma exchange filters with respect to removal of these agents.

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