Presentation Details
| Monitoring Bivalirudin Therapy Using a Bivalirudin-Specific Chromogenic Anti-IIa Assay Sean G Yates1, Ravi Sarode1, Sarita Paulino1, Ibrahim F Ibrahim2, Lisa K Skariah3. 1Department of Pathology, Division of Transfusion Medicine and Hemostasis, University of Texas Southwestern Medical Center, Dallas, TX, USA.2Department of Internal Medicine, Division of Hematology/Oncology, University of Texas Southwestern Medical Center, Dallas, TX, USA.3UT Southwestern Department of Pharmacy, University of Texas Southwestern Medical Center, Dallas, TX, USA |
Abstract
Background: Bivalirudin infusions are traditionally monitored with activated partial thromboplastin time (aPTT) despite demonstrating poor correlations with bivalirudin dose-response curves. The discordance between bivalirudin dose and aPTT may lead to over or under-anticoagulation, predisposing patients to a higher incidence of bleeding or thrombosis and requiring repeated dose adjustments. A bivalirudin-specific chromogenic anti-IIa assay that reports plasma concentrations of bivalirudin is available. Objectives: To evaluate the correlation between the bivalirudin dose, aPTT, and a chromogenic anti-IIa bivalirudin assay (bivalirudin-specific assay) to establish an anti-IIa therapeutic range for clinical use. We conducted a before-after retrospective cohort study to compare the incidence of adverse events and time in therapeutic range (TTR) for patients anticoagulated with bivalirudin using aPTT versus the bivalirudin assay. Methods: Fifty-three plasma samples from 6 adult patients anticoagulated with bivalirudin were evaluated using aPTT and a bivalirudin-specific assay. The correlation between the bivalirudin dose and results of aPTT and the bivalirudin-specific assay was determined with the strength of correlation defined as follows: 0.00 to 0.19, very weak; 0.20 to 0.39, weak; 0.40 to 0.59, moderate; 0.60 to 0.79, strong; and 0.80 to 1.0, very strong. For the before-after retrospective evaluation, the following clinical data was recorded for each cohort: age, sex, clinical indication for bivalirudin, creatinine clearance (CrCl), initial and median bivalirudin dose, TTR, major and minor bleeding events, and thromboembolic events. Results: A moderate dose-dependent correlation was observed between bivalirudin dose and aPTT results (R2=0.4). Conversely, a very strong correlation was observed between bivalirudin dose and bivalirudin plasma concentrations, as measured by the bivalirudin-specific assay (R2=0.8). A review of dose-response data led to the establishment of a bivalirudin-specific assay therapeutic range of 0.5-1.5 ug/mL. Of the patients undergoing bivalirudin anticoagulation included in the before-after analysis, aPTT was used to monitor therapy in 11 patients (11 encounters), and the bivalirudin-specific assay was used in 15 patients (16 encounters). Confirmed or suspected heparin-induced thrombocytopenia (HIT) were the two main indications for bivalirudin anticoagulation in either cohort. The mean TTR was significantly higher in patients monitored using the bivalirudin-specific assay versus aPTT (p=0.003). The incidence of minor bleeding events was not significantly different between the cohorts, and no major bleeding or thromboembolic events were observed in either cohort. Conclusions: This study suggests that a bivalirudin-specific assay demonstrated a stronger correlation with the bivalirudin dose relative to aPTT. Patients anticoagulated with bivalirudin whose therapy was monitored using a bivalirudin-specific assay showed a significantly higher percent TTR than those monitored using aPTT. No significant differences in thromboembolic, major, or minor bleeding events in patients anticoagulated with bivalirudin were observed when comparing aPTT-based monitoring or the bivalirudin-specific assay.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.