Heparin-Induced Thrombocytopenia in Patients with Ventricular Assist Devices: Are New Prevention Strategies Required? Theodore E. Warkentin, MD, Andreas.

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Presentation transcript:

Heparin-Induced Thrombocytopenia in Patients with Ventricular Assist Devices: Are New Prevention Strategies Required? Theodore E. Warkentin, MD, Andreas Greinacher, MD, Andreas Koster, MD The Annals of Thoracic Surgery Volume 87, Issue 5, Pages 1633-1640 (May 2009) DOI: 10.1016/j.athoracsur.2008.10.060 Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions

Fig 1 Iceberg model of heparin-induced thrombocytopenia (HIT): applicability to ventricular assist device (VAD) patients. Upper panel, generic iceberg. The model illustrates that there is a greater sensitivity for detecting clinically irrelevant anti-platelet factor 4 (PF4)/heparin antibodies, as follows: (EIA-IgGAM) (commercial enzyme immunoassays that detect any of the three immunoglobulin (Ig) classes, IgG, IgA, or IgM) > particle gel immunoassay (PaGIA) > EIA-IgG > platelet-activation assay (HIPA or SRA). The tip of the iceberg is represented by clinical HIT, comprising isolated HIT (HIT) and HIT with associated thrombosis (HIT-T). The dashed bracket for PaGIA indicates that some antibodies detectable by the EIA-IgG give a false-negative result in the PaGIA. Genetic Testing Institute (GTI) and Stago indicate two different manufacturers of the EIA-IgGAM. Ortho and cardiac denotes orthopedic and cardiac surgery patients, respectively. Lower panel, four differing clinical situations, indicating that VAD patients have a particularly high frequency of both antibody formation and clinical HIT. (LMWH = low-molecular weight heparin; UFH = unfractionated heparin.) The Annals of Thoracic Surgery 2009 87, 1633-1640DOI: (10.1016/j.athoracsur.2008.10.060) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions

Fig 2 Freedom from thromboembolic events during mechanical circulatory support. HIPA+/IgG+, indicates positive (or indeterminate) heparin-induced platelet activation (HIPA) test plus positive enzyme immunoassay (EIA)-immunoglobulin (Ig) G; HIPA–/EIA+, indicates that the HIPA test was negative, and at least one of the three EIAs that detect IgG, IgA, or IgM antibodies was positive; HIT– = indicates negative testing in all assays. (Reprinted with permission from Schenk S et al [29].) The Annals of Thoracic Surgery 2009 87, 1633-1640DOI: (10.1016/j.athoracsur.2008.10.060) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions

Fig 3 Antiplatelet factor 4 (PF4)/heparin antibody levels from the time of diagnosis of heparin-induced thrombocytopenia (HIT) to heart transplantation. The absolute change in antibody levels from diagnosis to transplantation is represented for each of 17 ventricular assist device (VAD) patients who tested positive for anti-PF4/heparin antibodies. The average decline in antibody levels is represented by the heavy line. The dashed line represents 0.40 optical density units (upper limit of normal for the enzyme immunoassay [EIA]). (Reprinted with permission from Schroder JN et al [31].) The Annals of Thoracic Surgery 2009 87, 1633-1640DOI: (10.1016/j.athoracsur.2008.10.060) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions

Fig 4 (A) Percentage change in platelet counts after transplantation. Comparison of the percentage change in mean daily platelet counts from 1 day before transplant (preTx) to 1 month after transplant (postTx). Ventricular assist device (VAD) patients positive for heparin-induced thrombocytopenia (HIT+; squares) had significantly greater decreases in platelet counts on postoperative day (POD) 1 through 4 compared with controls (triangles). Data are presented with the standard deviation. (B) Kaplan-Meier analysis of survival after transplantation in patients positive for HIT (HIT+, solid line) vs controls (dashed line). (C) Kaplan-Meier analysis of thromboembolic-free survival after transplantation in patients positive for HIT (HIT+) [solid line] vs controls (dashed line). (Reprinted with permission from Schroder JN et al [31].) The Annals of Thoracic Surgery 2009 87, 1633-1640DOI: (10.1016/j.athoracsur.2008.10.060) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions