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J Thorac Cardiovasc Surg 2006;131:1314-1322
© 2006 The American Association for Thoracic Surgery

Evolving Technology

Platelet function monitoring with the Sonoclot analyzer after in vitro tirofiban and heparin administration

Michael A. Tucci, MD, DEAA a , * , Michael T. Ganter, MD, DEAA b , * , Christine R. Hamiel, BS c , Richard Klaghofer, PhD d , Andreas Zollinger, MD e , Christoph K. Hofer, MD, DEAA e , *

a Institute of Anaesthesiology, University Hospital Lausanne, Lausanne, Switzerland
b Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, Calif
c Division of Cardiothoracic Surgery, University of Colorado Health Sciences Centre, Denver, Colo
d Department of Psychosocial Medicine, University Hospital Zurich, Zurich, Switzerland
e Institute of Anaesthesiology and Intensive Care Medicine, Triemli City Hospital Zurich, Zurich, Switzerland.

Received for publication October 16, 2005; revisions received December 20, 2005; accepted for publication January 12, 2006.

* Address for reprints: Christoph K. Hofer, MD, Institute of Anaesthesiology and Intensive Care Medicine, Triemli City Hospital Zurich, Birmensdorferstrasse 497, CH-8063 Zurich, Switzerland. (Email: Christoph.hofer{at}triemli.stzh.ch).

OBJECTIVE: Reliable platelet function monitoring is desirable in patients treated with glycoprotein IIb/IIIa receptor inhibitors. The aim of the present laboratory-based study was to assess platelet function after administration of clinically relevant doses of the glycoprotein IIb/IIIa antagonist tirofiban with or without heparin by using Sonoclot (Sienco Inc) and platelet aggregometry.

METHODS: Tirofiban (0-100 ng · mL–1) and heparin (0 or 1 U · mL–1) were added to blood samples obtained from 20 healthy volunteers. Coagulation analysis was performed on citrated whole blood by using the Sonoclot analyzer. The glass bead–activated test and the new glass bead test with heparinase were used. The results were compared with adenosine-5'-diphosphate–activated platelet aggregometry.

RESULTS: Administration of tirofiban showed a similar increase of platelet inhibition detected with the Sonoclot glass bead–activated test and glass bead test with heparinase, as well as by means of aggregometry. Bias between the different techniques was comparable; Spearman rank correlation was strong (glass bead–activated test vs aggregometry: {rho} = 0.823, P < .001; glass bead test with heparinase vs aggregometry: {rho} = 0.856, P < .001). After additional administration of heparin, platelet inhibition was only comparable for the glass bead test with heparinase and aggregometry, and the correlation coefficient remained unchanged for the glass bead test with heparinase versus aggregometry ({rho} = 0.878, P < .001). By contrast, the glass bead–activated test showed a nearly complete platelet inhibition with a significant bias compared with the glass bead test with heparinase and aggregometry. Correlation was weak for the glass bead–activated test versus aggregometry ({rho} = 0.407, P = .004).

CONCLUSIONS: When compared with platelet aggregometry, the glass bead–activated test from Sonoclot reliably detects glycoprotein IIb/IIIa receptor inhibition with tirofiban in unheparinized whole blood. However, in heparinized blood the glass bead test with heparinase is essential to accurately assess platelet function.

Abbreviations and Acronyms ACT = activated clotting time; CPB = cardiopulmonary bypass; GB = glass bead–activated test; GP = glycoprotein; hepGB = glass bead–activated test containing heparinase; PF = platelet function; PPP = platelet-poor plasma; PRP = platelet-rich plasma




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