Platelet function point-of-care tests in post-bypass cardiac surgery: are they relevant?

BACKGROUND: Platelet dysfunction is an important cause of excessive bleeding after cardiac surgery. We assessed two platelet function point-of-care tests: the platelet function analyser (PFA-100) and the Hemostatus(TM) in patients with and without excessive bleeding after cardiac surgery with cardiopulmonary bypass. METHODS: Mediastinal chest tube drainage (MCTD) was measured for the first 6 h in the intensive care unit (ICU). Haematology and coagulation tests were done on arrival in the ICU, and when excessive bleeding occurred (MCTD >1 ml kg(-1) h(-1)) or after 3 h. RESULTS: Eighteen patients bled excessively and 27 had normal MCTD. Hemostatus measurements were prolonged in those with excessive bleeding compared with the normal group. The times for PFA-100 adenosine diphosphate (ADP) and epinephrine were 91 vs 71 s (P=0.004) and 155 vs 114 s (P=0.02) in the bleeding and normal group s, respectively. None of the Hemostatus or PFA-100 values correlated with total MCTD. Depending on the agonist used, maximum aggregation was 33-81% and 52-86% in bleeding and normal groups, respectively. Only poor correlations were found between PFA-100 epinephrine and maximum aggregation in response to ADP (r=-0.52, P=0.03) or to collagen (r=-0.48, P=0.04). CONCLUSION: Patients bleeding excessively in the ICU had abnormal measurements in point-of-care tests without a dramatic decrease in aggregation. Except for patients with increased risk of postbypass bleeding, point-of-care tests are not useful for routine use after cardiac surgery.

Inhibition of platelet aggregation by abciximab but not by aspirin can be detected by a new point-of-care test, the hemostatus.

We have investigated the type of platelet defect that can be detected with the Hemostatus test performed with the Hepcon/HMS instrument (Medtronic) designed to investigate platelet function during and after surgery. This assay is based on the comparison of the activated clotting time of whole blood measured in cartridges containing kaolin or kaolin and platelet-activating factor in different concentrations. Addition of platelet-activating factor shortened the blood activated clotting time when the platelet counts were normal. However, when platelet counts were below 70000/microL, the activated clotting time was prolonged in all channels including those without platelet-activating factor showing the influence of platelets in the formation of the clot under the conditions tested. Inhibition of platelet aggregation with c7E3 (abciximab, ReoPro) also induced a much-prolonged activated clotting time, and a similar finding was seen with blood from a patient with Glanzmann's thrombasthenia confirming the need for platelet aggregation and/or the glycoprotein (GP) IIb-IIIa complex. In contrast, the interaction of GP Ib with von Willebrand Factor was not of major importance, since inhibition of this interaction with the anti-GP Ib murine monoclonal antibody, ALMA-12, did not modify the activated clotting time. Furthermore, the activated clotting time measured for patients with an acquired defect in von Willebrand Factor activity were unchanged. Finally, inhibition of thromboxane A2 formation by aspirin did not influence the results of this test. Globally, the Hemostatus test was able to detect major abnormalities of GP IIb-IIIa function in the presence or absence of platelet-activating factor.