Influence of selected antithrombotic treatment on thromboelastometric results

Abstract

Rotatory thromboelastometry (ROTEM^®) is used for diagnosing and monitoring bleeding patients. Some of these patients receive antithrombotic treatment, thus having an increased risk of bleeding. Only sparse knowledge exists about whether the ROTEM^® analysis is influenced by antithrombotic treatment. The objective of the present study was to examine if the ROTEM^® results are affected in patients receiving antithrombotic treatment. This prospective observational study included patients receiving either vitamin K-antagonists (VKA), aspirin (ASA) or ASA combined with an adenosine diphosphate (ADP) receptor antagonist (ASA + ADP). ROTEM^® analyses were performed using the standard assays EXTEM^®, INTEM^® and FIBTEM^®. Furthermore, haemoglobin, platelet count, International Normalized Ratio (INR), activated partial thromboplastin time, fibrinogen (functional), creatinine, estimated glomerular filtration rate, and C-reactive protein were determined. The study included 231 patients receiving antithrombotic treatment and compared the results to ROTEM^® previously collected data from 73 healthy subjects. The VKA (n = 73) patients had a consistently prolonged EXTEM clot initiation (p < .0001), which was significantly correlated to the INR (Spearman’s r = 0.53, p < .0001). Additionally, the VKA patients had significantly reduced clot propagation [reduced maximum velocity, maximum velocity (MaxVel) and increased time to maximum velocity (MaxVel_t)]. ASA (n = 80) and ASA + ADP patients (n = 78) revealed a prolonged clot initiation. ASA patients had decreased clot propagation (increased MaxVel_t), whereas ASA + ADP patients had an inconsistent change in clot propagation (increased MaxVel and MaxVel_t). In conclusion, VKA treatment was revealed by the ROTEM^® analysis. On the contrary, ASA and ASA + ADP treatment were not consistently revealed by the analysis.

Keywords:

• Antiplatelet drugs
• antithrombotic agents
• point-of-care system
• platelet inhibitors
• thromboelastography

Acknowledgements

The authors thank the laboratory technician M. S. Veirup and V. B. Mogensen at the Department of Clinical Biochemistry for laboratory assistance. We also thank M. Maegaard, L. Schou and K. Overgaard at the Anticoagulation Centre for the help with patient inclusion.

Disclosure statement

None of the authors have any conflicts of interest related to the present study. T.D.C. and A.-M.H. have the following general conflicts of interest: T.D.C. has been on the speaker bureaus for AstraZeneca, Boehringer-Ingelheim, Pfizer, Roche Diagnostics and Takeda and A.-M.H. has received speaker’s fees from CSL Behring, Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb and Leo Pharma and unrestricted research support from Octapharma, CSL Behring and Leo Pharma. M.H.H. has no conflict of interest to declare.

Additional information

Funding

The study was financially supported by Aarhus University, Oda & Hans Svenningsens Fond, Snedkermester Sophus Jacobsen & Hustru Astrid Jacobsens Fond, A.P. Møller & Hustru Chastine Mc-Kinney Møllers Fond for Almene Formaal – Fonden til Laegevidenskabens Fremme, and Helga & Peter Kornings Fond. The work was done independent of the funders.