Platelet function assessed by ROTEM^®platelet in patients receiving antiplatelet therapy during cardiac and vascular surgery

Abstract

Patients undergoing coronary artery bypass graft (CABG) surgery or carotid endarterectomy (CEA) continue antiplatelet therapy perioperatively, which may increase bleeding risk. We aimed to investigate whether Rotational thromboelastometry (ROTEM^®) platelet, a newly marketed platelet function analysis, would detect antiplatelet therapy in CABG and CEA patients; whether detection of reduced platelet function was associated with increased bleeding; and whether ex vivo desmopressin increased platelet function. We included 20 CABG patients continuing aspirin and 20 CEA patients continuing clopidogrel (n = 1) or clopidogrel and aspirin (n = 19). Platelet function was analyzed with ROTEM^® platelet and light transmission aggregometry (LTA). According to the lower reference limit, ROTEM^® platelet managed to detect aspirin, but clopidogrel detection was inadequate compared to LTA. Using a previously published cut-off for bleeding risk, 6 (30%) patients receiving aspirin and 4 (21%) patients receiving both clopidogrel and aspirin demonstrated platelet function below this cut-off. One of the four CEA patients below the cut-off died from intracerebral hemorrhage postoperatively. CABG patients below (n = 6) and above (n = 14) the cut-off did not differ in chest tube output (median [range]: 373 ml [250–900] vs. 368 ml [195–820]). Ex vivo addition of desmopressin did not increase platelet function. In conclusion, ROTEM^® platelet does reveal aspirin treatment whereas clopidogrel treatment is most often overlooked. Due to low bleeding in the study population, it was not possible to conclude on the association with bleeding risk.

Keywords:

• Platelet function tests
• antiplatelet drug
• cardiac surgery
• vascular surgical procedure
• bleeding
• Deamino Arginine Vasopressin

Acknowledgments

The authors thank TEM Innovations, Munich, Germany for providing ROTEM^® platelet reagents and utensils for this study. The authors thank laboratory technicians Mai Stenulm Veirup and Vivi Bo Mogensen for their help in the laboratory. Furthermore, we thank the Department of Cardiothoracic and Vascular Surgery, Aarhus University Hospital, for their kind help with recruitment of patients, and finally the Department of Neurology, Aarhus University Hospital, for their supporting assistance during enrollment.

Disclosure statement

AMH has no conflicts of interest regarding this work but has the following general conflicts of interest: speaker fees from CSL Behring, Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, and Astellas and unrestricted research support from CSL Behring and Octapharma. The remaining authors have no conflicts of interest to declare.

Author contributions

All authors contributed to the hypotheses and design of the study. ASL, TFP and MT carried out the enrollment of patients. ASL obtained blood samples and performed laboratory analyses. ASL, PHN and AMH analyzed data. All authors interpreted data. ASL provided first draft, and all authors revised the manuscript.

Additional information

Funding

The study was funded by Aarhus University Research Foundation, Aase and Ejnar Danielsen’s Foundation, and Helga and Peter Korning’s Foundation.