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

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.

Optimized tool for evaluation of platelet function measured by impedance aggregometry.

Platelet aggregation measured by impedance aggregometry is highly dependent on platelet count. We previously developed a tool to interpret impedance aggregometry based on the strong linear correlation between platelet counts and platelet aggregation at reduced platelet counts. The present study aimed to optimize the tool by expanding the model to include normal platelet counts. We combined data from three previous studies on 266 healthy individuals measuring impedance aggregometry with four agonists (collagen, adenosine diphosphate, thrombin receptor activating peptide-6, and ristocetin). Reduced platelet counts were established in vitro. The investigated platelet counts ranged from 26-425x109/L. A positive linear correlation was found between platelet counts and platelet aggregation across normal and reduced platelet counts (all p-values <0.001). We established 95% prediction intervals for healthy platelet aggregation in relation to platelet count. The new expanded model serves as an optimized tool for evaluation of platelet aggregation at normal and reduced platelet counts.