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Title: Global coagulation assays in healthy controls: are there compensatory mechanisms within the coagulation system?
Austin Authors: Lim, Hui Yin;Lui, Brandon;Tacey, Mark A ;Selan, Carly;Donnan, Geoffrey A ;Burrell, Louise M ;Nandurkar, Harshal;Ho, Prahlad
Affiliation: Department of Medicine and Radiology, University of Melbourne, Parkville, VIC, Australia
Medicine (University of Melbourne)
The Melbourne Brain Centre, Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia
The Northern Hospital, Epping, VIC, Australia
Department of Haematology, Northern Hospital, 185 Cooper St, Epping, VIC, 3076, Australia
Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia
Department of Medicine, Northern Health, University of Melbourne, Heidelberg, VIC, Australia
Issue Date: 24-Feb-2021
Date: 2021
Publication information: Journal of Thrombosis and Thrombolysis 2021; 52(2): 610-619
Abstract: Global coagulation assays (GCAs) may provide a more comprehensive individual hemostatic profiling. We aim to evaluate GCAs (thromboelastography, thrombin generation) in healthy controls, and correlate results with age, gender, lipid status, tissue factor pathway inhibitor (TFPI) and P-selectin. Blood samples were collected from healthy controls (> 18 years of age) not taking anticoagulation or antiplatelet agents and without known cardiovascular disease. Thromboelastography (TEG) was performed on citrated whole blood while calibrated automated thrombogram (CAT), P-selectin (endothelial marker) and TFPI (principle inhibitor of tissue factor-initiated coagulation) were performed on platelet-poor plasma. 153 healthy controls (mean age 42 years, 98 females (64%)) were recruited. Female controls demonstrated more hypercoagulable TEG and CAT parameters while those over 50 years of age demonstrated more hypercoagulable TEG parameters despite comparable thrombin generation. Paradoxically, individuals with "flattened" thrombin curves (lower velocity index (rate of thrombin generation) despite preserved endogenous thrombin potential (amount of thrombin)) were more likely to be male (49% vs 20%, p = 0.003) with increased low-density lipoprotein cholesterol (3.3 vs 2.6 mmol/L, p = 0.003), P-selectin (54.2 vs 47.3 ng/mL, p = 0.038) and TFPI (18.7 vs 8.6 ng/ml, p = 0.001). In addition to reduced velocity index and thrombin peak, controls in the highest TFPI tertile also demonstrated a poorer lipid profile. GCAs can detect subtle changes of the hemostatic profile. Interestingly, reduced thrombin generation was paradoxically associated with increased cardiovascular risk factors, possibly attributable to increased TFPI. This finding may suggest compensation by the coagulation system in response to endothelial activation and represent a biomarker for early cardiovascular disease. A larger prospective study evaluating these assays in the cardiovascular disease population is ongoing.
DOI: 10.1007/s11239-021-02400-y
ORCID: 0000-0003-2455-3155
Journal: Journal of Thrombosis and Thrombolysis
PubMed URL: 33625645
Type: Journal Article
Subjects: Blood coagulation tests
Cardiovascular disease
Tissue factor pathway inhibitor
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