Non vitamin K oral anticoagulants (NOACs) do not require regular monitoring but information about their pharmacodynamic effect may be importantin situations like trauma, stroke oremergent surgery. Currently, no standardized point-of-care test is available to evaluate the anticoagulant effects of NOACs. We evaluated the anticoagulant effect of NOACs with the next generation point-of-care TEG assay (TEG® 6S) based on a fully-automated thrombelastography system. We used two TEG® 6S assays, the DTI assay and Anti-Factor Xa (AFXa) assay, to detect anticoagulant effects and classify NOACs. Blood from healthy volunteers (n = 26) was used to obtain a baseline reference range. Data derived from patients on factor Xa inhibitors (FXi) (rivaroxaban and apixaban) (n = 39), and direct thrombin inhibitors (DTIs) (dabigatran) (n = 25) were compared against the reference range for detection of drug effect and drug classification. TEG®6s R-time highly correlated to each NOAC. Presence of NOACs caused elongation of R-time on the AFXa assay compared to the reference range (4.3 ± 1.7 vs. 1.3 ± 0.3 min. for FXi, p < 0.001 and 3.5 ± 1.2 vs. 1.3 ± 0.3 min. for DTI, p < 0.001). R-time on the DTI assay was elongated only in presence of a DTI (3.4 ± 1.0 vs. 1.5 ± 0.2 min, p < 0.001). The cutoff for detection of a DTI effect was an R time of 1.9 min and for anti-Xa effect was 1.95 min. For detection of NOAC therapy, there was ≥92% sensitivity and ≥95% specificity. The automated TEG®6s NOAC assay may be an effective tool to identify an anticoagulant effect from NOAC therapy and facilitate care of patients with bleeding or at risk of bleeding in the event of needing emergency surgery.

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Obese individuals, despite having increased cardiovascular (CV) risk factors experience adverse CV outcomes less frequently than non-obese. Little is known about association of long-term weight gain to development of coronary artery disease (CAD), inflammation and thrombogenicity. 418 consecutive patients with suspected CAD undergoing elective cardiac catheterization were included in a sub-analysis of the multi analyte, thrombogenic, and genetic markers of atherosclerosis study. Maximum weight gain (MWG) was defined as percentage increase in weight since age 17 years to year of heaviest weight and categorized as: minor (<30 %), moderate (30-47 %), severe (>47-69 %), and extreme (>69 %). Lipid profiling was determined by vertical density gradient ultracentrifugation, thrombin-induced platelet fibrin clot strength (TIP-FCS) by thrombelastography, and urinary 11-dehydrothromboxane B2 (11-dhTxB2) by ELISA. CAD severity was defined as minimal (<20 %), moderate (20-75 %), and severe (>75 %) luminal diameter obstruction of any major coronary vessel. The mean MWG was 53 ± 33 %. Extreme MWG group had a higher incidence of diabetes mellitus (48 %), hypertension (81 %), depression (25 %), and were most often female (60 %) (p < 0.05 for all). In women, CAD severity was inversely associated to MWG (p = 0.05), whereas in men no such association was observed (p = 0.18). TIP-FCS increased in a stepwise fashion with MWG (p = 0.001). 11-dTxB2 levels were higher in the extreme MWG group, regardless of lipid lowering therapy (p < 0.05). Our data suggest that maximal weight gain since age 17 years is associated with heightened thrombogenicity, inflammation and a poorer lipid profile but not an increased risk for severe CAD development.

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