Role of Thrombelastography (<scp>TEG</scp>) in Risk Assessment and Guidance of Antithrombotic Therapy in Patients with Coronary Artery Disease

Bitar, Abbas; Kreutz, Rolf P.

doi:10.1002/ddr.21112

Cited by 7 publications

(9 citation statements)

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“…In whole blood, maximal clot strength (MA) measured by TEG is the sum of the additive forces generated by aggregating and contracting platelets incorporated into the growing, initially soluble fibrin network, which is cross-linked and stabilized by FXIIIa [ 13 , 20 ]. In a large cohort study of subjects with coronary artery disease by Lev et al, DM was also independently associated with whole blood (platelet-fibrin) clot strength measured by TEG [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…Thrombelastography (TEG) is an established clinical laboratory method for analysis of coagulation and fibrinolysis and allows for quantitative measurement of the dynamic processes of clot formation and clot strength [ 12 , 13 ]. We have previously demonstrated the feasibility of measurement of plasma fibrin clot strength by TEG in platelet-poor plasma and correlation with whole blood fibrin TEG measurements [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

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Fibrin Clot Strength in Patients with Diabetes Mellitus Measured by Thrombelastography

Maatman

Schmeisser

Kreutz

2018

Journal of Diabetes Research

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Background Patients with diabetes mellitus (DM) exhibit increased risk of recurrent myocardial infarction. Maximal clot strength measured by thrombelastography (TEG) is a risk factor for recurrent ischemic events. We hypothesized that diabetic subjects exhibit increased fibrin clot strength in platelet-poor plasma and that glycemic control correlates with maximal fibrin clot strength. Methods We collected plasma samples from subjects with known or suspected coronary artery disease undergoing cardiac catheterization (n = 354). We measured kaolin-activated TEG in platelet-poor citrate plasma. Time to fibrin formation (R), clot formation time (K), and maximal fibrin clot strength (MA) were recorded. Results Plasma fibrin MA was increased among subjects with DM (n = 152) as compared to non-DM (n = 202) (37.0 ± 8 versus 34.1 ± 8 mm; p < 0.001). Hemoglobin A1c (HbA1c) (ρ = 0.22; p = 0.001) and fibrinogen (ρ = 0.29; p < 0.001) correlated with fibrin MA. In multivariable regression analysis, DM remained significantly associated with plasma MA after adjustment for fibrinogen level (p = 0.003). Conclusions Subjects with diabetes mellitus exhibit increased maximal fibrin clot strength measured by TEG in platelet-poor plasma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fibrin Clot Strength in Patients with Diabetes Mellitus Measured by Thrombelastography

Maatman

Schmeisser

Kreutz

2018

Journal of Diabetes Research

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“…Platelet rich plasma (PRP) and platelet poor plasma (PPP) were obtained by differential centrifugation as previously described [12,14,15]. In short, PRP was obtained from citrate blood after centrifugation at 180 g for 5 minutes.…”

Section: Methodsmentioning

confidence: 99%

“…Recently Kasahara et al reported that platelet-dependent clot retraction requires factor XIII (FXIII), which covalently associates fibrin polymers with protein located within the platelet plasma membrane at lipid rafts [10]. High clot strength in whole blood assays measured by thrombelastography (TEG) appears to be a risk factor for increased risk of coronary thrombosis after coronary stenting and coronary artery bypass grafting (CABG) [11,12]. Antiplatelet therapy may affect local thrombus generation dynamics and fibrin stabilization by inhibiting FXIIIa activity on the surface of platelets or preventing release of FXIIIa into plasma [13].…”

Section: Introductionmentioning

confidence: 99%

Platelet factor XIIIa release during platelet aggregation and plasma clot strength measured by thrombelastography in patients with coronary artery disease treated with clopidogrel

Kreutz

Owens

et al. 2014

Platelets

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It has been estimated that up to half of circulating Factor XIIIa (FXIIIa) is stored in platelets. The release of FXIIIa from platelets upon stimulation with ADP in patients with coronary artery disease treated with dual antiplatelet therapy has not been previously examined. Samples from 96 patients with established coronary artery disease treated with aspirin and clopidogrel were examined. Platelet aggregation was performed by light transmittance aggregometry (LTA) in platelet rich plasma (PRP) with platelet poor plasma (PPP) as reference and ADP 5μM as agonist. Kaolin activated TEG was performed in citrate PPP. PRP after aggregation was centrifuged and plasma supernatant (PSN) collected. FXIIIa was measured in PPP and PSN. Platelet aggregation after stimulation with ADP 5μM resulted in 24% additional FXIIIa release in PSN as compared to PPP (99.3 ± 27 vs. 80.3 ± 24 %, p<0.0001). FXIIIa concentration in PSN correlated with maximal plasma clot strength (TEG-G) (r=0.48, p<0.0001), but not in PPP (r=0.15, p=0.14). Increasing quartiles of platelet derived FXIIIa were associated with incrementally higher TEG-G (p=0.012). FXIIIa release was similar between clopidogrel responders and non-responders (p=0.18). In summary, platelets treated with aspirin and clopidogrel release a significant amount of FXIIIa upon aggregation by ADP. Platelet derived FXIIIa may contribute to differences in plasma TEG-G, and thus in part provide a mechanistic explanation for high clot strength observed as a consequence of platelet activation. Variability in clopidogrel response does not significantly influence FXIIIa release from platelets.

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“…It also allows for quantitatively determining whether the body environment has a hypercoagulable state, low coagulation, fibrinolysis, or other symptoms. Based on the scope of TEG parameters, personalized approaches to guide antithrombotic therapies could be determined [23][24][25]. Our TEG results revealed that the level of TEG-R was prominently decreased and levels of TEG-MA, TEG-CI, and TEG-α were significantly increased, indicating that the activation of plasma clotting factors and platelet function might account for the enhanced coagulation in cirrhosis with PVT.…”

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confidence: 89%

A Preclinical Porcine Model of Portal Vein Thrombosis in Liver Cirrhosis

Zhang

Jiang

et al. 2020

BioMed Research International

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Background. This study aimed at presenting a novel method of developing a porcine model of portal vein thrombosis (PVT) in cirrhosis by intravenous administration of thrombin and insertion of a fibered coil. We further investigated changes of biochemical parameters, coagulation, and proinflammatory cytokine expression in the cirrhosis-PVT group. Methods. Twelve male pigs were randomized into the control group (n=3) and cirrhosis group (n=9). In cirrhotic pigs, three were randomly selected to establish PVT by ultrasound-guided percutaneous puncture of the main portal vein (MPV) followed by intravenous thrombin administration and fibered coil insertion. Thrombosis in the MPV was detected by abdominal enhanced computer tomography (CT). The changes of hepatic function, coagulation system, and inflammation cytokines were compared among normal, cirrhosis, and cirrhosis with PVT groups. Results. As manifested by the presence of a filling defect in MPV on portal venous-phase CT angiography, fibrin thrombi were formed in the MPV in cirrhotic pigs within one week and persisted for four weeks. Five weeks after surgery, abnormal liver functions occurred in association with PVT formation in cirrhosis. Both coagulation and thromboelastography parameters showed that cirrhosis-PVT pigs exhibited a procoagulant state through hyperfunction of platelets and clotting factors. Interleukin 6 (IL-6) as a potential inflammatory marker stimulated PVT-mediated inflammation activation in cirrhosis. Conclusions. Our study provides in vivo evidence that intravenous injection of a coil and thrombin into MPV under interventional guided devices enables a feasible method in thrombus creation. Further exploration and validation of large-sample cases are required to characterize utilities of this model.

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Role of Thrombelastography (TEG) in Risk Assessment and Guidance of Antithrombotic Therapy in Patients with Coronary Artery Disease

Cited by 7 publications

References 54 publications

Fibrin Clot Strength in Patients with Diabetes Mellitus Measured by Thrombelastography

Fibrin Clot Strength in Patients with Diabetes Mellitus Measured by Thrombelastography

Platelet factor XIIIa release during platelet aggregation and plasma clot strength measured by thrombelastography in patients with coronary artery disease treated with clopidogrel

A Preclinical Porcine Model of Portal Vein Thrombosis in Liver Cirrhosis

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