Endogenous thrombin potential (ETP) in plasma from patients with AMI during antithrombotic treatment

Brodin, Ellen; Seljeflot, Ingebjørg; Arnesen, Harald; Hurlen, Mette; Appelbom, Hege I.; Hansen, John‐Bjarne

doi:10.1016/j.thromres.2008.03.018

Cited by 22 publications

(16 citation statements)

References 31 publications

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“…Our findings of a median ETP in warfarin-treated patients of 597nM.min concur with other reported observations that patients on warfarin with an INR between 2.0-3.0, have been shown to have an ETP range of approximately 500-700nM.min [30]. This range is equivalent to 30%-50% of the pre-warfarin result [31] or that in normal controls [32]. In patients treated with rivaroxaban, the median ETP at 903nM.min (range 224-1287), was significantly higher than in patients on warfarin.…”

Section: Discussionsupporting

confidence: 91%

Rivaroxaban and warfarin achieve effective anticoagulation, as assessed by inhibition of TG and in-vivo markers of coagulation activation, in patients with venous thromboembolism

Arachchillage

Efthymiou

Mackie

et al. 2015

Thrombosis Research

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Section: Discussionsupporting

confidence: 91%

Rivaroxaban and warfarin achieve effective anticoagulation, as assessed by inhibition of TG and in-vivo markers of coagulation activation, in patients with venous thromboembolism

Arachchillage

Efthymiou

Mackie

et al. 2015

Thrombosis Research

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“…During antiplatelet treatment this might decrease levels of F1+2, the most sensitive marker for in vivo thrombin generation [34]. Our results are in accordance with some previous reports, although, conflicting results exist [10,35]. …”

Section: Discussionsupporting

confidence: 90%

Markers of hypercoagulability in CAD patients. Effects of single aspirin and clopidogrel treatment

et al. 2012

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BackgroundCardiovascular disease with disturbances in the haemostatic system, might lead to thrombotic complications with clinical manifestations like acute myocardial infarction (AMI) and stroke. Activation of the coagulation cascade with subsequent increased thrombin generation, characterizes a prothrombotic phenotype. In the present study we investigated whether prothrombotic markers were associated with risk factors and clinical subgroups in a cohort of patients with angiographically verified coronary artery disease (CAD). The patients were randomized to long-term treatment with the antiplatelet drugs aspirin or clopidogrel, and we further investigated the effect on hypercoagulability of such treatment for 1 year, of which limited data exists.MethodsVenous blood samples were collected in fasting condition between 08:00 and 10:30 am, at baseline when all patients were on aspirin therapy (n = 1001) and in 276 patients after 1 year follow-up on aspirin or clopidogrel. In vivo thrombin generation was assessed by prothrombin fragment 1 + 2 (F1+2) and D-dimer, and the endogenous thrombin potentiale (ETP) in the calibrated automated thrombogram (CAT) assay, representing ex vivo thrombin generation. In addition soluble tissue factor (sTF) and free- and total tissue factor pathway inhibitor (TFPI) were measured.ResultsWe found age to be significantly associated with F1+2 and D-dimer (β = 0.229 and β =0.417 respectively, p <0.001, both). Otherwise, only weak associations were found. F1+2 and D-dimer were higher in women compared to men (p <0.001 and p = 0.033, respectively). Smokers had elevated levels of ETP compared to non-smokers (p = 0.014). Additionally, patients on renin-angiotensin system (RAS) inhibition showed significantly higher levels of F1+2, compared to non-users (p = 0.013). Both aspirin and clopidogrel reduced levels of ETP after 12 months intervention (p = 0.003 and p <0.001, respectively) and the levels of F1+2 were significantly more reduced on aspirin compared to clopidogrel (p = 0.023).ConclusionsIn the present population of stable CAD, we could demonstrate a more hypercoagulable profile among women, smokers and patients on RAS medication, assessed by the prothrombotic markers F1+2, D-dimer and ETP. Long-term antiplatelet treatment with aspirin alone seems to attenuate thrombin generation to a greater extent than with clopidogrel alone. The study is registered at http://www.clinicaltrials.gov: NCT00222261.

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“…Contrarily, injection of heparinized blood results in less perihematomal edema formation [31], and brain edema formation is also reduced after the administration of thrombin inhibitors [32]. Thrombin formation is inhibited by the effect of warfarin or other related compounds [33], and it is conceivable that a lower concentration of thrombin at the clot in patients with OAC-ICH facilitates the formation of larger hematomas and longer bleedings. Yet, the lower disposal of thrombin within the clot would also result in less toxicity to the surrounding brain parenchyma.…”

Section: Pathophysiologymentioning

confidence: 99%

Oral anticoagulant-associated intracerebral hemorrhage

2011

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The incidence of oral anticoagulation-associated intracerebral hemorrhage (OAC-ICH) is growing due to the increasing use of warfarin and the older age of treated patients. Recent population studies reveal that OAC-ICH currently occurs at a frequency comparable to that of subarachnoid hemorrhage. Most frequently, OAC-ICH are located in deep or lobar regions of the brain, although it may also occur in the brainstem. These hemorrhages are larger than spontaneous hematomas and may be fatal in at least 50% of cases. The primary cause of brain injury in patients with OAC-ICH is the direct mechanical disruption of the brain tissue but secondary damage may occur through the intervention of matrix metalloproteinases, glutamate, cytokines, heme, iron, and the chemical toxicity of products such as thrombin, which are released from the clot. The pathogenesis of OAC-ICH also includes the effects of aging, the level of anticoagulation, genetic factors, and a high prevalence of concurrent cerebrovascular conditions, such as cerebral amyloid angiopathy, leukoaraiosis or previous strokes. The treatment of OAC-ICH is challenging and involves rapid reversal of anticoagulation with hemostatic drug therapies such as vitamin K, fresh frozen plasma, prothrombin complex concentrates or recombinant factor VIIa. These therapies may not always be sufficient to stabilize the patient's clinical condition and lacking randomized controlled trials, the best hematological approach to reverse oral anticoagulation is debated. Other difficult decisions reviewed in this article are whether anticoagulation should be restarted after OAC-ICH, and when anticoagulant treatment should be resumed. The newer oral anticoagulants, which are increasingly being introduced for thromboembolism prevention, may confer a lower risk of intracranial bleeding than warfarin, although they do not have an antidote and their anticoagulant effect is difficult to monitor.

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Endogenous thrombin potential (ETP) in plasma from patients with AMI during antithrombotic treatment

Cited by 22 publications

References 31 publications

Rivaroxaban and warfarin achieve effective anticoagulation, as assessed by inhibition of TG and in-vivo markers of coagulation activation, in patients with venous thromboembolism

Rivaroxaban and warfarin achieve effective anticoagulation, as assessed by inhibition of TG and in-vivo markers of coagulation activation, in patients with venous thromboembolism

Markers of hypercoagulability in CAD patients. Effects of single aspirin and clopidogrel treatment

Oral anticoagulant-associated intracerebral hemorrhage

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