Anticoagulant Effect of Unfractionated Heparin in Antithrombin-Depleted Plasma in vitro

Krulder, J.W.M.; Strebus, A.; Meinders, A. E.; Briët, E.

doi:10.1159/000217192

Cited by 4 publications

(5 citation statements)

References 17 publications

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“…It is known that AT concentrations correlate with heparin's effect to inhibit coagulation: lower AT levels are associated with a decreased heparin dose response as measured by the ACT. However, in vitro data showed that only AT levels <30% are associated with impaired heparin action [15].…”

Section: Discussionmentioning

confidence: 99%

Monitoring activated clotting time for combined heparin and aprotinin application: in vivo evaluation of a new aprotinin-insensitive test using Sonoclot☆

Ganter

Monn

Tavakoli

et al. 2006

European Journal of Cardio-Thoracic Surgery

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Section: Discussionmentioning

confidence: 99%

Monitoring activated clotting time for combined heparin and aprotinin application: in vivo evaluation of a new aprotinin-insensitive test using Sonoclot☆

Ganter

Monn

Tavakoli

et al. 2006

European Journal of Cardio-Thoracic Surgery

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“…In a laboratory study, as antithrombin concentrations declined, there was a progressive reduction in the activated partial thromboplastin time (aPTT) response to specific concentrations of UFH and a significant increase in the concentration of UFH required to reach a therapeutic in vitro aPTT. 8 Clinically, this resistance to UFH manifests as a need for significantly increased doses of UFH to maintain the aPTT within the therapeutic range. Time to therapeutic heparinization is directly correlated with clinical outcomes in patients with VTE.…”

Section: Special Considerations In Management Of Acute Vte Heparin Rementioning

confidence: 99%

Anticoagulation in Hypercoagulable Conditions: Special Considerations in the Treatment and Prevention of Venous Thromboembolism

Wittkowsky

2004

Journal of Pharmacy Practice

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Patients with hypercoagulable conditions, including malignancy, are at increased risk of recurrent venous thromboembolic events (VTE). The general approach to treatment and prevention of VTE in patients with thrombophilia is similar to that of patients who present with VTE associated with transient risk factors, including immobility, trauma, and surgery. However, several important issues must be considered in the initial management of acute VTE, in the long-term prevention of VTE following an initial event, and in VTE prophylaxis in patients with hypercoagulable conditions. Patients with antithrombin deficiency are prone to heparin resistance and may require concurrent antithrombin concentrates or anticoagulation with direct thrombin inhibitors for adequate treatment of acute VTE. In patients with malignancy, lowmolecular-weight heparins have been found to be more effective than unfractionated heparin for the initial treatment of VTE. Long-term prevention is preferred for most patients with hypercoagulable conditions, and the latest trials show that low-intensity warfarin is not as effective as typical moderateintensity therapy for chronic therapy. Primary prophylaxis of asymptomatic carriers is not warranted unless they are exposed to additional risk factors, including surgery, trauma, immobilization, and pregnancy. Prolonged prophylaxis may be appropriate in patients with malignancy who undergo surgical procedures.

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“…The mechanisms of heparin-induced antithrombosis are still not completely defined. Although much of the activity of unfractionated heparin is due to potentiation of antithrombin III-mediated inhibition of thrombin and factor Xa, antithrombosis by heparin is still possible in plasma depleted of antithrombin III (3,4). Recent studies have suggested that tissue factor pathway inhibitor (TFPI) may play a significant role in heparin-induced antithrombosis (3,5,6).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Unfractionated vs. Low Molecular Weight Heparin on Tissue Factor Pathway Inhibitor Levels in Hospital Inpatients

Brown

Kuter²

2001

Thromb Haemost

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SummaryAlthough heparin is widely used as an antithrombotic agent, its multiple mechanisms of action are not fully defined. Recent work has suggested that tissue factor pathway inhibitor (TFPI) may contribute to the antithrombotic activity of heparin by inhibiting the extrinsic pathway of coagulation. We have investigated the effect of heparin on TFPI and have found that when unfractionated heparin is given by continuous intravenous infusion to hospitalized inpatients, TFPI levels increase 2.3-fold and remain high as long as heparin is continued, but return to baseline levels soon after the infusion is stopped. In contrast, therapeutic doses of the low molecular weight heparin, dalteparin, resulted in significantly less TFPI induction. Given the increasing number of studies establishing the clinical efficacy of low molecular weight heparins as antithrombotic agents, these results suggest that TFPI may not be a major contributor to the antithrombotic effect of heparin.

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Anticoagulant Effect of Unfractionated Heparin in Antithrombin-Depleted Plasma in vitro

Cited by 4 publications

References 17 publications

Monitoring activated clotting time for combined heparin and aprotinin application: in vivo evaluation of a new aprotinin-insensitive test using Sonoclot☆

Monitoring activated clotting time for combined heparin and aprotinin application: in vivo evaluation of a new aprotinin-insensitive test using Sonoclot☆

Anticoagulation in Hypercoagulable Conditions: Special Considerations in the Treatment and Prevention of Venous Thromboembolism

The Effect of Unfractionated vs. Low Molecular Weight Heparin on Tissue Factor Pathway Inhibitor Levels in Hospital Inpatients

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