Bivalirudin in Peripheral Interventions

MacLean, Alexandra A.; Peña, Constantino; Katzen, Barry T.

doi:10.1053/j.tvir.2006.12.007

Cited by 5 publications

(2 citation statements)

References 9 publications

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“…Further, mortality and incidence of MI and ATEC were not statistically significant different. Thus, a reduction of bleeding complications when using a direct thrombin antagonist (bivalirudin) instead of heparin, as documented for coronary and peripheral endovascular procedures, 28,29 could not be established for EVAR.…”

Section: Discussionmentioning

confidence: 99%

Prophylactic Perioperative Anti-Thrombotics in Open and Endovascular Abdominal Aortic Aneurysm (AAA) Surgery: A Systematic Review

Wiersema

Jongkind

Bruijninckx³

et al. 2012

European Journal of Vascular and Endovascular Surgery

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Section: Discussionmentioning

confidence: 99%

Prophylactic Perioperative Anti-Thrombotics in Open and Endovascular Abdominal Aortic Aneurysm (AAA) Surgery: A Systematic Review

Wiersema

Jongkind

Bruijninckx³

et al. 2012

European Journal of Vascular and Endovascular Surgery

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“…New alternative anticoagulants have now become available in many countries: sodium danaparoid (N.V. Orgaran; Oss, The Netherlands), fondaparinux (Arixtra; GlaxoSmithKline, Marly-le-Roi, France), hirudin and its derivatives (lepirudin; bivalirudin), and argatroban. 45,46 Making the right diagnosis is of prime importance because it is not always optimal to deprive a patient the benefit of heparin therapy, unless this patient is at risk of HIT/HITTT. Also, alternative therapies require careful handling and they frequently present side effects.…”

Section: How Heparin-dependent Antibodies Produce Hit or Hittmentioning

confidence: 99%

Mechanisms Involved in Heparin-Induced Thrombocytopenia and Associated Thrombosis

Vissac¹,

Amiral²

2008

Semin Thromb Hemost

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Heparin-induced thrombocytopenia (HIT), sometimes complicated by the occurrence of thrombosis (HITT), is a rare but severe complication of heparin therapy (both unfractionated and low molecular weight heparin). It is induced by the generation of antibodies targeted to complexes of platelet factor (PF) 4 and heparin (H), mainly IgG isotypes with the highest avidity. Laboratory studies and clinical surveys help elucidate the mechanisms of HIT/HITT. The presence of stoichiometric complexes of H-PF4 is probably the immunogenic stimulus that induces the generation of antibodies, via a T-cell response. In pathologies, where a large extent of platelet activation occurs, especially at the vicinity of pathological sites, large amounts of H-PF4 complexes can be formed that bind to platelet surfaces (mainly activated platelets), but also to endothelial cells and other blood cells such as monocytes. This induces cell-cell interactions and the release of microparticles, which can amplify to a hypercoagulable state resulting from release of tissue factor, microparticles, and expression of procoagulant phospholipids. The clinical consequence is the development of thrombocytopenia, which can be complicated by a rapid evolution to thrombosis that becomes life threatening. The present understanding of the mechanisms of HIT/HITT, the advances in clinical investigations, and the availability of alternative anticoagulants have progressively introduced new tools for a better diagnosis and management of patients with this disease.Heparin-induced thrombocytopenia (HIT) type II, sometimes complicated by the occurrence of thrombosis (HITT), is a severe immune-mediated complication of heparin therapy that can be life threatening. 1 It develops more frequently in individuals treated with unfractionated heparin (UFH) than in those receiving low molecular weight heparin (LMWH) (respective incidences of 0.5 to 2% for UFH and 0.2 to 0.5% for LMWH).HIT is characterized by the occurrence of thrombocytopenia, usually moderate (50 to 120 g/L or a decrease of > 30% on two successive platelet counts, rarely < 50 g/L), developing 5 to 15 days following the onset of heparin therapy or more rapidly if there was a previous heparin exposure. [2][3][4] Platelet count normalizes when heparin is withdrawn and replaced by another antithrombotic therapy. This typical pattern is frequently complicated by the clinical state of the patient,

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Subclavian and Upper Extremity Interventions

Yeo¹,

Laird²

2011

Peripheral and Cerebrovascular Intervention

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Bivalirudin in Peripheral Interventions

Cited by 5 publications

References 9 publications

Prophylactic Perioperative Anti-Thrombotics in Open and Endovascular Abdominal Aortic Aneurysm (AAA) Surgery: A Systematic Review

Prophylactic Perioperative Anti-Thrombotics in Open and Endovascular Abdominal Aortic Aneurysm (AAA) Surgery: A Systematic Review

Mechanisms Involved in Heparin-Induced Thrombocytopenia and Associated Thrombosis

Subclavian and Upper Extremity Interventions

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