Assessment of hemostatic activation during cardiopulmonary bypass for coronary artery bypass grafting with bivalirudin: Results of a pilot study

Koster, Andreas; Yeter, R.; Buz, Semih; Kuppe, Hermann; Hetzer, Roland; Lincoff, A. Michael; Dyke, Cornelius; Smedira, Nicholas G.; Spiess, Bruce D.

doi:10.1016/j.jtcvs.2004.09.016

Cited by 51 publications

(42 citation statements)

References 10 publications

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“…The concentrations of bivalirudin and aprotinin employed in our experiments are similar to those used in heart surgery [10,12,15,16,20,21] and are defined as pharmacologic concentrations.…”

Section: Resultsmentioning

confidence: 99%

“…The relatively fast in-vivo clearance of bivalirudin (halflife ¼ 25 min) [9] makes it useful for short-term acute treatment in coronary interventions and vascular surgery. Bivalirudin is approved for anticoagulation during percutaneous coronary intervention and is presently being evaluated in coronary artery bypass graft surgery [10][11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Influence of bivalirudin on tissue factor-triggered coagulation

Butenas

Orfeo

Brummel‐Ziedins

et al. 2007

Blood Coagulation &Amp; Fibrinolysis

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Bivalirudin, a synthetic analog of the carboxy-terminus of hirudin, is a reversible thrombin inhibitor used during coronary balloon angioplasty. The objective of this study was to evaluate the influence of bivalirudin on thrombin generation. Three in-vitro models (numerical simulations, synthetic coagulation proteome and whole blood) of contact pathway-independent blood coagulation triggered with tissue factor were used in this study. Increasing concentrations of bivalirudin prolong the initiation phase of thrombin generation in a concentration-dependent manner. At subpharmacologic bivalirudin concentrations (0.5-2 micromol/l), total thrombin generation was significantly increased. At a pharmacologic concentration (5 micromol/l), bivalirudin suppressed thrombin generation in the synthetic coagulation proteome; in numerical simulations and contact pathway-inhibited whole blood, no thrombin generation was detected over 1200-2000 s and platelet activation was inhibited by 80%. The addition of a pharmacologic concentration (9 micromol/l) of a naturally occurring protease inhibitor aprotinin in the presence of at least 0.5 micromol/l bivalirudin provided limited enhancement of the bivalirudin inhibitory effect. In conclusion, bivalirudin at pharmacologic concentrations is an efficient inhibitor of thrombin generation, platelet activation and clot formation, which acts not as a modulator but as an 'on-off' switch of blood coagulation.

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“…The concentrations of bivalirudin and aprotinin employed in our experiments are similar to those used in heart surgery [10,12,15,16,20,21] and are defined as pharmacologic concentrations.…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of bivalirudin on tissue factor-triggered coagulation

Butenas

Orfeo

Brummel‐Ziedins

et al. 2007

Blood Coagulation &Amp; Fibrinolysis

View full text Add to dashboard Cite

show abstract

“…Koster and colleagues described two cases of acute oxygenator thrombosis at the start of CPB [9]. Bakaeen and colleagues reported a case of bilateral adrenal haemorrhage after coronary artery bypass grafting (CABG) [10] and HIT has been recently described as cause of a right free-floating thrombus [11].…”

Section: Discussionmentioning

confidence: 99%

Early heparin-induced thrombocytopaenia (HIT) after cardiac surgery

Pappalardo

Crescenzi

Franco

et al. 2006

European Journal of Anaesthesiology

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“…However, the anticoagulation effect of bivalirudin diminishes rapidly in LVAD because the enzymatic cleavage can happen more easily in stagnant blood. 126 This can potentially create thromboembolism in the arterial system. Monitoring aPTT is not specific for the level of bivalirudin.…”

Section: Left Ventricular Assist Device and Cardiac Transplantationmentioning

confidence: 99%

Heparin-Induced Thrombocytopenia in Cardiovascular Patients

Yoon

Jang²

2011

Cardiology in Review

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Heparin-induced thrombocytopenia is a life-threatening immune-mediated platelet activation condition that can cause arterial and venous thromboembolism. The triggering complex, platelet factor 4/heparin antibody, has several unique immunologic characteristics that have not been well elucidated until recently. In patients undergoing cardiovascular procedures such as percutaneous coronary intervention and coronary artery bypass graft surgery, the prevalence of platelet factor 4/heparin antibody is significantly higher than that in the general population. The acuity and graveness of the thromboembolic phenomenon requires early diagnosis and empirical initiation of treatment, even before confirmatory test results are available. Also, although multiple therapeutic modalities exist, the safety and efficacy of each option depends upon the clinical setting. Therefore, this review will focus on the updated pathophysiology of heparin-induced thrombocytopenia, new diagnostic criteria, and the various treatment options for cardiovascular patients with different conditions.

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Assessment of hemostatic activation during cardiopulmonary bypass for coronary artery bypass grafting with bivalirudin: Results of a pilot study

Cited by 51 publications

References 10 publications

Influence of bivalirudin on tissue factor-triggered coagulation

Influence of bivalirudin on tissue factor-triggered coagulation

Early heparin-induced thrombocytopaenia (HIT) after cardiac surgery

Heparin-Induced Thrombocytopenia in Cardiovascular Patients

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