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1. A Controlled Trial of Rivaroxaban after Transcatheter Aortic-Valve Replacement

Author

Dangas, George D., Tijssen, Jan G. P., Wöhrle, Jochen, Søndergaard, Lars, Gilard, Martine, Möllmann, Helge, Makkar, Raj R., Herrmann, Howard C., Giustino, Gennaro, Baldus, Stephan, de Backer, Ole, Guimarães, Ana H. C., Gullestad, Lars, Kini, Annapoorna, von Lewinski, Dirk, Mack, Michael, Moreno, Raúl, Schäfer, Ulrich, Seeger, Julia, Tchétché, Didier, Thomitzek, Karen, Valgimigli, Marco, Vranckx, Pascal, Welsh, Robert C., Wildgoose, Peter, Volkl, Albert A., Zazula, Ana, van Amsterdam, Ronald G. M., Mehran, Roxana, Windecker, Stephan, Dangas, G. D., Windecker, S., Mehran, R., Tijssen, J. G. P., Welsh, R. C., Vranckx, P., Valgimigli, M., van Amsterdam, R. G. M., Thomitzek, K., Wildgoose, P., Colombo, A., Prendergast, B., Makkar, R., Mack, M., Webb, J., Marx, Steven O., Corvaja, Nicola, Ghodsi, Newsha, DiStefano, Douglas, Kaufman, David, Bugger, Heiko/0000-0002-3524-0405, Avanzas, Pablo/0000-0002-4958-6108, Twerenbold, Raphael/0000-0003-3814-6542, Kalkman, Deborah/0000-0002-1900-2116, Academic Medical Center, Cardiology, ACS - Heart failure & arrhythmias, University of Zurich, and Windecker, Stephan

Subjects
medicine.medical_specialty, Catheters, Transcatheter aortic, medicine.drug_mechanism_of_action, medicine.medical_treatment, Factor Xa Inhibitor, MEDLINE, 610 Medicine & health, 2700 General Medicine, 030204 cardiovascular system & hematology, 11171 Cardiocentro Ticino, law.invention, 03 medical and health sciences, 0302 clinical medicine, Pharmacotherapy, Randomized controlled trial, Valve replacement, law, Ús terapèutic, medicine, 030212 general & internal medicine, Aspirina, Rivaroxaban, Intention-to-treat analysis, Aspirin, business.industry, 10031 Clinic for Angiology, Catèters, Therapeutic use, food and beverages, General Medicine, Surgery, 10209 Clinic for Cardiology, business, medicine.drug
Abstract

Background Whether the direct factor Xa inhibitor rivaroxaban can prevent thromboembolic events after transcatheter aortic-valve replacement (TAVR) is unclear. Methods We randomly assigned 1644 patients without an established indication for oral anticoagulation after successful TAVR to receive rivaroxaban at a dose of 10 mg daily (with aspirin at a dose of 75 to 100 mg daily for the first 3 months) (rivaroxaban group) or aspirin at a dose of 75 to 100 mg daily (with clopidogrel at a dose of 75 mg daily for the first 3 months) (antiplatelet group). The primary efficacy outcome was the composite of death or thromboembolic events. The primary safety outcome was major, disabling, or life-threatening bleeding. The trial was terminated prematurely by the data and safety monitoring board because of safety concerns. Results After a median of 17 months, death or a first thromboembolic event (intention-to-treat analysis) had occurred in 105 patients in the rivaroxaban group and in 78 patients in the antiplatelet group (incidence rates, 9.8 and 7.2 per 100 person-years, respectively; hazard ratio with rivaroxaban, 1.35; 95% confidence interval [CI], 1.01 to 1.81; P=0.04). Major, disabling, or life-threatening bleeding (intention-to-treat analysis) had occurred in 46 and 31 patients, respectively (4.3 and 2.8 per 100 person-years; hazard ratio, 1.50; 95% CI, 0.95 to 2.37; P=0.08). A total of 64 deaths occurred in the rivaroxaban group and 38 in the antiplatelet group (5.8 and 3.4 per 100 person-years, respectively; hazard ratio, 1.69; 95% CI, 1.13 to 2.53). Conclusions In patients without an established indication for oral anticoagulation after successful TAVR, a treatment strategy including rivaroxaban at a dose of 10 mg daily was associated with a higher risk of death or thromboembolic complications and a higher risk of bleeding than an antiplatelet-based strategy. (Funded by Bayer and Janssen Pharmaceuticals; GALILEO ClinicalTrials.gov number, NCT02556203.) Supported by Bayer in collaboration with Janssen Pharmaceuticals. Dr. Dangas reports iving lecture lees from Bayer, receiving grant support, paid to his institution, and lecture fees from Daiichi Sankyo, and previously holding equity in Medtronic; Dr. Mollmann, receiving lecture fees from AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, and Pfizer; Dr. Makkar, receiving grant support, consulting fees, and travel support from Abbott Vascular, grant support, lecture fees, and travel support from Edwards Lifesciences, and grant support and consulting fees from Medtronic and Boston Scientific; Dr. FIerrmann, receiving grant support, paid to his institution, from Abbott Vascular and Boston Scientific and grant support, paid to his institution, and consulting fees from Edwards Lifesciences and Medtronic; Dr. Giusrino, receiving consulting fees from Bristol-Myers Squibb/Pfizer; Dr. De Backer, receiving lecture fees from Boston Scientific; Dr. Guimaraes, being employed by Cardialysis; Dr. Mack, serving as a trial coprimary investigator for Edwards Lifesciences and Abbott Vascular and serving as a study chair for Medtronic; Dr. Schafer, receiving grant support from the Medicines Company; Dr. Thomitzek, being employed by and holding stock in Bayer; Dr. Valgimigli, receiving lecture fees from AstraZeneca, Als'imedical CID, Vifor Pharma, and Medscape, grant support and lecture fees from 'Ceram, consulting fees and lecture fees from Abbott Vascular, Bayer, and Bristol-Myers Squibb, and consulting fees from Daiichi Sankyo, Opsens, CoreFIDW, Idorsia Pharmaceuticals, and iVascular; Dr. Vranekx, receiving fees for serving on a speakers bureau from Daiichi Sankyo, lecture tees from AstraZeneca, and fees for serving on a steering committee and travel support from CSL Behring; Dr. Welsh, receiving grant support and honoraria from AstraZeneca, Bayer, and Boehringer Ingelheim; Dr. Wildgoose, being employed by and holding stock in Janssen Pharmaceuticals; Dr. Volkl, being employed by Janssen Pharmaceuticals; Dr. van Amsterdam, being employed by Cardialysis; Dr. Zazula, being employed by Bayer; Dr. Mehran, receiving advisory board fees and consulting fees from Sanofi-Aventis and Janssen, receiving lecture fees from Bayer, receiving grant support, paid to her institution, and lecture fees from Daiichi Sankyo, and previously holding equity in Medtronic; and Dr. Windecker, receiving grant support, paid to his institution, advisory board fees, and travel support from Amgen and grant support, paid ro his institution, from Abbott Vascular, Bayer, Bristol-Myers Squibb, CSL Behring, Boston Scientific, Bic rronik, Medtronic, Edwards Lifesciences, Polares Medical, and Sinomed. No other potential conflict of interest relevant to this article was reported. Windecker, S (reprint author), Windecker, S (reprint author) stephan.windecker@insel.ch

Published
2020

2. A Controlled Trial of Rivaroxaban after Transcatheter Aortic-Valve Replacement

Author

Dangas, George D, Tijssen, Jan G P, Wöhrle, Jochen, Søndergaard, Lars, Gilard, Martine, Möllmann, Helge, Makkar, Raj R, Herrmann, Howard C, Giustino, Gennaro, Baldus, Stephan, De Backer, Ole, Guimarães, Ana H C, Gullestad, Lars, Kini, Annapoorna, von Lewinski, Dirk, Mack, Michael, Moreno, Raúl, Schäfer, Ulrich, Seeger, Julia, Tchétché, Didier, Thomitzek, Karen, Valgimigli, Marco, Vranckx, Pascal, Welsh, Robert C, Wildgoose, Peter, Volkl, Albert A, Zazula, Ana, van Amsterdam, Ronald G M, Mehran, Roxana, Windecker, Stephan, Kreuzpointner, Robert, Dangas, George D, Tijssen, Jan G P, Wöhrle, Jochen, Søndergaard, Lars, Gilard, Martine, Möllmann, Helge, Makkar, Raj R, Herrmann, Howard C, Giustino, Gennaro, Baldus, Stephan, De Backer, Ole, Guimarães, Ana H C, Gullestad, Lars, Kini, Annapoorna, von Lewinski, Dirk, Mack, Michael, Moreno, Raúl, Schäfer, Ulrich, Seeger, Julia, Tchétché, Didier, Thomitzek, Karen, Valgimigli, Marco, Vranckx, Pascal, Welsh, Robert C, Wildgoose, Peter, Volkl, Albert A, Zazula, Ana, van Amsterdam, Ronald G M, Mehran, Roxana, Windecker, Stephan, and Kreuzpointner, Robert

Abstract

BACKGROUND Whether the direct factor Xa inhibitor rivaroxaban can prevent thromboembolic events after transcatheter aortic-valve replacement (TAVR) is unclear. METHODS We randomly assigned 1644 patients without an established indication for oral anticoagulation after successful TAVR to receive rivaroxaban at a dose of 10 mg daily (with aspirin at a dose of 75 to 100 mg daily for the first 3 months) (rivaroxaban group) or aspirin at a dose of 75 to 100 mg daily (with clopidogrel at a dose of 75 mg daily for the first 3 months) (antiplatelet group). The primary efficacy outcome was the composite of death or thromboembolic events. The primary safety outcome was major, disabling, or life-threatening bleeding. The trial was terminated prematurely by the data and safety monitoring board because of safety concerns. RESULTS After a median of 17 months, death or a first thromboembolic event (intention-to-treat analysis) had occurred in 105 patients in the rivaroxaban group and in 78 patients in the antiplatelet group (incidence rates, 9.8 and 7.2 per 100 person-years, respectively; hazard ratio with rivaroxaban, 1.35; 95% confidence interval [CI], 1.01 to 1.81; P = 0.04). Major, disabling, or life-threatening bleeding (intention-to-treat analysis) had occurred in 46 and 31 patients, respectively (4.3 and 2.8 per 100 person-years; hazard ratio, 1.50; 95% CI, 0.95 to 2.37; P = 0.08). A total of 64 deaths occurred in the rivaroxaban group and 38 in the antiplatelet group (5.8 and 3.4 per 100 person-years, respectively; hazard ratio, 1.69; 95% CI, 1.13 to 2.53). CONCLUSIONS In patients without an established indication for oral anticoagulation after successful TAVR, a treatment strategy including rivaroxaban at a dose of 10 mg daily was associated with a higher risk of death or thromboembolic complications and a higher risk of bleeding than an antiplatelet-based strategy. (Funded by Bayer and Janssen Pharmaceuticals; GALILEO ClinicalTrials.gov number, NCT02556203.).

Published
2020

3. Impaired fibrinolysis as a risk factor for Budd-Chiari syndrome

Author

Hoekstra, Jildou, Guimarães, Ana H. C., Leebeek, Frank W. G., Darwish Murad, Sarwa, Malfliet, Joyce J. M. C., Plessier, Aurelie, Hernandez-Guerra, Manuel, Langlet, Philippe, Elias, Elwyn, Trebicka, Jonel, Primignani, Massimo, Garcia-Pagan, Juan-Carlos, Valla, Dominique C., Rijken, Dingeman C., and Janssen, Harry L. A.

Abstract

In Budd-Chiari syndrome (BCS), thrombosis develops in the hepatic veins or inferior vena cava. To study the relationship between hypofibrinolysis and BCS, we measured plasma levels of fibrinolysis proteins in 101 BCS patients and 101 healthy controls and performed a plasma-based clot lysis assay. In BCS patients, plasminogen activator inhibitor 1 (PAI-1) levels were significantly higher than in controls (median, 6.3 vs 1.4 IU/mL, P < .001). Thrombin-activatable fibrinolysis inhibitor and plasmin inhibitor levels were lower than in controls (13.8 vs 16.9 μg/mL and 0.91 vs 1.02 U/L, both P < .001). Median plasma clot lysis time (CLT) was 73.9 minutes in cases and 73.0 minutes in controls (P = .329). A subgroup of cases displayed clearly elevated CLTs. A CLT above the 90th or 95th percentile of controls was associated with an increased risk of BCS, with odds ratios of 2.4 (95% confidence interval, 1.1-5.5) and 3.4 (95% confidence interval, 1.2-9.7), respectively. In controls, only PAI-1 activity was significantly associated with CLT. Analysis of single nucleotide polymorphisms of fibrinolysis proteins revealed no significant differences between cases and controls. This case-control study provides the first evidence that an impaired fibrinolytic potential, at least partially caused by elevated PAI-1 levels, is related to the presence of BCS.

Published
2010
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4. TAFI and pancreatic carboxypeptidase B modulate in vitro capillary tube formation by human microvascular endothelial cells.

Author

Guimarães AH, Laurens N, Weijers EM, Koolwijk P, van Hinsbergh VW, and Rijken DC

Subjects
Angiogenesis Inhibitors pharmacology, Atherosclerosis enzymology, Capillaries cytology, Carboxypeptidase B pharmacology, Carboxypeptidase B2 antagonists & inhibitors, Cell Adhesion, Cell Culture Techniques, Cell Proliferation, Cells, Cultured, Dose-Response Relationship, Drug, Endothelial Cells drug effects, Endothelial Cells enzymology, Fibrin metabolism, Fibrin Fibrinogen Degradation Products metabolism, Fibroblast Growth Factor 2 metabolism, Humans, Plant Proteins pharmacology, Plasminogen metabolism, Protease Inhibitors pharmacology, Time Factors, Tumor Necrosis Factor-alpha metabolism, Urokinase-Type Plasminogen Activator metabolism, Wound Healing, Angiogenesis Inhibitors metabolism, Carboxypeptidase B metabolism, Carboxypeptidase B2 metabolism, Cell Movement drug effects, Endothelial Cells metabolism, Neovascularization, Physiologic drug effects
Abstract

Objective: Besides having a key role in fibrinolysis, the plasminogen system has been implicated in cell migration and angiogenesis. A common mechanism is the binding of plasminogen to carboxy-terminal lysine residues in partially degraded fibrin or on cellular surfaces. Here we examined the involvement of thrombin activatable fibrinolysis inhibitor (TAFI) and pancreatic carboxypeptidase B (CPB) in an in vitro capillary tube formation system, which is largely plasminogen-dependent., Methods and Results: Human microvascular endothelial cells (hMVECs) were seeded on a 3D plasma clot matrix and subsequently stimulated with bFGF/tumor necrosis factor (TNF)-alpha. Tube formation was analyzed and fibrin degradation products (FbDP) were determined in the medium. Supplementation of the matrix with additional TAFI or CPB produced a reduction in tube formation. Pretreatment of hMVECs with CPB before seeding resulted in a similar effect. FbDP-levels indicated a concomitant reduction in matrix proteolysis. A TAFIa inhibitor increased tube formation and FbDP release into the medium. In separate assays, CPB impaired the migration of hMVECs in a dose-dependent manner, whereas proliferation and adhesion remained unaffected., Conclusions: Overall, these results demonstrate that TAFI and CPB in these systems modulate the plasminogen system both in the matrix and on the cell surface, thus leading to the inhibition of endothelial cell movement and tube formation.

Published
2007
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