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3. Antithrombotic Therapy: Prevention and Treatment of Atherosclerosis and Atherothrombosis

Author

Olie, R. H., van der Meijden, P. E. J., Spronk, H. M. H., ten Cate, H., Barrett, James E., Editor-in-Chief, Flockerzi, Veit, Editorial Board Member, Frohman, Michael A., Editorial Board Member, Geppetti, Pierangelo, Editorial Board Member, Hofmann, Franz B., Editorial Board Member, Kuner, Rohini, Editorial Board Member, Michel, Martin C., Editorial Board Member, Page, Clive P., Editorial Board Member, Wang, KeWei, Editorial Board Member, von Eckardstein, Arnold, editor, and Binder, Christoph J., editor

Published
2022
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4. Lupus anticoagulant associates with thrombosis in patients with COVID‐19 admitted to intensive care units: A retrospective cohort study

Author

Noordermeer, Tessa, Schutgens, Roger E.G., Visser, Chantal, Rademaker, Emma, de Maat, Moniek P.M., Jansen, A.J. Gerard, Limper, Maarten, Cremer, Olaf L., Kruip, Marieke J.H.A., Endeman, Henrik, Maas, Coen, de Laat, Bas, Urbanus, Rolf T., van de Beek, D., Brouwer, M.C., de Bruin, S., Coppens, M., van Es, N., van Haaps, T.F., Juffermans, N.P., Muller, M.C.A., Vlaar, A.P.J., Hertogh, C.M.P.M., Heunks, L.M.A., Hugtenburg, J.G., van Kooten, J., Nossent, E.J., Smulders, Y., Tuinman, P.R., Vonk Noordegraaf, A., Grootenboers, M.J.J.H., van Guldener, C., Kant, M., Lansbergen, A., Faber, J., Hajer, G., Stemerdink, A., van den Akker, J., Bierings, R., Endeman, H., Goeijenbier, M., Hunfeld, N.G.M., van Gorp, E.C.M., Gommers, D.A.M.P.J., Koopmans, M.P.G., Kruip, M.J.H.A., Kuiken, T., Langerak, T., Leebeek, Lauw, M.N., de Maat, M.P.M., Noack, D., Paats, M.S., Raadsen, M.P., Rockx, B., Rokx, C., Schurink, C.A.M., Tong‐Minh, K., van den Toorn, L., den Uil, C.A., Visser, C., Boutkourt, F., Roest, T., Douma, R.A., de Haan, L.R., ten Wolde, M., Bemelmans, R.H.H., Festen, B., Stads, S., de Jager, C.P.C., Simons, K.S., Antoni, M.L., Bos, M.H., Burggraaf, J.L.I., Cannegieter, S.C., Eikenboom, H.C.J., den Exter, P.L., Geelhoed, J.J.M., Huisman, M.V., de Jonge, E., Kaptein, F.H.J., Klok, F.A., Kroft, L.J.M., Lijfering, W.M., Nab, L., Ninaber, M.K., Putter, H., Ramai, S.R.S., da Rocha Rondon, A.M., Roukens, A.H.E., Stals, M.A.M., Versteeg, H.H., Vliegen, H.W., van Vlijmen, B.J.M., van de Berg, T., Bruggemann, R., van Bussel, B.C.T., ten Cate, H., ten Cate‐Hoek, A., Hackeng, T.M., Henskens, ir.Y., Hulshof, A., Mulder, M., Olie, R.H., Schurgers, L., Spaetgens, B., Spronk, H., Winckers, K., Nieuwenhuizen, L., Franken, B., Schrover, I.M., de Waal, E.G.M., Beishuizen, A., Cornet, A., Krabbe, J., Kramers, K., Leentjens, J., de Mast, Q., Middeldorp, S., Brouwer, R.E., Ellerbroek, J.L.J., Tijmensen, J., Hovens, M.M C., Oostdijk, E.A.N., Westerhof, B.D., Faber, L.M., van den Biggelaar, M., Meijers, J.C.M., Voorberg, J., Kevenaar, M.E., Soei, Y.L., Wils, E.J., Croles, F.N., de Laat, B., Kamphuisen, P.W., Vink, R., Lisman, T., Meijer, K., van Tichelaar, Y.I.G., Cremer, O.L., Geersing, G., Kaasjager, H.A.H., Kusadasi, N., Huisman, A., Maas, C., Nijkeuter, M., Schutgens, R.E.G., Creveldkliniek, Van, Urbanus, R.T., Westerink, J., Faber, H.J., Koster, S.C.E., van Montfort, P., and van Twist, D.J.L.

Published
2022
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12. Translational insights into mechanisms underlying residual venous obstruction and the role of factor XI, P-selectin and GPVI in recurrent venous thromboembolism

Author

Iding, A F J, Kremers, B M M, Nagy, M, Robles, A Pallares, Ten Cate, H, Spronk, H M H, Ten Cate-Hoek, A J, Biochemie, MUMC+: HVC Trombosedienst (9), RS: Carim - B04 Clinical thrombosis and Haemostasis, Interne Geneeskunde, MUMC+: MA Alg Interne Geneeskunde (9), MUMC+: HVC Trombosezorg (8), and MUMC+: HVC Pieken Trombose (9)

Subjects
Hematology
Abstract

Background: Residual venous obstruction (RVO) after deep vein thrombosis (DVT) is considered a risk factor of recurrent venous thromboembolism (VTE), arterial events and post-thrombotic syndrome (PTS). We hypothe-sized thrombo-inflammatory markers might be associated with RVO and clinical outcomes.Materials and methods: In a DVT cohort with routine RVO-assessment and 5-year follow-up, patients were invited for blood withdrawal after stopping anticoagulants. Thrombin generation potential, coagulation enzyme:inhib-itor complexes, soluble platelet markers and clinical markers were measured in platelet-poor plasma. Associa-tions were represented as odds ratio (OR) or hazard ratio (HR) per standard deviation.Results: Patients with RVO (102/306, 33 %) had higher rates of PTS (24 vs. 12 %, p = 0.008), but similar rates of recurrence (16 vs. 15 %, p = 0.91) and arterial events (7 vs. 4 %, p = 0.26). RVO was associated with thrombin peak height (OR 1.40 [1.04-1.88]), endogenous thrombin potential (ETP, OR 1.35 [1.02-1.79]), and CRP (OR 1.74 [1.10-2.75]). Recurrent VTE was associated with ETP (HR 1.36 [1.03-1.81]), FXIa:C1-inhibitor (HR 1.34 [1.04-1.72]), thrombin:antithrombin (HR 1.36 [1.16-1.59]), soluble P-selectin (HR 2.30 [1.69-3.11]), soluble glycoprotein VI (sGPVI, HR 1.30 [1.01-1.69]), D-dimer (HR 1.56 [1.31-1.86]), and factor VIII (HR 1.44 [1.15-1.82]). Arterial events were associated with sGPVI (HR 1.80 [1.25-2.59]). PTS was not associated with any marker.Conclusions: Our findings indicate RVO was associated with thrombo-inflammation, but this did not predict clinical outcomes in this setting. Importantly, we found recurrent VTE was associated with ongoing coagulation and platelet activation in patients well beyond the acute phase of DVT. Furthermore, sGPVI indicated an increased risk of arterial events, highlighting the role of platelets in arterial thrombosis following DVT.

Published
2022

13. The 3S-AF scheme, rather than the 4S-AF scheme, predicts progression in patients with paroxysmal atrial fibrillation: data from RACE V study

Author

Artola, V, primary, Geelhoed, B, additional, Van Lande, M, additional, Khalilian Ekrami, N, additional, De With, R, additional, Weberndorfer, V, additional, Linz, D, additional, Ten Cate, H, additional, Spronk, H, additional, Koldenhof, T, additional, Tieleman, RG, additional, Schotten, U, additional, Crijns, HJG, additional, Van Gelder, I, additional, and Rienstra, M, additional

Published
2022
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17. Sustained endothelial, coagulation and inflammatory cytokine activation without macrovascular dysfunction at 3 months after COVID-19: a reflection on SARS-CoV-2 induced thrombo-inflammation

Author

Willems, L H, primary, Nagy, M, additional, Ten Cate, H, additional, Spronk, H M H, additional, Groh, L A, additional, Leentjes, J, additional, Janssen, N A F, additional, Netea, M G, additional, Thijssen, D H J, additional, Hannink, G J, additional, Van Petersen, A S, additional, and Warle, M C, additional

Published
2021
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20. Design and synthesis of a multivalent catch-and-release assay to measure circulating FXIa

Author

van der Beelen, S H E, van der Beelen, S H E, Agten, S M, Suylen, D P L, Wichapong, K, Hrdinova, J, Mees, B M E, Spronk, H M H, Hackeng, T M, van der Beelen, S H E, van der Beelen, S H E, Agten, S M, Suylen, D P L, Wichapong, K, Hrdinova, J, Mees, B M E, Spronk, H M H, and Hackeng, T M

Abstract

BACKGROUND: Decreased blood coagulation factor (F)XIa levels have been shown to protect from thrombosis without bleeding side effects, but less is known on effects of increased FXIa levels. Studies are hampered by lack of a reliable and robust method for FXIa quantification in blood. We aim to develop a new assay employing a unique multivalent catch-and-release system. The system selectively isolates and protects homodimeric FXIa from plasma and releases free FXIa allowing subsequent quantification.METHODS: A dynamic multivalent construct was synthesized by complexing four identical FXIa inhibitors from the snake Bungarus Fasxiatus to avidin through desthiobiotin-PEG-linkers, allowing dissociation of FXIa by excess biotin. PEG-linker lengths were optimised for FXIa inhibitory activity and analysed by Michaelis-Menten kinetics. Finally, the catch-and-release assay was validated in buffer and plasma model systems.RESULTS: Monovalent and multivalent inhibitor constructs were successfully obtained by total chemical synthesis. Multimerisation of Fasxiator resulted in a 30-fold increase in affinity for FXIa from 1.6 nM to 0.05 nM. With use of this system, FXIa could be quantified down to a concentration of 7 pM in buffer and 20 pM in plasma.CONCLUSION: In this proof-of-concept study, we have shown that the catch-and-release approach is a promising technique to quantify FXIa in plasma or buffer. By binding FXIa to the multivalent construct directly after blood drawing, FXIa is hypothesized to be inaccessible for serpin inhibition or auto inactivation. This results in a close reflection of actual circulating FXIa levels at the moment of blood drawing.

Published
2021

43. Atherothrombosis and Thromboembolism: Position Paper from the Second Maastricht Consensus Conference on Thrombosis

Author

Spronk, H. M. H., Spronk, H. M. H., Padro, T., Siland, J. E., Prochaska, J. H., Winters, J., van der Wal, A. C., Posthuma, J. J., Lowe, G., d'Alessandro, E., Wenzel, P., Coenen, D. M., Reitsma, P. H., Ruf, W., van Gorp, R. H., Koenen, R. R., Vajen, T., Alshaikh, N. A., Wolberg, A. S., Macrae, F. L., Asquith, N., Heemskerk, J., Heinzmann, A., Moorlag, M., Mackman, N., van der Meijden, P., Meijers, J. C. M., Heestermans, M., Renne, T., Dolleman, S., Chayoua, W., Ariens, R. A. S., Baaten, C. C., Nagy, M., Kuliopulos, A., Posma, J. J., Harrison, P., Vries, M. J., Crijns, H. J. G. M., Dudink, E. A. M. P., Buller, H. R., Henskens, Y. M. C., Sjalander, A., Zwaveling, S., Erkuner, O., Eikelboom, J. W., Gulpen, A., Peeters, F. E. C. M., Douxfils, J., Olie, R. H., Baglin, T., Leader, A., Schotten, U., Scaf, B., van Beusekom, H. M. M., Mosnier, L. O., van der Vorm, L., Declerck, P., Visser, M., Dippel, D. W. J., Strijbis, V. J., Pertiwi, K., ten Cate-Hoek, A. J., ten Cate, H., Spronk, H. M. H., Spronk, H. M. H., Padro, T., Siland, J. E., Prochaska, J. H., Winters, J., van der Wal, A. C., Posthuma, J. J., Lowe, G., d'Alessandro, E., Wenzel, P., Coenen, D. M., Reitsma, P. H., Ruf, W., van Gorp, R. H., Koenen, R. R., Vajen, T., Alshaikh, N. A., Wolberg, A. S., Macrae, F. L., Asquith, N., Heemskerk, J., Heinzmann, A., Moorlag, M., Mackman, N., van der Meijden, P., Meijers, J. C. M., Heestermans, M., Renne, T., Dolleman, S., Chayoua, W., Ariens, R. A. S., Baaten, C. C., Nagy, M., Kuliopulos, A., Posma, J. J., Harrison, P., Vries, M. J., Crijns, H. J. G. M., Dudink, E. A. M. P., Buller, H. R., Henskens, Y. M. C., Sjalander, A., Zwaveling, S., Erkuner, O., Eikelboom, J. W., Gulpen, A., Peeters, F. E. C. M., Douxfils, J., Olie, R. H., Baglin, T., Leader, A., Schotten, U., Scaf, B., van Beusekom, H. M. M., Mosnier, L. O., van der Vorm, L., Declerck, P., Visser, M., Dippel, D. W. J., Strijbis, V. J., Pertiwi, K., ten Cate-Hoek, A. J., and ten Cate, H.

Abstract

Atherothrombosis is a leading cause of cardiovascular mortality and long-term morbidity. Platelets and coagulation proteases, interacting with circulating cells and in different vascular beds, modify several complex pathologies including atherosclerosis. In the second Maastricht Consensus Conference on Thrombosis, this theme was addressed by diverse scientists from bench to bedside. All presentations were discussed with audience members and the results of these discussions were incorporated in the final document that presents a state-of-the-art reflection of expert opinions and consensus recommendations regarding the following five topics: 1. Risk factors, biomarkers and plaque instability: In atherothrombosis research, more focus on the contribution of specific risk factors like ectopic fat needs to be considered; definitions of atherothrombosis are important distinguishing different phases of disease, including plaque (in) stability; proteomic and metabolomics data are to be added to genetic information. 2. Circulating cells including platelets and atherothrombosis: Mechanisms of leukocyte and macrophage plasticity, migration, and transformation in murine atherosclerosis need to be considered; diseasemechanism-based biomarkers need to be identified; experimental systems are needed that incorporatewhole-blood flow to understand how red blood cells influence thrombus formation and stability; knowledge on platelet heterogeneity and priming conditions needs to be translated toward the in vivo situation. 3. Coagulation proteases, fibrin(ogen) and thrombus formation: The role of factor (F) XI in thrombosis including the lower margins of this factor related to safe and effective antithrombotic therapy needs to be established; FXI is a key regulator in linking platelets, thrombin generation, and inflammatory mechanisms in a renin-angiotensin dependent manner; however, the impact on thrombin-dependent PAR signaling needs further study; the fundamental mechanisms in FXIII b

Published
2018

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