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Your search keyword '"Joyner, C.D."' showing total 3 results
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3 results on '"Joyner, C.D."'

1. Final Study Report of Andexanet Alfa for Major Bleeding With Factor Xa Inhibitors

Author

Milling, Truman J., Jr, Middeldorp, Saskia, Xu, Lizhen, Koch, Bruce, Demchuk, Andrew, Eikelboom, John W., Verhamme, Peter, Cohen, Alexander T., Beyer-Westendorf, Jan, Michael Gibson, C., Lopez-Sendon, Jose, Crowther, Mark, Shoamanesh, Ashkan, Coppens, Michiel, Schmidt, Jeannot, Albaladejo, Pierre, Connolly, Stuart J., Anand, R., Bastani, A., Clark, C., Concha, M., Cornell, J., Dombrowski, K., Fermann, G., Fulmer, J., Goldstein, J., Kereiakes, D., Milling, T., Pallin, D., Patel, N., Refaai, M., Rehman, M., Schmaier, A., Schwarz, E., Shillinglaw, W., Spohn, M., Takata, T., Venkat, A., Welker, J., Welsby, I., Wilson, J., Van Keer, L., Verschuren, F., Blostein, M., Eikelboom, J., Althaus, K., Berrouschot, J., Braun, G., Doeppner, T., Dziewas, R., Genth-Zotz, S., Greinacher, P., Hamann, F., Hanses, F., Heide, W., Kallmuenzer, B., Kermer, P., Poli, S., Royl, G., Schellong, S., Schnupp, S., Schwarze, J., Spies, C., Thomalla, G., von Mering, M., Weissenborn, K., Wollenweber, F., Gumbinger, C., Jaschinski, U., Maschke, M., Mochmann, H-C., Pfeilschifter, W., Pohlmann, C., Zahn, R., Bouzat, P., Schmidt, J., Vallejo, C., Floccard, B., Coppens, M., van Wissen, S., Arellano-Rodrigo, E., Valles, E., Alikhan, R., Breen, K., Hall, R., Crowther, M., Albaladejo, P., Cohen, A., Demchuk, A.M., Schmidt, J., Wyse, D.G., Garcia, D.A., Prins, M., Nakamya, J., Büller, H.R., Mahaffey, K. W., Alexander, J. H., Cairns, J.A., Hart, R.G., Joyner, C.D., Raskob, G.E., Schulman, S., Veltkamp, R., Meeks, B., Zotova, E., Ahmad, S., Pinto, T., Baker, K., Dykstra, A., Holadyk-Gris, I., Malvaso, A., and Demchuk, A.M.

Published
2023
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2. Irbesartan in patients with atrial fibrillation

Author

UCL - (MGD) Service de cardiologie, UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire, Yusuf, S., Healey, J.S., Pogue, J., Chrolavicius, S., Flather, M., Hart, R.G., Hohnloser, S.H., Joyner, C.D., Pfeffer, M.A., Connolly, S.J., De Roy, Luc, UCL - (MGD) Service de cardiologie, UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire, Yusuf, S., Healey, J.S., Pogue, J., Chrolavicius, S., Flather, M., Hart, R.G., Hohnloser, S.H., Joyner, C.D., Pfeffer, M.A., Connolly, S.J., and De Roy, Luc

Abstract

BACKGROUND: The risk of cardiovascular events among patients with atrial fibrillation is high. We evaluated whether irbesartan, an angiotensin-receptor blocker, would reduce this risk. METHODS: We randomly assigned patients with a history of risk factors for stroke and a systolic blood pressure of at least 110 mm Hg to receive either irbesartan at a target dose of 300 mg once daily or double-blind placebo. These patients were already enrolled in one of two trials (of clopidogrel plus aspirin versus aspirin alone or versus oral anti-coagulants). The first coprimary outcome was stroke, myocardial infarction, or death from vascular causes; the second was this composite outcome plus hospitalization for heart failure. RESULTS: A total of 9016 patients were enrolled and followed for a mean of 4.1 years. The mean reduction in systolic blood pressure was 2.9 mm Hg greater in the irbesartan group than in the placebo group, and the mean reduction in diastolic blood pressure was 1.9 mm Hg greater. The first coprimary outcome occurred at a rate of 5.4% per 100 person-years in both groups (hazard ratio with irbesartan, 0.99; 95% confidence interval [CI], 0.91 to 1.08; P = 0.85). The second coprimary outcome occurred at a rate of 7.3% per 100 person-years among patients receiving irbesartan and 7.7% per 100 person-years among patients receiving placebo (hazard ratio, 0.94; 95% CI, 0.87 to 1.02; P = 0.12). The rates of first hospitalization for heart failure (a pre-specified secondary outcome) were 2.7% per 100 person-years among patients receiving irbesartan and 3.2% per 100 person-years among patients receiving placebo (hazard ratio, 0.86; 95% CI, 0.76 to 0.98). Among patients who were in sinus rhythm at baseline, there was no benefit of irbesartan in preventing hospitalization for atrial fibrillation or atrial fibrillation recorded on 12-lead electrocardiography, nor was there a benefit in a subgroup that underwent transtelephonic monitoring. More patients in the irbesartan gro

Published
2011

3. Reactivation of coagulation after stopping infusions of recombinant hirudin and unfractionated heparin in unstable angina and myocardial infarction without ST elevation: results of a randomized trial.

Author

Flather, M.D, Weitz, J.I, Yusuf, S, Pogue, J, Sussex, B, Campeau, J, Gill, J, Schuld, R, Joyner, C.D, Morris, A.L, Lai, C, Théroux, P, Marquis, J.F, Chan, Y.K, Venkatesh, G, and Jessel, A

Abstract

Aims To compare effects of heparin and hirudin on biochemical markers of coagulation.Methods and Results Patients (n=395) with unstable angina or myocardial infarction without ST elevation were randomized to a 72-h infusion of one of three regimens: unfractionated heparin (bolus of 5000IU followed by an infusion of 1200IU.h−1), low-dose hirudin (HBW 023; 0·2mg.kg−1bolus followed by 0·10mg.kg−1.h−1) or medium-dose hirudin (0·4mg.kg−1bolus followed by 0·15mg.kg−1.h−1). Infusions were adjusted to maintain an activated partial thromboplastin time of between 60–100s. Activated partial thromboplastin time, prothrombin fragment 1.2 (F1.2), thrombin antithrombin III complex and D-dimer were measured before, during and after the infusion. Median activated partial thromboplastin time was similar in the two groups early on, but was significantly lower in the heparin group than in the combined hirudin group 48h after starting the infusion (53s and 75s, respectively;P<0·001), and 6h after stopping (31s and 46s, respectively;P<0·001). Median F1.2 levels were not significantly different between the groups during the infusion. Median thrombin antithrombin III levels in the heparin and hirudin groups were 2·8μg.l−1and 2·3μg.l−1, respectively, at 6h (P<0·001), and 3·0μg.l−1and 2·3μg.l−1, respectively, at 48h (P<0·001). Median D-dimer levels were 320ng.ml−1and 260ng.ml−148h after starting the infusion in the heparin and hirudin groups, respectively (P<0·001), and 415ng.ml−1and 280ng.ml−1, respectively (P<0·001) 6h after stopping. D-dimer levels were significantly elevated above baseline values in both groups 24–48h after stopping the infusions.Conclusions The greater reduction of thrombin antithrombin III and D-dimer during the hirudin infusion supports the hypothesis that hirudin is a more potent antithrombin agent than heparin. Increased D-dimer levels after stopping heparin or hirudin suggest that there is an ongoing pro-coagulant state. These results point to the greater efficacy of hirudin in preventing early clinical events (death, myocardial infarction and refractory ischaemia) compared with heparin that have been observed in large randomized trials. Persistent activation of coagulation afterstopping infusions in our study suggests that a longer course of antithrombotic treatment may be needed to pacify the thrombus. [ABSTRACT FROM PUBLISHER]

Published
2000
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