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7 results on '"Hord, Edward"'

1. Abstract 145: Thrombus Composition is Associated With Endothelial Injury and Stroke Etiology in Patients Undergoing Mechanical Thrombectomy for Emergent Large Vessel Occlusion

Author

Elijovich, Lucas, primary, Arthur, Adam, additional, Hoit, Daniel, additional, Nickele, Chris, additional, Morris, David, additional, Vachhani, Jay, additional, Belayev, Andrei, additional, Kotha, JP, additional, Hord, Edward, additional, Price, Susan, additional, Derrick, Vanessa, additional, Cardenas, Juan, additional, and Jennings, Lisa, additional

Published
2018
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4. Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes

Author

Smyth, Susan S., primary, Moliterno, David J., primary, Rorick, Tyrus L., primary, Moccetti, Tiziano, primary, Valgimigli, Marco, primary, Dery, Jean Pierre, primary, Cornel, Jan H., primary, Thomas, Gregory S., primary, Huber, Kurt, primary, Harrington, Robert A., primary, Hord, Edward, primary, Judge, Heather M., primary, Chen, Edmond, primary, Strony, John, primary, Mahaffey, Kenneth W., primary, Tricoci, Pierluigi, primary, Becker, Richard C., primary, Storey, Robert F., additional, Kotha, Jayaprakash, additional, and Jennings, Lisa K., additional

Published
2014
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5. PHARMACODYNAMICS OF VORAPAXAR, A PLATELET PAR-1 ANTAGONIST, AND ITS INTERACTION WITH P2Y12 RECEPTOR PATHWAY IN THE TRACER TRIAL

Author

Jennings, Lisa K., primary, Moliterno, David, additional, Storey, Robert, additional, Hord, Edward, additional, Kotha, Jayaprakash, additional, Becker, Richard, additional, Smyth, Susan, additional, Providencia, Luis, additional, Moccetti, Tiziano, additional, Valgimigli, Marco, additional, Dery, Jean-Pierre, additional, Cornel, J.H., additional, Thomas, Gregory, additional, Huber, Kurt, additional, Chen, Edmond, additional, Strony, John, additional, Rorick, Tyrus, additional, Tricoci, Pierluigi, additional, and Mahaffey, Kenneth, additional

Published
2012
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6. PAR1 antagonists inhibit thrombin-induced platelet activation whilst leaving the PAR4-mediated response intact.

Author

Judge, Heather M., Jennings, Lisa K., Moliterno, David J., Hord, Edward, Ecob, Rosemary, Tricoci, Pierluigi, Rorick, Tyrus, Kotha, Jayaprakash, and Storey, Robert F.

Subjects
ACUTE coronary syndrome, PLATELET aggregation inhibitors, PROTEASE-activated receptors, THROMBIN, PLATELET-rich plasma, THROMBIN receptors
Abstract

Thrombin-induced platelet activation is initiated by PAR1 and PAR4 receptors. Vorapaxar, a PAR1 antagonist, has been assessed in patients with acute coronary syndromes (ACS) and stable atherosclerotic disease in addition to standard-of-care treatment. In clinical trials, vorapaxar has been observed to reduce the frequency of ischaemic events in some subgroups though in others has increased the frequency of bleeding events. Among patients undergoing CABG surgery, which is associated with excess thrombin generation, bleeding was not increased. The aim of these studies was to investigate the effects of selective PAR1 antagonism on thrombin-induced platelet activation in patients receiving vorapaxar or placebo in the TRACER trial and to explore the roles of PAR1 and PAR4 in thrombin-induced platelet activation in healthy volunteers. ACS patients receiving vorapaxar or placebo in the TRACER trial were studied at baseline and 4 hours, 1 and 4 months during drug administration. Thrombin-induced calcium mobilisation in platelet-rich plasma was assessed by flow cytometry. In vitro studies were performed in healthy volunteers using the PAR1 antagonist SCH79797 or PAR4 receptor desensitisation. Vorapaxar treatment significantly inhibited thrombin-induced calcium mobilisation, leaving a residual, delayed response. These findings were consistent with calcium mobilisation mediated via the PAR4 receptor and were reproduced in vitro using SCH79797. PAR4 receptor desensitization, in combination with SCH79797, completely inhibited thrombin-induced calcium mobilisation confirming that the residual calcium mobilisation was mediated via PAR4. In conclusion vorapaxar selectively antagonises the PAR1-mediated component of thrombin-induced platelet activation, leaving the PAR4-mediated response intact, which may explain why vorapaxar is well tolerated in patients undergoing CABG surgery since higher thrombin levels in this setting may override the effects of PAR1 antagonism through PAR4 activation, thus preserving haemostasis. Further assessment may be warranted. [ABSTRACT FROM AUTHOR]

Published
2015
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7. Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes

Author

Storey, Robert F., Kotha, Jayaprakash, Smyth, Susan S., Moliterno, David J., Rorick, Tyrus L., Moccetti, Tiziano, Valgimigli, Marco, Dery, Jean Pierre, Cornel, Jan H., Thomas, Gregory S., Huber, Kurt, Harrington, Robert A., Hord, Edward, Judge, Heather M., Chen, Edmond, Strony, John, Mahaffey, Kenneth W., Tricoci, Pierluigi, Becker, Richard C., and Jennings, Lisa K.

Published
2014
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