Details

Autor(en) / Beteiligte

• Tricoci, Pierluigi
• Huang, Zhen
• Held, Claes
• Moliterno, David J
• Armstrong, Paul W
• Van de Werf, Frans
• White, Harvey D
• Aylward, Philip E
• Wallentin, Lars
• Chen, Edmond
• Lokhnygina, Yuliya
• Pei, Jinglan
• Leonardi, Sergio
• Rorick, Tyrus L
• Kilian, Ann M
• Jennings, Lisa H.K
• Ambrosio, Giuseppe
• Bode, Christoph
• Cequier, Angel
• Cornel, Jan H
• Diaz, Rafael
• Erkan, Aycan
• Huber, Kurt
• Hudson, Michael P
• Jiang, Lixin
• Jukema, J. Wouter
• Lewis, Basil S
• Lincoff, A. Michael
• Montalescot, Gilles
• Nicolau, José Carlos
• Ogawa, Hisao
• Pfisterer, Matthias
• Prieto, Juan Carlos
• Ruzyllo, Witold
• Sinnaeve, Peter R
• Storey, Robert F
• Valgimigli, Marco
• Whellan, David J
• Widimsky, Petr
• Strony, John
• Harrington, Robert A
• Mahaffey, Kenneth W

Titel

Thrombin-Receptor Antagonist Vorapaxar in Acute Coronary Syndromes

Ist Teil von

• The New England journal of medicine, 2012-01, Vol.366 (1), p.20-33

Ort / Verlag

Waltham, MA: Massachusetts Medical Society

Erscheinungsjahr

2012

Quelle

MEDLINE

Beschreibungen/Notizen

• In this trial, vorapaxar, a protease-activated–receptor 1 antagonist that inhibits thrombin-induced platelet activation, was not effective in reducing the primary cardiovascular efficacy end point, and it increased rates of bleeding, including serious bleeding and intracranial hemorrhage. The risk of recurrent ischemic complications among patients with acute coronary syndromes without ST-segment elevation remains high despite contemporary treatment strategies, including the use of early revascularization and dual antiplatelet therapy. 1 , 2 Hence, the assessment of new platelet inhibitors has continued to be an important avenue of investigation. 3 – 5 Thrombin activates platelets through two protease-activated receptors (PARs), PAR-1 and PAR-4. 6 PAR-1 is activated by lower concentrations of thrombin than PAR-4 and mediates a more rapid platelet-activation response. 7 In preclinical models, selective PAR-1 blockade resulted in potent inhibition of thrombin-induced platelet aggregation but appeared to preserve primary hemostatic function. 8 Vorapaxar (SCH . . .