Small peptide GP IIb/IIIa receptor inhibitors as upstream therapy in non-ST-segment elevation acute coronary syndromes: results of the PURSUIT, PRISM, PRISM-PLUS, TACTICS, and PARAGON trials
Rg. Mckay et We. Boden, Small peptide GP IIb/IIIa receptor inhibitors as upstream therapy in non-ST-segment elevation acute coronary syndromes: results of the PURSUIT, PRISM, PRISM-PLUS, TACTICS, and PARAGON trials, CURR OPIN C, 16(6), 2001, pp. 364-369
The primary pathophysiologic mechanism underlying all non-ST-segment elevat
ion acute coronary syndromes (NSTE ACS) is the formation of platelet-rich c
oronary thrombi in response to spontaneous or intervention-induced endothel
ial damage with exposure of subendothelial substrates. Antagonists of the g
lycoprotein (GP) IIb/IIIa receptor ameliorate this process by blocking the
final common pathway for platelet aggregation. Based upon collective data i
n over 24,000 patients, clinical trials have demonstrated that treatment of
NSTE ACS patients with GP IIb/IIIa agents results in an approximate 12% re
lative risk reduction in the incidence of death or myocardial infarction at
30 days. The magnitude of this clinical benefit is increased in patients w
ho are troponin-positive and who are referred for early percutaneous interv
ention. Potential benefits of GP IIb/IIIa inhibitor use must be weighed aga
inst an increased risk of bleeding. Ongoing controversies exist concerning
the relative efficacy of different GP IIb/IIIa antagonists, the accurate us
e of platelet function tests to define safe and efficacious drug dosing, th
e adjunctive use of additional anti-thrombotic agents, and the optimal timi
ng of upstream therapy before diagnostic cardiac catheterization and revasc
ularization. (C) 2001 Lippincott Williams & Wilkins, Inc.