Glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: pathophysiologic foundation and clinical findings

Am Heart J. 1998 Oct;136(4 Pt 2 Su):S32-42. doi: 10.1053/hj.1998.v136.93434.

Abstract

The pathophysiologic basis for potent platelet inhibition in the acute coronary syndromes has been established. In the setting of PTCA for unstable angina and non-Q-wave myocardial infarction, there are clear data for a benefit of GP IIb/IIIa inhibition, whereas for primary PTCA in evolving myocardial infarction, preliminary data are very encouraging and a large-scale clinical trial is nearly completed. Glycoprotein IIb/IIIa inhibition as an adjunct to medical therapy for unstable angina is also the subject of encouraging preliminary data, and 3 large-scale clinical trials have just been completed. Preliminary data have also been accrued for GP IIb/IIIa inhibition as conjunctive therapy with thrombolytic agents, and large clinical trials are now commencing.

Publication types

  • Review

MeSH terms

  • Acute Disease
  • Angina, Unstable / drug therapy
  • Angina, Unstable / metabolism
  • Clinical Trials as Topic
  • Coronary Disease / drug therapy*
  • Coronary Disease / metabolism*
  • Coronary Disease / physiopathology
  • Heart Conduction System / drug effects
  • Humans
  • Myocardial Infarction / drug therapy
  • Myocardial Infarction / metabolism
  • Platelet Aggregation Inhibitors / therapeutic use*
  • Platelet Glycoprotein GPIIb-IIIa Complex / antagonists & inhibitors*
  • Platelet Glycoprotein GPIIb-IIIa Complex / metabolism*
  • Syndrome
  • Thrombolytic Therapy

Substances

  • Platelet Aggregation Inhibitors
  • Platelet Glycoprotein GPIIb-IIIa Complex