Key result
Glycoprotein IIb/IIIa inhibitors reduce non-fatal MI and death ~21% vs conventional treatment in ACS.
Odds Ratio: 0.79
This report summarizes the pathophysiology of acute coronary syndromes and the pharmacological role of glycoprotein IIb/IIIa inhibitors.
Acute coronary syndromes constitute a spectrum of clinical conditions and can be divided into non-ST segment elevation (unstable angina and non-Q wave myocardial infarction) and ST segment elevation myocardial infarction. They are major causes of morbidity and mortality. Hospital admissions for unstable angina are increasing (estimated approximately 130 000 patients per year in the UK) and have now exceeded those for acute myocardial infarction, with the incidence of death or myocardial infarction in hospital at 4.9% and by six months 12%.1 Plaque disruption, platelet adherence, platelet activation2 (mediated by various agents3) and an ensuing platelet thrombus lead to subtotal or complete occlusion of the coronary artery. It is hypothesised that platelet thrombi can embolise downstream giving rise to microvascular platelet aggregation and myocardial damage. The evidence for inflammation as a significant factor in patients with acute coronary syndromes is raised C-reactive protein (a measure of interleukin 6 and cytokine activation) which carries a worse prognosis. The glycoprotein (GP) IIb/IIIa receptor represents a pathway for platelet aggregation and is the most abundant receptor found on platelet membrane surfaces (40 000 to 80 000 per platelet). The activated GP IIb/IIIa receptor binds with the soluble ligands fibrinogen and von Willebrand factor causing platelet adherence, generation of a platelet mass, and thrombus formation.4 Pioneering research by Coller and colleagues with a murine derived monoclonal antibody directed against the GP IIb/IIIa receptor5 led to the development of a chimeric monoclonal antibody Fab fragment compound known as c7E3 Fab or abciximab (Reopro). Development of synthetic molecules of low molecular weight followed and two are commercially available (tirofiban (Aggrastat) and eptifibatide (Integrilin)). They differ from abciximab by mimicking the arginine-glycine-aspartic acid sequence and thus competitively inhibit fibrinogen binding to the GP IIb/IIIa receptor.6 They have a shorter duration of action and are specific …
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Manoharan et al. (2001) conducted a review in Acute coronary syndromes (n=30,000). Glycoprotein IIb/IIIa inhibitors vs. Conventional treatment (aspirin and heparin alone) was evaluated on Non-fatal myocardial infarction and death (OR 0.79). Glycoprotein IIb/IIIa inhibitors reduced non-fatal myocardial infarction and death by up to 25% compared with conventional treatment in patients with acute coronary syndromes (OR 0.79).
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