Treatment of unstable angina: the role of platelet inhibitors and anticoagulants
Cohen, M.
Journal of Invasive Cardiology 11(3): 147-159
1999
ISSN/ISBN: 1042-3931 PMID: 10745504 Document Number: 502101
Thrombo-occlusive events at sites of atherosclerotic stenosis and plaque rupture are caused by exposure of the sub-endothelial layer of the vasculature to platelets and their subsequent aggregation at the locus of injury. Thrombi are generated by the activation of platelets, which are not always inhibited by aspirin or heparin. Both unstable angina and myocardial infarction are ultimately linked to thrombus formation. In addition, various invasive procedures used to re-establish patency of coronary vessels are often followed by thrombotic events that can be life threatening. New antagonists to thrombin and the development of glycoprotein (GP) IIb/IIIa platelet receptor inhibitors have been the main focus of recent large clinical trials that have demonstrated both the efficacy and safety of these new agents. The new antithrombotics include hirudin, hirulog, and the low molecular weight heparins. Representative GP IIb/IIIa receptor blockers include: abciximab, a human-murine chimeric monoclonal antibody; tirofiban, a non-peptide tyrosine derivative with a short half-life; and eptifibatide, a cyclic heptapeptide. All three are available for clinical use, but their approved indications vary. The GP IIb/IIIa receptor antagonists are anticipated to gain wide clinical acceptance by both cardiologists and internists and should have a prominent role in the management of acute coronary syndromes, most likely in combination with an antithrombin.