title: Antiplatelet strategies: evaluating their current role in the setting of acute coronary syndromes.
abstract: Numerous clinical trials have established the value of antiplatelet therapies for acute coronary syndromes (ACS). Aspirin (ASA), thienopyridines (i.e., clopidogrel and ticlopidine) and GP IIb/IIIa antagonists comprise the major classes of antiplatelet therapies demonstrated to be of benefit in the treatment of ACS and for the prevention of thrombotic complications of percutaneous coronary intervention (PCI). Clopidogrel is beneficial when administered before and after PCI, and is more effective when combined with either ASA or GP IIb/IIIa inhibitors in preventing post-PCI complications, coronary subacute stent thrombosis, and thrombotic events in general. It is currently unclear whether a higher loading dose of clopidogrel (600 mg) is better than the standard loading dose (300 mg), how long therapy should continue, and which maintenance dose is optimal. The role of the GP IIb/IIIa antagonists in ACS is less clear due to conflicting data from several studies with different patient populations. Currently, it appears that the use of GP IIb/IIIa antagonists might be most beneficial in high-risk ACS patients scheduled to undergo PCI, who demonstrate non-ST-segment elevation myocardial infarction and elevated troponin levels.
authors.affiliation: TIMI Study Group, Cardiovascular Division, Brigham and Women's Hospital, Department of Medicine, Harvard Medical School, 350 Longwood Avenue, Boston, Massachusetts 02115, USA. ebraunwald@partners.org
authors.forename: Eugene
authors.initials: E
authors.lastname: Braunwald
authors.forename: Dominick
authors.initials: D
authors.lastname: Angiolillo
authors.forename: Eric
authors.initials: E
authors.lastname: Bates
authors.forename: Peter B
authors.initials: PB
authors.lastname: Berger
authors.forename: Deepak
authors.initials: D
authors.lastname: Bhatt
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
authors.forename: Mark I
authors.initials: MI
authors.lastname: Furman
authors.forename: Paul
authors.initials: P
authors.lastname: Gurbel
authors.forename: Alan D
authors.initials: AD
authors.lastname: Michelson
authors.forename: Eric
authors.initials: E
authors.lastname: Peterson
authors.forename: Stephen
authors.initials: S
authors.lastname: Wiviott
mesh_terms: D000077284:Abciximab; D054058:Acute Coronary Syndrome / Q000097:blood / Q000150:complications / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects*; D000077144:Clopidogrel; D004334:Drug Administration Schedule; D004351:Drug Resistance; D004359:Drug Therapy, Combination; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000209:etiology / Q000628:therapy; D018579:Patient Selection; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D010979:Platelet Function Tests; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D018570:Risk Assessment; D013927:Thrombosis / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab