Antiplatelet strategies: evaluating their current role in the setting of acute coronary syndromes
Authors
Braunwald, EugeneAngiolillo, Dominick J.
Bates, Eric
Berger, Peter B.
Bhatt, Deepak
Cannon, Christopher P.
Furman, Mark I.
Gurbel, Paul A.
Michelson, Alan D.
Peterson, Eric D.
Wiviott, Stephen D.
UMass Chan Affiliations
Department of PediatricsDocument Type
Journal ArticlePublication Date
2008-03-01Keywords
Acute Coronary SyndromeAngioplasty, Balloon, Coronary
Antibodies, Monoclonal
Aspirin
Blood Platelets
Drug Administration Schedule
Drug Resistance
Drug Therapy, Combination
Humans
Immunoglobulin Fab Fragments
Myocardial Infarction
Patient Selection
Platelet Aggregation Inhibitors
Platelet Function Tests
Platelet Glycoprotein GPIIb-IIIa Complex
Risk Assessment
Thrombosis
Ticlopidine
Time Factors
Treatment Outcome
Hematology
Oncology
Pediatrics
Metadata
Show full item recordAbstract
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.Source
Clin Cardiol. 2008 Mar;31(3 Suppl 1):I2-9. doi 10.1002/clc.20362DOI
10.1002/clc.20362Permanent Link to this Item
http://hdl.handle.net/20.500.14038/43301PubMed ID
18481818Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1002/clc.20362