title: Antiplatelet and anticoagulation agents in acute coronary syndromes: what is the current status and what does the future hold?
abstract: Mortality and morbidity in acute coronary syndromes (ACSs), caused principally by plaque erosion or rupture leading to thrombus formation and myocardial ischemia, have been reduced by a combination of antithrombotic agents (antiplatelet drugs and anticoagulants) and early revascularization. Aspirin is the foundation antiplatelet agent. New P2Y12 receptor inhibitors (prasugrel and ticagrelor) have clear benefits compared with clopidogrel for dual antiplatelet therapy, and cangrelor or vorapaxar, a thrombin receptor inhibitor, may be of value in specific settings. Anticoagulation uses 1 of 4 choices: bivalirudin, unfractionated heparin, enoxaparin, and fondaparinux. Moreover, some patients (such as those who have chronic atrial fibrillation) require triple therapy with aspirin, clopidogrel, plus an anticoagulant, frequently a vitamin K antagonist. New oral anticoagulants have been shown to be at least as effective as vitamin K antagonists in atrial fibrillation and led to fewer bleeding complications. Finally, the combination of aspirin, clopidogrel, and low-dose rivaroxaban has recently been approved by the European Medicines Agency (but not the Food and Drug Administration) for secondary prevention after ACS. Several strategies have been developed to balance the potential benefit of antithrombotic therapy against the risk of bleeding complications, for example, radial access in coronary angiography or restricted use of combination therapy, and others are under investigation, such as discontinuation of aspirin. This overview summarizes the current status of antithrombotic therapy in ACS and describes strategies currently explored to optimize its benefit/risk ratio.
authors.affiliation: 3rd Medical Department, Cardiology and Intensive Care Unit, Wilhelminen Hospital, Vienna, Austria.
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
authors.affiliation: Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI.
authors.forename: Eric R
authors.initials: ER
authors.lastname: Bates
authors.affiliation: Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands.
authors.forename: Marco
authors.initials: M
authors.lastname: Valgimigli
authors.affiliation: Uppsala Clinical Research Center and Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: Lars
authors.initials: L
authors.lastname: Wallentin
authors.affiliation: Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
authors.forename: Steen Dalby
authors.initials: SD
authors.lastname: Kristensen
authors.affiliation: University of Utah, Intermountain Healthcare, Salt Lake City, UT.
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Anderson
authors.affiliation: La Paz University Hospital and Research Institute IdiPaz, Madrid, Spain.
authors.forename: Jose Luis
authors.initials: JL
authors.lastname: Lopez Sendon
authors.affiliation: San Filippo Neri Hospital, Rome, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Tubaro
authors.affiliation: Duke Heart Center, Durham, NC.
authors.forename: Christopher B
authors.initials: CB
authors.lastname: Granger
authors.affiliation: University of Freiburg, Freiburg, Germany.
authors.forename: Christoph
authors.initials: C
authors.lastname: Bode
authors.affiliation: Duke Heart Center, Durham, NC.
authors.forename: Erik Magnus
authors.initials: EM
authors.lastname: Ohman
authors.affiliation: Departement Hospitalo-Universitaire FIRE, Hôpital Bichat, AP-HP, and Universite Paris-Diderot, INSERM U, Paris, France. Electronic address: gabriel.steg@bch.aphp.fr.
authors.forename: Philippe Gabriel
authors.initials: PG
authors.lastname: Steg
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy*; D000241:Adenosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000249:Adenosine Monophosphate / Q000031:analogs & derivatives / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D017984:Enoxaparin / Q000627:therapeutic use; D000077542:Eptifibatide; D000077425:Fondaparinux; D006493:Heparin / Q000627:therapeutic use; D006629:Hirudins; D006801:Humans; D007783:Lactones / Q000627:therapeutic use; D010446:Peptide Fragments / Q000627:therapeutic use; D010455:Peptides / Q000627:therapeutic use; D010879:Piperazines / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011134:Polysaccharides / Q000627:therapeutic use; D000068799:Prasugrel Hydrochloride; D058921:Purinergic P2Y Receptor Antagonists / Q000627:therapeutic use*; D011725:Pyridines / Q000627:therapeutic use; D018179:Receptors, Thrombin / Q000037:antagonists & inhibitors*; D011994:Recombinant Proteins / Q000627:therapeutic use; D013876:Thiophenes / Q000627:therapeutic use; D000077486:Ticagrelor; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D017984:Enoxaparin; D006629:Hirudins; D007783:Lactones; D010446:Peptide Fragments; D010455:Peptides; D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D011134:Polysaccharides; D058921:Purinergic P2Y Receptor Antagonists; D011725:Pyridines; D018179:Receptors, Thrombin; D011994:Recombinant Proteins; D013876:Thiophenes; D000249:Adenosine Monophosphate; D014443:Tyrosine; D014859:Warfarin; C117446:cangrelor; D006493:Heparin; D000068799:Prasugrel Hydrochloride; D000077466:Tirofiban; D000077486:Ticagrelor; D000077425:Fondaparinux; D000241:Adenosine; D000077542:Eptifibatide; D001241:Aspirin; C074619:bivalirudin; C530299:vorapaxar