title: Switching antiplatelet regimens: alternatives to clopidogrel in patients with acute coronary syndrome undergoing PCI: a review of the literature and practical considerations for the interventional cardiologist.
abstract: Dual antiplatelet therapy with aspirin plus a P2Y(12) receptor inhibitor is the cornerstone of treatment for patients with acute coronary syndrome and in those undergoing percutaneous coronary intervention. Clopidogrel is the most widely used P2Y(12) receptor inhibitor. Despite the clinical benefits associated with adjunctive clopidogrel therapy, a considerable number of patients continue to experience recurrent cardiovascular events. Importantly, the interindividual response to clopidogrel is variable and is affected by multiple factors, including genetic polymorphisms and drugs that interfere with the conversion of clopidogrel to its active metabolite. The individual variability to clopidogrel-induced antiplatelet effects has significant clinical implications that can result in an increased risk of atherothrombotic recurrences, including stent thrombosis. The introduction of novel P2Y(12) receptor inhibitors, such as prasugrel or ticagrelor, characterized by more potent and consistent platelet inhibitory effects, represents an opportunity for clinicians to consider these alternative therapies to overcome the limitations of clopidogrel. Understanding the strategies and implications of switching antiplatelet treatment regimens is, therefore, key in the clinical setting. This article provides an overview of the literature on switching antiplatelet treatment strategies and practical considerations for the interventional cardiologist.
authors.affiliation: Division of Cardiology, University of Florida College of Medicine, Jacksonville, Florida 32209, USA.
authors.forename: Shahdad
authors.initials: S
authors.lastname: Azmoon
authors.forename: Dominick J
authors.initials: DJ
authors.lastname: Angiolillo
mesh_terms: D054058:Acute Coronary Syndrome / Q000628:therapy*; D000241:Adenosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D000077144:Clopidogrel; D003328:Coronary Thrombosis / Q000209:etiology / Q000517:prevention & control; D004347:Drug Interactions; D057915:Drug Substitution; D004359:Drug Therapy, Combination; D006801:Humans; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D010597:Pharmacogenetics; D010879:Piperazines / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000493:pharmacokinetics / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D000068799:Prasugrel Hydrochloride; D058921:Purinergic P2Y Receptor Antagonists / Q000009:adverse effects / Q000493:pharmacokinetics / Q000627:therapeutic use*; D013876:Thiophenes / Q000627:therapeutic use; D000077486:Ticagrelor; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000493:pharmacokinetics / Q000627:therapeutic use; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D010879:Piperazines; D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D013876:Thiophenes; D000077144:Clopidogrel; D000068799:Prasugrel Hydrochloride; D000077486:Ticagrelor; D000241:Adenosine; D013988:Ticlopidine; D001241:Aspirin