title: Genetically Determined Platelet Reactivity and Related Clinical Implications.
abstract: Many drugs are nowadays available to inhibit platelet activation and aggregation, especially in patients with acute coronary syndromes and undergoing percutaneous coronary intervention with stent implantation. Primary targets are represented by enzymes or receptors involved in platelet activation. Genetic mutations in these targets contribute to the inter-individual variability in platelet responses therefore weakening the efficacy of antiplatelet agents. High on treatment platelet reactivity is a condition characterized by low levels of platelet inhibition despite the use of antiplatelet drugs. This could be responsible for re-infarction, stent-thrombosis and strokes, affecting short and long-term prognosis after coronary revascularization. So far, to test antiplatelet resistance either the assessment of platelet function or the identification of genetic carriers of poly morphisms have been pursued. Although several methods are now available to test platelet reactivity, it is still debated whether its routine assessment gives real benefits in clinical practice. The present review aims at examining current evidences on genetic polymorphisms affecting optimal platelet inhibition.
authors.affiliation: Divisione di Cardiologia, Dipartimento di Scienze Biomediche Avanzate, Università Federico II Napoli, Naples, Italy.
authors.forename: Teresa
authors.initials: T
authors.lastname: Strisciuglio
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Di Gioia
authors.forename: Chiara
authors.initials: C
authors.lastname: De Biase
authors.forename: Massimiliano
authors.initials: M
authors.lastname: Esposito
authors.forename: Danilo
authors.initials: D
authors.lastname: Franco
authors.forename: Bruno
authors.initials: B
authors.lastname: Trimarco
authors.forename: Emanuele
authors.initials: E
authors.lastname: Barbato
mesh_terms: D001792:Blood Platelets / Q000187:drug effects* / Q000502:physiology; D000077144:Clopidogrel; D065731:Cytochrome P-450 CYP2C19 / Q000235:genetics* / Q000378:metabolism; D004351:Drug Resistance / Q000235:genetics*; D006801:Humans; D008562:Membrane Glycoproteins / Q000235:genetics*; D009154:Mutation; D015539:Platelet Activation / Q000187:drug effects / Q000235:genetics*; D010973:Platelet Adhesiveness / Q000235:genetics; D010974:Platelet Aggregation / Q000187:drug effects / Q000235:genetics; D010975:Platelet Aggregation Inhibitors / Q000378:metabolism / Q000494:pharmacology*; D011110:Polymorphism, Genetic; D011942:Receptors, Adrenergic, alpha / Q000235:genetics; D011943:Receptors, Adrenergic, beta / Q000235:genetics; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology
chemical_list: D008562:Membrane Glycoproteins; D010975:Platelet Aggregation Inhibitors; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D000077144:Clopidogrel; D065731:Cytochrome P-450 CYP2C19; D013988:Ticlopidine