title: Stent thrombosis is associated with an impaired response to antiplatelet therapy.
abstract: OBJECTIVE
  We sought to evaluate the response to antiplatelet therapy in patients with stent thrombosis (ST).
  
  
  BACKGROUND
  Stent thrombosis is associated with considerable morbidity and mortality. An impaired response to antiplatelet therapy might be related to an increased risk for ST.
  
  
  METHODS
  Eighty-two patients were included in the present study: 23 patients with previous ST, 50 matched controls (coronary stenting without ST), and 9 healthy volunteers. Platelet aggregation (PA) was studied (optical aggregometry) under monotherapy with acetylsalicylic acid (ASA) 100 mg daily for one month, followed by dual therapy with ASA 100 mg and clopidogrel 75 mg daily (loading dose 300 mg) for another month.
  
  
  RESULTS
  Maximal (5 and 20 micromol) adenosine diphosphate-induced PA was significantly higher in patients with ST compared with controls (5 micromol, p < 0.005; 20 micromol, p < 0.05) and volunteers (5 micromol, p < 0.005; 20 micromol, p < 0.05). Resistance to ASA (>20% aggregation with 0.5 mg/ml arachidonic acid) was more prevalent in patients with ST (48%) compared with control patients (32%, p = ns) and volunteers (0%, p = 0.01). Clopidogrel significantly reduced PA in all three groups, but intergroup differences persisted. Clopidogrel resistance (<10% relative change) was similar in patients with ST, control patients, and volunteers (4%, 6%, and 11%, respectively, all p = NS). However, combined ASA and clopidogrel resistance was more prevalent in patients with ST (52%) compared with controls (38%, p = NS) and volunteers (11%, p < 0.05).
  
  
  CONCLUSIONS
  Patients with previous ST show an impaired response to antiplatelet therapy with ASA compared with controls and volunteers. Additional treatment with clopidogrel is not able to overcome these differences in PA. Acetylsalicylic acid but not clopidogrel resistance appears to be associated with ST.
authors.affiliation: Department of Cardiology, Swiss Cardiovascular Center, University Hospital, Bern, Switzerland.
authors.forename: Peter
authors.initials: P
authors.lastname: Wenaweser
authors.forename: Janine
authors.initials: J
authors.lastname: Dörffler-Melly
authors.forename: Katja
authors.initials: K
authors.lastname: Imboden
authors.forename: Stephan
authors.initials: S
authors.lastname: Windecker
authors.forename: Mario
authors.initials: M
authors.lastname: Togni
authors.forename: Bernhard
authors.initials: B
authors.lastname: Meier
authors.forename: Andre
authors.initials: A
authors.lastname: Haeberli
authors.forename: Otto M
authors.initials: OM
authors.lastname: Hess
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000077144:Clopidogrel; D003327:Coronary Disease / Q000628:therapy*; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D012189:Retrospective Studies; D015607:Stents / Q000009:adverse effects*; D013927:Thrombosis / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D013988:Ticlopidine / Q000008:administration & dosage* / Q000031:analogs & derivatives*
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine