title: Clopidogrel resistance and the effect of combination cilostazol in patients with ischemic stroke or carotid artery stenting using the VerifyNow P2Y12 Assay.
abstract: OBJECTIVE
  The inhibitory response to clopidogrel considerably varies among individuals and clopidogrel resistance is a risk factor for thrombotic events in patients with cardiovascular disease. Based on the platelet aggregation evaluated by the VerifyNow P2Y12 Assay, the present study investigated clopidogrel resistance and the effect of cilostazol addition.
  
  
  METHODS
  We measured the ability of 20 µM ADP to aggregate platelets using the VerifyNow P2Y12 Assay. Clopidogrel resistance was defined as % inhibition of <20% in this assay.
  
  
  METHODS
  We examined 77 patients (53 men and 24 women, aged 65.8 ± 9.9 years) with ischemic stroke or carotid artery stenting who received clopidogrel (75 mg) for >7 days at our hospital between October 2009 and March 2010. For 62 patients (42 men and 20 women, aged 65.3 ± 9.9 years) 75 mg clopidogrel alone was administered (clopidogrel only group); the other 15 patients (11 men and 4 women, aged 67.9 ± 9.9 years) received 75 mg of clopidogrel plus 100 or 200 mg of cilostazol (cilostazol combination group).
  
  
  RESULTS
  Clopidogrel resistance was identified in 18 (29%) of the 62 patients in the clopidogrel only group. The percent inhibition was significantly higher in the cilostazol combination group than in the clopidogrel only group (41.7 ± 28.0% vs. 64.9 ± 22.7%, p=0.005). None of the patients in the cilostazol combination group had % inhibition of <20%.
  
  
  CONCLUSIONS
  Clopidogrel resistance developed in 29% of patients given clopidogrel alone. The addition of cilostazol to clopidogrel may have intensified platelet inhibition.
authors.affiliation: Department of Neurology, International Medical Center, Saitama Medical University, Japan. hmaruyam@saitama-med.ac.jp
authors.forename: Hajime
authors.initials: H
authors.lastname: Maruyama
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Takeda
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Dembo
authors.forename: Harumitsu
authors.initials: H
authors.lastname: Nagoya
authors.forename: Yuji
authors.initials: Y
authors.lastname: Kato
authors.forename: Takuya
authors.initials: T
authors.lastname: Fukuoka
authors.forename: Ichiro
authors.initials: I
authors.lastname: Deguchi
authors.forename: Yohsuke
authors.initials: Y
authors.lastname: Horiuchi
authors.forename: Norio
authors.initials: N
authors.lastname: Tanahashi
mesh_terms: D000368:Aged; D001780:Blood Coagulation Tests / Q000379:methods*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D002340:Carotid Artery Diseases / Q000517:prevention & control* / Q000628:therapy; D000077407:Cilostazol; D000077144:Clopidogrel; D004351:Drug Resistance; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D058921:Purinergic P2Y Receptor Antagonists / Q000494:pharmacology; D012189:Retrospective Studies; D055502:Secondary Prevention; D015607:Stents; D020521:Stroke / Q000503:physiopathology / Q000517:prevention & control*; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use*; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D013777:Tetrazoles; D000077144:Clopidogrel; D000077407:Cilostazol; D013988:Ticlopidine