title: Predictors of biochemical aspirin and clopidogrel resistance in patients with ischemic stroke.
abstract: Variable platelet response to aspirin and clopidogrel is a well-established phenomenon in patients with coronary artery disease. We sought to determine the predictors of an impaired biochemical response to aspirin and clopidogrel in patients with ischemic stroke. Patients with established cerebrovascular disease who underwent an aspirin/clopidogrel response panel (ie, light transmittance aggregometry) between June 2003 and March 2007 were identified through an electronic database. The medical records of these patients were retrospectively reviewed, and demographic characteristics, medical history, and laboratory results were recorded. Univariate and multivariate logistic regression analyses were performed to assess for factors associated with antiplatelet resistance. Of the 465 patients included in this study, 120 (28%) were biochemical aspirin nonresponders and 83 (28%) were biochemical clopidogrel nonresponders. Of the 270 patients on dual antiplatelet therapy, 25 (9.3%) were dual biochemical nonresponders. In binary logistic regression modeling, patients with congestive heart failure (odds ratio [OR] = 4.54; 95% confidence interval [CI] = 1.33-15.5; P = .02) and those with higher hemoglobin A1c values (OR = 1.41; 95% CI = 1.12-1.79; P = .004) had a significantly greater likelihood of having a biochemical nonresponse to aspirin therapy. African-American patients (OR = 2.19; 95% CI = 1.23-3.91; P < .007) were significantly more likely to be nonresponders to clopidogrel. This preliminary study shows that aspirin and clopidogrel biochemical nonresponse frequently occurs in ischemic stroke patients. In addition, some associated variables may affect the biochemical response to antiplatelet therapy. Further study is needed to explore whether this nonresponse has an impact on clinical outcomes.
authors.affiliation: Department of Neurology, Cleveland Clinic Neurological Institute, Cleveland, Ohio, USA.
authors.forename: Joanna
authors.initials: J
authors.lastname: Fong
authors.forename: Esteban
authors.initials: E
authors.lastname: Cheng-Ching
authors.forename: Muhammad Shazam
authors.initials: MS
authors.lastname: Hussain
authors.forename: Irene
authors.initials: I
authors.lastname: Katzan
authors.forename: Rishi
authors.initials: R
authors.lastname: Gupta
mesh_terms: D001741:Black or African American / Q000706:statistics & numerical data; D000368:Aged; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000097:blood / Q000188:drug therapy* / Q000208:ethnology; D000077144:Clopidogrel; D004351:Drug Resistance; D004359:Drug Therapy, Combination; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006333:Heart Failure / Q000097:blood / Q000150:complications; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D009820:Ohio; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000188:drug therapy* / Q000208:ethnology; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D001241:Aspirin; D015415:Biomarkers; D000077144:Clopidogrel; D006442:Glycated Hemoglobin; D010975:Platelet Aggregation Inhibitors; D013988:Ticlopidine; C517652:hemoglobin A1c protein, human