Clinical outcomes using a platelet function-guided approach for secondary prevention in patients with ischemic stroke or transient ischemic attack.
OBJECTIVE
Antiplatelet therapy nonresponse is associated with worse clinical outcomes. We studied the clinical outcomes associated with platelet function-guided modifications in antiplatelet therapy in patients with ischemic stroke or transient ischemic attack.


METHODS
From January 2005 to August 2007, 324 patients with ischemic stroke underwent platelet function testing using platelet aggregometry. Aspirin nonresponse was defined as a mean platelet aggregation ≥20% with 0.5 mg/mL arachidonic acid and/or ≥70% with 5 μmol/L adenosine diphosphate. Clopidogrel nonresponse was defined as a mean platelet aggregation ≥40% with 5 μmol/L adenosine diphosphate. A modification was any increase in antiplatelet therapy occurring after testing. Clinical outcomes were compared between patients with and without platelet function-guided antiplatelet therapy modifications using univariate and propensity score-adjusted analyses.


RESULTS
In patients with ischemic stroke or transient ischemic attack, 43% (n=128) and 35% (n=54) were nonresponders to aspirin and clopidogrel, respectively. After platelet function testing, antiplatelet therapy was increased in 23% of patients (n=73). After propensity score matching (n=61 in each group), antiplatelet therapy modification was associated with significantly increased rates of death, ischemic events, or bleeding (hazard ratio, 2.24; 95% CI, 1.12-4.47; P=0.02) compared with no modification in antiplatelet therapy and a trend toward increased bleeding (hazard ratio, 3.56; 95% CI, 0.98-12.95; P=0.05). No differences in ischemic events were observed.


CONCLUSIONS
Platelet function-guided modification in antiplatelet therapy after an ischemic stroke or transient ischemic attack was associated with significantly higher rates of adverse clinical outcomes.
VA Boston Healthcare System, 1400 VFW Parkway, Boston, MA 02132, USA.
Jeremiah P
JP
Depta
Jeffrey
J
Fowler
Eric
E
Novak
Irene
I
Katzan
Suzanne
S
Bakdash
Kandice
K
Kottke-Marchant
Deepak L
DL
Bhatt
D000244:Adenosine Diphosphate; D000368:Aged; D016718:Arachidonic Acid; D002545:Brain Ischemia / Q000097:blood / Q000453:epidemiology / Q000517:prevention & control*; D002543:Cerebral Hemorrhage / Q000453:epidemiology; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood / Q000517:prevention & control*; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D010979:Platelet Function Tests; D016016:Proportional Hazards Models; D055502:Secondary Prevention / Q000379:methods*; D020521:Stroke / Q000097:blood / Q000517:prevention & control*; D016019:Survival Analysis; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
D010975:Platelet Aggregation Inhibitors; D016718:Arachidonic Acid; D000244:Adenosine Diphosphate; D000077144:Clopidogrel; D013988:Ticlopidine