Abstract

Aspirin and clopidogrel combined irreversibly inhibits cyclooxygenase and reversibly inhibits ADP -dependent platelet aggregation. The combined effect on platelet recruitment is not described. Individual patient response to therapy is measurable. Thirty chronic ischemic stroke patients had platelet reactivity tests performed while taking aspirin alone followed by combination aspirin-clopidogrel over 3 months: ex-vivo platelet aggregation using a PAP 4 platelet aggregometer, recruitment by the method described by Valles et al., [2002] and urinary 11-dhTxB <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sub> excretion by competitive enzyme linked immunosorbent assay. Compliance was monitored. Statistical methods included analysis of variance to compare variables of inhibition of platelet aggregation and recruitment between those on aspirin alone and combination therapy and longitudinal regression analysis with time as covariate to estimate inhibition of platelet recruitment. Non-linear mapping defined variable associations and interconnections in each patient. No bleeding or recurrent stroke occurred. One patient was non-compliant. Statistically significant difference was found (1) in favor of combination therapy for inhibition of ADP and collagen-induced platelet aggregation and maximum inhibition of platelet recruitment for all methods tested, and (2) increasing inhibition of platelet recruitment over time. No statistical difference was found in urinary 11-dhTxB <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sub> excretion between aspirin resistant and non resistant patients defined by platelet aggregation. Non-linear mapping showed patient-unique variable interconnections. Platelet inhibition with combination aspirin-clopidogrel increases over time in most patients. Urinary TxB <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sub> excretion may not differentiate between aspirin resistant and non resistant patients defined by other measures of inhibition of platelet reactivity which uniquely connect in each patient.

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