Dissociation of inhibitory effects of low-dose ASA on thromboxane production and platelet aggregation in ischemic stroke patients.

Acetylsalicylic acid (ASA) inhibits thromboxane production and hence platelet aggregation. However, individual variations in platelet aggregability and serum thromboxane B2 (TxB2) concentration after a low dose of ASA (40 mg/day) have been reported. To clarify this issue, we studied plasma thromboxane levels and platelet aggregation in 43 ischemic stroke patients. Of the 22 patients who received 100 mg of ASA daily, dissociation between inhibitory effects of ASA on the plasma TxB2 level and threshold concentrations of adenosine diphosphate was found in three cases after one month of drug administration, and in three cases after six, 12 and 18 months of ASA therapy. This dissociation also developed in two patients after one month and six months, respectively, of treatment in the 21 patients who received 300 mg of ASA daily. The dissociation between the inhibitory effects on plasma TxB2 and the circulating platelet aggregate ratio was found in two cases after taking medication for one month, and in four cases after six, 12, 18 and 24 months of therapy in the 100 mg ASA group. In the 300 mg ASA group, dissociation was noted in two cases after one month of medication, and in two cases after six and 12 months of medication. In these patients, although their TxB2 levels were inhibited to almost unmeasurable levels, platelet aggregation was still not inhibited. This ASA inhibitory dissociation phenomenon on platelet function may be due to the low dose of ASA, individual differences in platelet function in response to ASA therapy, or factors other than those involved in the cyclooxygenase system.