BACKGROUND AND PURPOSE: We examined the effect of ticlopidine hydrochloride on the enhanced erythrocyte aggregability in 14 patients with cerebral infarction during the chronic phase (over 1 month after onset). SUMMARY OF REPORT: Ticlopidine (100 mg BID) was administered for 8 weeks. We measured the rate of erythrocyte aggregation (aggregability), using the whole-blood erythrocyte aggregometer that we developed, before and at 4 and 8 weeks after the initiation of ticlopidine administration. Concomitant measurements were made of such blood factors as the hematocrit, albumin-globulin ratio, and fibrinogen concentration. The erythrocyte aggregation rates before and at 4 and 8 weeks after were 0.147 +/- 0.017/s, 0.138 +/- 0.019/s, and 0.133 +/- 0.017/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly lower (P < .05 by Bonferroni's modified t test) than those before ticlopidine administration. At 4 and 8 weeks after the initiation of ticlopidine treatment, the hematocrit value and concentration of fibrinogen were also significantly (P < .05) reduced. CONCLUSIONS: Our results suggest that ticlopidine can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.
BACKGROUND AND PURPOSE: We examined the effect of ticlopidine hydrochloride on the enhanced erythrocyte aggregability in 14 patients with cerebral infarction during the chronic phase (over 1 month after onset). SUMMARY OF REPORT: Ticlopidine (100 mg BID) was administered for 8 weeks. We measured the rate of erythrocyte aggregation (aggregability), using the whole-blood erythrocyte aggregometer that we developed, before and at 4 and 8 weeks after the initiation of ticlopidine administration. Concomitant measurements were made of such blood factors as the hematocrit, albumin-globulin ratio, and fibrinogen concentration. The erythrocyte aggregation rates before and at 4 and 8 weeks after were 0.147 +/- 0.017/s, 0.138 +/- 0.019/s, and 0.133 +/- 0.017/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly lower (P < .05 by Bonferroni's modified t test) than those before ticlopidine administration. At 4 and 8 weeks after the initiation of ticlopidine treatment, the hematocrit value and concentration of fibrinogen were also significantly (P < .05) reduced. CONCLUSIONS: Our results suggest that ticlopidine can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.