Objective: To investigate the changes of platelet-leukocyte aggregation (PLA) in patients with cerebral infarction and the effects of antiplatelet agents on it.
Methods: The levels of plasma soluble P-selectin (sP-sel), serum C-reactive protein (CRP), platelet aggregation rate (PAR) and PLA were measured in 40 patients with acute cerebral infarction and 20 cases of controls. The 40 patients with cerebral infarction were randomly divided into aspirin-treated group (20 cases) and clopidogrel-treated group (20 cases) scandinavian neurological stroke score (SNSS), plasma sP-sel, serum CRP, PAR and PLA were observed before and after the treatment.
Results: Compared with controls, the percentage of monocyte-platelet aggregation (PMA) was significantly increased in the patients (P < 0.001). The level of plasma sP-sel, serum CRP and PAR in the case group were significantly greater than those in the control group (P < 0.05). The level of PMA was positively related with the plasma sP-sel, serum CRP and PAR in cerebral infarction patients before treatment (P < 0.05), and it showed a significant inverse correlation between the percentage of PMA and the score of SNSS (P < 0.05). After treatment, the levels of PMA and PAR were decreased in both groups of cerebral infarction patients (P < or = 0.001), and the level of PMA and PAR (ADP) in clopidogrel-treated group was lower than those in aspirin-treated group (P < 0.05). However, the CRP in the patients was no significant difference before and after treatment. The level of sP-sel was no significant difference before and after treatment in aspirin-treated group, but it was significantly decreased after treatment in clopidogrel-treated group (P < 0.001).
Conclusions: The levels of PMA in patients with cerebral infarction was significantly higher than in the controls. PMA may be a sensitive marker of platelet activation. Aspirin and Clopidogrel could decline the level of PMA in the patients with acute cerebral infarction, and Clopidogrel was more effective than aspirin in inhibiting the activation of platelet.