I Mattiasson1, S Lethagen, A Hillarp. 1. Department of Vascular Diseases, University Hospital, Malmö, Sweden. ingrid.mattiasson@skane.se
Abstract
AIM: Antiplatelet therapy in order to reduce the platelet aggregability is widely used to prevent recurrent stroke events. Data from several studies indicates that the inter-individual variation concerning the ability of standard doses of aspirin to inhibit platelet aggregation is substantial. The rationale of the present study was to test whether platelet aggregation in whole blood was enhanced in subjects that had suffered an ischemic stroke event under aspirin treatment. METHODS: Two groups of patients were included: 1) patients that have suffered 1 stroke event and were thereafter under continuous treatment with aspirin 75-160 mg once daily (n=17); 2) patients that have suffered at least 2 stroke events, and aspirin 75-160 mg was prescribed after the 1(st) event (n=17). Platelet aggregation was tested in whole blood with collagen (5 microg/mL and 1 microg/mL), ADP (5 microMol/L) and arachidonic acid (0.5 microg/mL). Aggregation was recorded as change in impedance and release of ATP after the addition of a luciferin-luciferase reagent. RESULTS: The inhibitory effect of aspirin tested with arachidonic acid as an agonist was complete in all the tested subjects. Aggregation induced by ADP 5 microMol/L was significantly higher in the subjects with recurrent stroke compared to those with a single stroke, when tested as impedance change. ATP release with ADP as an agonist was the same in both groups. CONCLUSION: The present study gives some indication that differences in ADP-induced aggregation, with a higher remaining aggregating ability after ASA treatment, might be of importance for the risk of stroke recurrence.
AIM: Antiplatelet therapy in order to reduce the platelet aggregability is widely used to prevent recurrent stroke events. Data from several studies indicates that the inter-individual variation concerning the ability of standard doses of aspirin to inhibit platelet aggregation is substantial. The rationale of the present study was to test whether platelet aggregation in whole blood was enhanced in subjects that had suffered an ischemic stroke event under aspirin treatment. METHODS: Two groups of patients were included: 1) patients that have suffered 1 stroke event and were thereafter under continuous treatment with aspirin 75-160 mg once daily (n=17); 2) patients that have suffered at least 2 stroke events, and aspirin 75-160 mg was prescribed after the 1(st) event (n=17). Platelet aggregation was tested in whole blood with collagen (5 microg/mL and 1 microg/mL), ADP (5 microMol/L) and arachidonic acid (0.5 microg/mL). Aggregation was recorded as change in impedance and release of ATP after the addition of a luciferin-luciferase reagent. RESULTS: The inhibitory effect of aspirin tested with arachidonic acid as an agonist was complete in all the tested subjects. Aggregation induced by ADP 5 microMol/L was significantly higher in the subjects with recurrent stroke compared to those with a single stroke, when tested as impedance change. ATP release with ADP as an agonist was the same in both groups. CONCLUSION: The present study gives some indication that differences in ADP-induced aggregation, with a higher remaining aggregating ability after ASA treatment, might be of importance for the risk of stroke recurrence.
Authors: Nadia A V Motta; Milla M Fumian; Renata F Medeiros; Gabriel F Lima; Christianne B V Scaramello; Karen J Oliveira; Antonio C L Nóbrega; Fernanda C F Brito Journal: Int J Endocrinol Date: 2019-01-06 Impact factor: 3.257