Abstract 5497: Platelet Activation in Patients Undergoing Carotid Artery Stenting Procedure
Background. Carotid Artery Stenting (CAS) is an evolving method to treat carotid stenosis. A limitation of CAS is the periprocedural risk of temporary or permanent ischemic neurological deficits resulting from local thrombosis and distal embolization. Platelet activation in CAS occurs as a result of vessel wall damage and subendothelium exposure. The dual antiplatelet regimen (aspirin+thienopyridine) has a significant impact on reducing adverse neurological outcomes.
Aim. To analyze platelet activation during dual antiplatelet therapy and two months after thienopyridine discontinuation in patients who underwent CAS procedure.
Methods. We enrolled 40 patients with high-grade carotid artery stenosis (≥ 70% NASCET criteria). Blood was withdrawn 1 day before (T0), 1 (T1) and 30 days (T2) after CAS and 2 months after thienopyridine discontinuation (T3). Platelet activation markers (PAC1, CD62 and Tissue Factor [TF] and the percentage of monocyte-platelet aggregates [MPA]) were assessed by whole blood flow cytometry in resting conditions and upon in vitro ADP stimulation and reported as %UR. As a comparison, platelet activation in 16 healthy subjects was also analyzed (Controls).
Results. In resting conditions, CD62 and PAC1 positive platelets and MPA were constant throughout the time points examined (average T0-T3: 0.22±0.02, 0.16±0.01, 9.51±0.68 respectively) and similar to those found in Controls. In vitro ADP-induced CD62, PAC1 and MPA levels were significantly higher at T3 when thienopyridine was discontinued compared to T0, T1 and T2 and similar to that observed in Controls. Levels of TF positive platelets were constant, in resting conditions, throughout the time points examined (average T0-T3: 5.04±0.43), but 3 fold higher that those found in Controls (1.95±0.56, p<0.01). Drug treatment does not inhibit ADP-induced TF expression being the values similar to those found in Controls.
Conclusions. Significant higher levels, compared to Controls, of TF-positive platelets circulating in peripheral blood of CAS patients. Dual antiplatelet therapy inhibits the expression of all ADP-induced platelet activation markers, but TF. This prothrombotic platelet phenotype may have implications for CAS complications.