Platelet function during carotid endarterectomy and the antiplatelet effect of dextran 40

Abstract Background Dextran 40 has been shown to reduce cerebral embolization following carotid endarterectomy (CEA). This study aimed to determine changes in platelet function during CEA and the antiplatelet effect of dextran 40. Methods Platelet function was measured by whole-blood flow cytometry in the peripheral arterial blood of patients during CEA and 24 h later. The binding index of P-selectin and PAC-1 expression were measured as markers of activation and aggregation. Patients were kept on aspirin 75–150 mg until the day of surgery and received an intravenous bolus of 5000 units unfractionated heparin before carotid artery clamping. High-intensity transient signals (HITS) in the ipsilateral middle cerebral artery were measured with transcranial Doppler (TCD) ultrasonography before, during and after operation. Results are presented as median (interquartile range) and statistical significance was determined using the Mann–Whitney U test. Results Thirty-eight patients undergoing CEA were studied. The P-selectin binding index rose significantly from incision (0·9 (0·2–2·7)) after carotid clamping (1·5 (0·6–3·6); P < 0·01), clamp release (1·7 (0·3–3·0); P < 0·01), 1 h after operation (1·5 (0·3–2·6); P < 0·05) and 24 h after operation (1·3 (0·6–2·5); P < 0·05). PAC-1 binding index increased from incision (0·4 (0·1–0·8)) after carotid clamping (2·0 (0·4–4·2); P < 0·01) and clamp release (1·8 (0·3–2·9); P < 0·05). TCD monitoring showed an increase in preoperative HITS per 30 min (2 (0–3)) during dissection (8 (1–15); P < 0·05), after clamp release (16 (2–27); P < 0·01) and during recovery (10 (2–29); P < 0·01). After operation, patients with more than 50 HITS per 30 min were started on an infusion of dextran 40. Six patients had a dextran 40 infusion. The P-selectin binding index decreased from 1·6 (0·7–1·9) to 0·6 (0·3–1·5) 1 h after dextran (P < 0·05) and 0·1 (0·1–0·2) 24 h after dextran (P < 0·05). PAC-1 expression decreased from 0·4 (0·3–0·5) to 0·1 (0·1–0·1) 24 h after dextran (P < 0·05). Conclusion Significant platelet activation and aggregation occurs during CEA despite the use of antiplatelet treatment. A simultaneous increase in HITS was demonstrated with TCD. Dextran 40 was shown to have an antiplatelet effect after CEA; this is further evidence that it may have a role in reducing thromboembolic complications.