Background:
Carotid artery stenosis (CAS) is a marker of atherosclerosis, a disease mediated by abnormalities in platelet and monocyte function, and a significant cause of stroke. Moreover, the effect of carotid artery revascularization via carotid endarterectomy (CEA) on platelet and monocyte markers is unknown.
Objective:
This study aims to investigate platelet activity, monocyte subsets and monocyte platelet aggregates (MPA) in CAS and changes with CEA.
Methods:
This prospective cohort study evaluated 48 patients who underwent non emergent CEA. Peripheral venous blood samples were obtained before, immediately postoperative and at 24 hours postoperative. Twenty healthy subjects served as controls. Platelet surface expression of P-selectin and PAC-1, monocyte subsets, and MPA were assessed using flow cytometry. Three distinct monocyte subsets were measured: anti-inflammatory (i.e. classical CD14
++
CD16
-
) and pro-inflammatory (i.e. intermediate CD14
++
CD16
+
and nonclassical CD14
+
CD16
++
) monocytes. Differences between two matched samples and between the study and control groups were statistically analyzed.
Results:
Compared to healthy subjects, CAS subjects had significantly greater markers of platelet activity (P-selectin [p=0.003] and PAC-1 [p=0.01]), pro-inflammatory monocytes (intermediate [p<0.0001] and nonclassical [p=0.009]) and MPA (p=0.0002). Following CEA, anti-inflammatory monocytes increased and pro-inflammatory monocytes decreased (Figure 1A). Platelet expression of P-selectin and MPA did not change, while PAC-1 transiently increased but then returned to baseline by 24 hours postoperative (Figure 1B &C).
Conclusions:
Subjects with CAS have elevated markers of thrombosis, inflammation, and their interface. However, only the pro-inflammatory monocytes are significantly reduced following CEA. Future studies investigating the clinical consequences of this reduction are warranted.
Monocyte Subsets and Related Chemokines in Carotid Artery Stenosis and Ischemic Stroke