scholarly journals Monocyte Subsets, Stanford-A Acute Aortic Dissection, and Carotid Artery Stenosis: New Evidences

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Noemi Cifani ◽  
Maria Proietta ◽  
Maurizio Taurino ◽  
Luigi Tritapepe ◽  
Flavia Del Porto
Keyword(s):  
Carotid Artery ◽  
Aortic Dissection ◽  
Carotid Artery Stenosis ◽  
Acute Aortic Dissection ◽  
Group Versus ◽  
Artery Stenosis ◽  
Monocyte Subset ◽  
Monocyte Subsets ◽  
Cd4 Lymphocyte ◽  
Classical Monocytes

Monocytes are a heterogeneous cell population distinguished into three subsets with distinctive phenotypic and functional properties: “classical” (CD14++CD16-), “intermediate” (CD14++CD16+), and “nonclassical” (CD14+CD16++). Monocyte subsets play a pivotal role in many inflammatory systemic diseases including atherosclerosis (ATS). Only a low number of studies evaluated monocyte behavior in patients affected by cardiovascular diseases, and data about their role in acute aortic dissection (AAD) are lacking. Thus, the aim of this study was to investigate CD14++CD16-, CD14++CD16+, and CD14+CD16++ cells in patients with Stanford-A AAD and in patients with carotid artery stenosis (CAS).Methods. 20 patients with carotid artery stenosis (CAS group), 17 patients with Stanford-A AAD (AAD group), and 17 subjects with traditional cardiovascular risk factors (RF group) were enrolled. Monocyte subset frequency was determined by flow cytometry.Results. Classical monocytes were significantly increased in the AAD group versus CAS and RF groups, whereas intermediate monocytes were significantly decreased in the AAD group versus CAS and RF groups.Conclusions. Results of this study identify in AAD patients a peculiar monocyte array that can partly explain depletion of T CD4+ lymphocyte subpopulations observed in patients affected by AAD.

Abstract 113: Platelet and Monocyte Activity in Carotid Artery Stenosis Treated with Carotid Endarterectomy

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Arvind Reddy Devanabanda ◽  
Caron Rockman ◽  
Nicole Allen ◽  
Maya Rubin ◽  
Binita Shah ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Endarterectomy ◽  
Carotid Artery Stenosis ◽  
Healthy Subjects ◽  
Artery Stenosis ◽  
Monocyte Subsets ◽  
Platelet Activity ◽  
Platelet Surface ◽  
Inflammatory Monocytes ◽  
Anti Inflammatory

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.

scholarly journals Monocyte Subsets and Related Chemokines in Carotid Artery Stenosis and Ischemic Stroke

2016 ◽  
Vol 17 (4) ◽  
pp. 433 ◽  
Author(s):  
Gerrit Grosse ◽  
Walter Schulz-Schaeffer ◽  
Omke Teebken ◽  
Ramona Schuppner ◽  
Meike Dirks ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Monocyte Subsets

Oxidative injury associated with stenting of asymptomatic carotid artery stenosis

VASA ◽  
2017 ◽  
Vol 46 (4) ◽  
pp. 268-274
Author(s):  
Erhan Saraçoğlu ◽  
Ertan Vuruşkan ◽  
Yusuf Çekici ◽  
Salih Kiliç ◽  
Halil Ay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carotid Artery ◽  
Oxidative Damage ◽  
Carotid Artery Stenosis ◽  
Artery Stenosis ◽  
Oxidative Stress Marker ◽  
Asymptomatic Carotid ◽  
Imaging Methods ◽  
Neurological Findings ◽  
Asymptomatic Carotid Artery Stenosis

Abstract. Background: After carotid artery stenting (CAS), neurological complications that cannot be explained with imaging methods may develop. In our study we aimed to show, using oxidative stress markers, isolated oxidative damage and resulting neurological findings following CAS in patients with asymptomatic carotid artery stenosis. Patients and methods: We included 131 neurologically asymptomatic patients requiring CAS. The neurological findings were evaluated using the modified Rankin Scale (mRS) prior to the procedure, one hour post-procedure, and two days after. Patients with elevated mRS scores but with or without typical hyperintense lesions observed on an MRI and with changes of oxidative stress marker levels at the time (Δtotal-thiol, Δtotal antioxidative status [TAS], and Δtotal oxidant status [TOS]) were evaluated. Results: In the neurological examination carried out one hour prior to the procedure, there were 92 patients with mRS = 0, 20 with mRS = 1, and 12 with mRS = 2. When Δtotal-thiol, ΔTAS, and ΔTOS values and the mRS were compared, it was observed that as the difference in oxidative parameters increased, clinical deterioration also increased proportionally (p = 0.001). Conclusions: We demonstrate a possible correlation between oxidative damage and neurological findings after CAS which could not be explained by routine imaging methods.

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