The results of this study suggest that Th17 are related to the late stages of CAS but not to plaque instability. Moreover, Treg expansion seems to represent a specific cellular pattern displayed by patients with symptomatic CAS and associated with brain injury. KEY MESSAGES Tregs expansion seems to represent a specific cellular pattern displayed by patients with symptomatic CAS and associated with CD4+ effector depletion and brain ischemic injury. Th17 lymphocytes are related to the late stages of CAS but not to plaque instability.
C-CEA has the same rate of postoperative hypertension of standard-CEA, which is probably related to the sparing of baroreceptor apparatus, compared to standard E-CEA. The Chevalier procedure could represent an E-CEA technique with its inherent advantages, without penalties related to postoperative hypertension, commonly observed after E-CEA.
The aim of this study was to evaluate fibroblast growth factor (FGF)-23 serum levels and its tissue expression in patients with critical carotid artery stenosis (CAS). We selected 35 patients with critical CAS undergoing carotid thromboendoarterectomy. In each patient, FGF-23 serum levels were evaluated just prior to the surgery (t0) and 30 min (t1) thereafter. Moreover, macrophage cytokines were measured at baselines. Carotid artery specimens were used for immune histochemistry. On the basis of the histology, the patients were divided into 2 groups: A with complicated plaque and B with uncomplicated plaque. Twenty complicated plaques (57.14%, group A,) and 15 uncomplicated (42.86%, group B) were evaluated: calcifications were present in 16/20 (80%) complicated plaques and in 6/15 (40%) uncomplicated plaques. An inflammatory infiltrate was observed in 26/35 carotid samples: 18/26 (69.23%) complicated and 8/26 (30.76%) uncomplicated. FGF-23(+) cells were present in 17/20 complicated (85%) and in 8 uncomplicated (53%) plaques. The double-staining immunofluorescence confirmed that macrophage cells (CD68(+)) were also positive for FGF-23 staining. Serum levels of FGF-23 were significantly higher in group A versus group B at t0 (p < 0.05) and t1 (p 0.0047). Moreover, in group A patients a significant increase of FGF-23 serum levels was observed at t1 in comparison with t0 (p 0.0011). Our results suggest that FGF-23 acts in the late phases of atherosclerotic disease and may potentially represent a marker of complications in critical CAS.
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