Circulating Ageing Neutrophils as a Marker of Asymptomatic Polyvascular Atherosclerosis in Statin-Naïve Patients without Established Cardiovascular Disease

Abstract

Background: Current data on the possible involvement of aging neutrophils in atherogenesis are limited. This study aimed to research the diagnostic value of aging neutrophils in their relation to subclinical atherosclerosis in statin-naïve patients without established atherosclerotic cardiovascular diseases (ASCVD). Methods: The study was carried out on 151 statin-naïve patients aged 40–64 years old without ASCVD. All patients underwent duplex scanning of the carotid arteries, lower limb arteries and abdominal aorta. Phenotyping and differentiation of neutrophil subpopulations were performed through flow cytometry (Navios 6/2, Beckman Coulter, USA). Results: The number of CD62LloCXCR4hi-neutrophils is known to be significantly higher in patients with subclinical atherosclerosis compared with patients without atherosclerosis (p = 0.006). An increase in the number of CD62LloCXCR4hi-neutrophils above cut-off values makes it possible to predict atherosclerosis in at least one vascular bed with sensitivity of 35.4–50.5% and specificity of 80.0–92.1%, in two vascular beds with sensitivity of 44.7–84.4% and specificity of 80.8–33.3%. Conclusion: In statin-naïve patients 40–64 years old without established ASCVD with subclinical atherosclerosis, there is an increase in circulating CD62LloCXCR4hi-neutrophils. It was also concluded that the increase in the number of circulating CD62LloCXCR4hi-neutrophils demonstrated moderate diagnostic efficiency (AUC 0.617–0.656) in relation to the detection of subclinical atherosclerosis, including polyvascular atherosclerosis.

Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice

“…Furthermore, neutrophil cells can extrude their nuclear material, defined as neutrophil extracellular traps (NETs), which can bind to VSMCs and induce cell lysis and plaque destabilization [10,[90][91][92]. Data on the possible involvement of aging neutrophils in atherogenesis are limited [93]. Aged neutrophils change phenotype, form NETs, produce ROS, and consequently are involved in the development and progression of atherosclerosis [93].…”

“…Data on the possible involvement of aging neutrophils in atherogenesis are limited [93]. Aged neutrophils change phenotype, form NETs, produce ROS, and consequently are involved in the development and progression of atherosclerosis [93].…”