Abstract
AbstractThe aim of this study was to detect the concentrations of PCSK9 in various subclinical stages of atherosclerosis and to highlight its relationship with inflammation. One hundred and fifty-nine healthy patients were divided into three groups, based on the extent of atherosclerotic changes in the carotid artery: a group without identifiable atherosclerosis, cIMT>75‰and an asymptomatic plaque group. The PCSK9 was measured by ELISA and hsCRP by the immunoturbidimetric method. Vascular changes were identified by a carotid ultrasound. PCSK9 was elevated, when comparing the healthy group with the cIMT>75‰group; however, no significant increase was detected between cIMT>75‰and the asymptomatic plaque group. A positive linear correlation of the PCSK9 concentration and atherosclerotic changes was found; however, after the re-analysis in each group, this correlation persisted only in the group with still normal values. Additionally, a significant linear correlation was found between the PCSK9 concentrations and lipid parameters. However, no significant association was found with hsCRP. PCSK9 was found to be elevated only in cIMT>75‰, but not in the later plaque stage. A linear correlation of PCSK9 values was detected only in the group with still reference values. Based on this fact, we assumed the direct linear role of PCSK9 in initiating atherosclerosis; however, in the later phases, the relationship, which highlights other risk factors such as inflammation, is not linear.
Highlights
Atherosclerosis is an inflammatory-degenerative disease characterized by the accumulation of lipids and white blood cells and the proliferation of smooth muscle into the intima of the vascular wall
Higher weight and BMI were detected in the groups with more advanced subclinical vascular changes in comparison with carotid artery intima-media thickness (cIMT)75‰
The analysis revealed a significant effect of age, sex and Proprotein convertase subtilisin/kexin-9 (PCSK9) levels on cIMT values and assumed that PCSK9 levels may act as a significant mediator of vascular changes side by side from LDL-C
Summary
Atherosclerosis is an inflammatory-degenerative disease characterized by the accumulation of lipids and white blood cells and the proliferation of smooth muscle into the intima of the vascular wall. The lesion is called an atheroma/plaque that affects the vascular flow through the luminal constriction and, in case of rupture, can cause occlusion and ischaemia, and eventually necrotic changes in the target organ [1,2]. The recognition that dyslipidaemia is one of the most critical risk factors for cardiovascular disease has caused researchers to tightly focus on the lowering of cholesterol (LDL-C) in both primary and secondary prevention, by inhibiting formation, increased uptake or reduced resorption [3]. In addition to the lipid factors involved in the initiation and progression of atherosclerotic lesions, the inflammatory components of the atherosclerotic process are well known, and they manifest as an intravascular inflammation affecting the plaque progression and stability itself [4]. This study provided evidence of a significant reduction in the primary end
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