Atherosclerosis in Psoriatic Arthritis: A Multiparametric Analysis Using Imaging Technique and Laboratory Markers of Inflammation and Vascular Function

Abstract

Cardiovascular disease is one of the leading causes of death in psoriatic arthritis (PsA). Pathogenesis of accelerated atherosclerosis in PsA remains to be elucidated. Endothelial dysfunction (ED) often precedes manifesting atherosclerosis. This study aims to assess carotid intima-media thickness (CIMT), a marker of atherosclerosis in PsA, in context of markers of inflammation and vascular function. A cross-sectional study was performed in 18 PsA patients who were compared with 18 controls matched for age and sex. Flow-mediated dilatation (FMD) assessed by AngioDefender (Everist Health, Ann Arbor, MI), endothelial progenitor cells (EPCs) quantified by flow cytometry and CIMT measured ultrasonographically. Inflammatory measures included disease activity score of 28 joints count and disease activity index in psoriatic arthritis. We also assayed markers of inflammation, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), proinflammatory cytokines (interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]-?), and endothelial dysfunction, including lipids, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and EPCs. CIMT is significantly higher in PsA patients compared with controls (0.062???0.18 vs. 0.045???0.10 cm, p?<?0.01) whereas FMD%, EPCs%, and high-density lipoproteins (HDL) cholesterol are significantly reduced in PsA compared with controls (p?<?0.05). Compared with controls, PsA patients had significantly increased concentrations of ESR, CRP, TNF-?, IL-6, ICAM-1, and VCAM-1. In PsA, CIMT positively correlated with IL-6 and ICAM-1 and inversely correlated with FMD, HDL, and EPCs (p?<?0.05). In PsA, FMD and CIMT were impaired, indicating endothelial dysfunction and accelerated atherosclerosis, respectively. PsA-related inflammatory mechanisms (TNF-?, IL-6) and markers of vascular function (CRP, ICAM-1, and EPCs) may all be involved in the development of vascular disease in PsA. Cytokine-triggered inflammation upregulates expression of adhesion molecules, depletes EPCs with endothelial dysfunction, and increased CIMT in PsA.

Usefullnes of atherogenic indices and Ca-LDL level to predict subclinical atherosclerosis in patients with psoriatic arthritis?

“…Similarly to our study, Gonzalez-Juanatey et al demonstrated there was no significant correlation between ESR, CRP and CIMT [14]. Garg et al observed no correlation between ESR, CRP, IL-1 and CIMT although CIMT was positively correlation with IL-6 [47].…”

Associations of IL-18 with Altered Cardiovascular Risk Profile in Psoriatic Arthritis and Ankylosing Spondylitis

“…So far, several studies have investigated factors suspected of being associated with an increased cardiovascular risk and with disease activity in patients with PsA. Among the most indicated factors were ESR, CRP [29,31], proinflammatory cytokines (TNF, IL-17, IL-1β) [32][33][34], and particular clinical symptoms such as peripheral arthritis and dactylitis [31,35]. Interestingly, none of these factors seemed to be connected directly to a highly proatherogenic metabolic profile in PsA.…”

Systemic Inflammatory Response and Atherosclerosis: The Paradigm of Chronic Inflammatory Rheumatic Diseases

“…Regarding SLE, data is more limited, but studies have shown increased levels of certain soluble endothelial damage biomarkers, such as ICAM-1 and thrombomodulin (TM) in SLE women and VCAM-1 in patients with lupus nephritis [ 126 , 127 ] Similarly, AS studies indicate that increased levels of ICAM-1, TM and IL-6, as well as increased ADMA serum concentrations are not correlated however with disease activity [ 128 , 129 , 130 ]. In PsA, both ICAM-1 and VCAM-1 levels have been found to be increased compared to controls and ICAM and IL6 were correlated with Cimt [ 131 , 132 ].…”