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Published on: March 1, 2024
Atherosclerosis in Psoriatic Arthritis: A Multiparametric Analysis Using Imaging Technique and Laboratory Markers of
Nidhi Garg1, Pawan Krishan1, Ashit Syngle2
1Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India.
Insights
Psoriatic arthritis (PsA) patients show higher carotid intima-media thickness (CIMT) and impaired vascular function, indicating accelerated atherosclerosis. Inflammation and endothelial dysfunction markers are elevated, contributing to cardiovascular disease risk in PsA.
Area of Science:
- Rheumatology and Cardiovascular Medicine
- Immunology and Vascular Biology
Background:
- Cardiovascular disease is a major cause of mortality in psoriatic arthritis (PsA).
- The mechanisms driving accelerated atherosclerosis in PsA are not fully understood.
- Endothelial dysfunction (ED) is an early indicator of atherosclerosis.
Purpose of the Study:
- To evaluate carotid intima-media thickness (CIMT) as a marker of atherosclerosis in PsA.
- To assess CIMT in relation to inflammatory markers and vascular function indicators in PsA patients.
Main Methods:
- A cross-sectional study comparing 18 PsA patients with 18 matched controls.
- Measurements included carotid intima-media thickness (CIMT), flow-mediated dilatation (FMD), endothelial progenitor cells (EPCs), and various inflammatory markers (ESR, CRP, IL-1, IL-6, TNF-α).
- Vascular dysfunction markers such as intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were also analyzed.
Main Results:
- PsA patients exhibited significantly higher CIMT compared to controls (p < 0.01).
- PsA patients showed significantly reduced FMD, EPCs, and high-density lipoproteins (HDL) cholesterol (p < 0.05).
- Elevated levels of ESR, CRP, TNF-α, IL-6, ICAM-1, and VCAM-1 were observed in PsA patients.
Conclusions:
- PsA is associated with endothelial dysfunction and accelerated atherosclerosis, evidenced by impaired FMD and increased CIMT.
- Inflammatory pathways (TNF-α, IL-6) and vascular markers (CRP, ICAM-1, EPCs) are implicated in PsA's vascular disease.
- Cytokine-driven inflammation may contribute to endothelial dysfunction and increased CIMT in PsA through adhesion molecule upregulation and EPC depletion.
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]-α), 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-α, 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-α, 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.
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