Abstract
Accelerated atherosclerosis has become a major problem in rheumatic inflammatory disease. The aim here was to analyze carotid intima-media thickness (IMT) in spondyloarthritis (SpA) patients and correlate this with clinical parameters and inflammatory markers. Cross-sectional analytical study at Rheumatology Outpatient Clinic, Evangelical University Hospital, Curitiba. IMTs (measured using Doppler ultrasonography) of 36 SpA patients were compared with controls. The IMT in SpA patients was associated with inflammatory markers, like erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI); and with clinical parameters, like axial or peripheral involvement, dactylitis, HLA B27, uveitis occurrence, Bath Ankylosing Spondylitis Functional Index (BASFI) and lipid profile. The mean IMT in SpA patients was 0.72 ± 0.21 mm; in controls, 0.57 ± 0.13 mm (P = 0.0007). There were no associations with ESR, CRP, BASDAI or clinical data. In univariate analysis, greater IMT was seen in patients with longer disease duration (P = 0.014; Pearson R = 0.40; 95% confidence interval, CI = 0.06 to 0.65); higher triglycerides (P = 0.02; Spearman R = 0.37; 95% CI = 0.03 to 0.64); and older age (P = 0.0014; Pearson R 0.51; 95% CI = 0.21 to 0.72). SpA patients have a higher degree of subclinical atherosclerosis than in controls, thus supporting clinical evidence of increased cardiovascular risk in rheumatic patients.
Highlights
Chronic inflammatory rheumatic diseases are considered nowadays to present a risk of cardiovascular events and increased cardiovascular mortality.[1]
We found that 90.62% had axial involvement, 53.12% entheseal involvement, 50% peripheral arthritis, 25% uveitis and none dactylitis
52.7% were using non-steroidal anti-inflammatory drugs; 11.1% were on methotrexate; 38.8% were using sulphasalazine, 19.4% were carotid intima-media thickness (IMT)
Summary
Chronic inflammatory rheumatic diseases are considered nowadays to present a risk of cardiovascular events and increased cardiovascular mortality.[1] Circulating mediators such as interleukin (IL)-6, tumor necrosis factor-alpha (TNF-alpha), C-reactive protein (CRP) and adhesion molecules secondary to rheumatic inflammatory processes contribute to all stages of atherosclerosis: from endothelial dysfunction to atheroma formation, plaque instability and thrombus development.[2]. The association between subclinical atherosclerosis and severity of inflammatory response has been clearly demonstrated in patients with rheumatoid arthritis[3,4] and systemic lupus erythematosus.[4] in relation to spondyloarthritis (SpA), studies have produced divergent results.[5,6] In this latter group of diseases, inflammatory markers do not accurately reflect the underlying pathological events. It is well known that the association between CRP levels and inflammation is lower in SpA than in rheumatoid arthritis.[7]
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