Background Patients with rheumatoid arthritis (RA) are at higher risk of cardiovascular (CV) disease. Emerging evidence suggests that this accelerated risk is present in the early stages of RA.
Objectives Our objective was to describe the CV profile of those with a new diagnosis of inflammatory arthritis (IA).
Methods 339 patients (pts) with IA enrolled into the Inflammatory Arthritis disease CONtinuum (IACON) registry in Leeds were assessed for known CV disease (CVD) and CV risk factors (RFs) including; hypertension, diabetes, smoking, family history of CVD, blood pressure, body mass index, waist/hip circumference and lipid profile. In a sub-group of those meeting ACR RA criteria (n=92); insulin resistance (homeostasis model assessment of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI)) and NT-proBNP were measured. Pts were split into 3 groups; RA1; pts meeting 1987 ACR RA criteria (n=143, 42%), RA2; pts meeting 2010 ACR RA criteria (n=55, 16%) and UIA; those not meeting either ACR criteria for RA i.e. undifferentiated IA (n=141, 42%). Descriptive statistics and analysis for correlation, chi-squared and ANOVA tests were performed.
Results Positivity for RF (p<0.001), ACPA (p<0.001) and presence of erosions (p<0.014) were more frequently observed in RA1, along with a higher DAS28-CRP score (p<0.001). There were no significant differences across the groups for age, gender or symptom duration (median (IQR); 6 (4-12), 5 (4-8), 6 (3-12) months respectively).
No differences in the prevalence of traditional CV RFs, overt CVD or metabolic syndrome (according to WHO and IDF criteria) were seen. Hypertension was prevalent across all groups (28, 27 and 25% respectively). There was a trend to significance in the prevalence of hypercholesterolaemia (26, 13 and 17% respectively, p=0.067). Similar proportions of pts within the groups were receiving anti-hypertensive, anti-platelet and lipid-lowering (LLT) therapies.
Total cholesterol (TC) was lower in RA1 vs. RA2 (p=0.041) but this lost significance when results were adjusted for CRP. There was no significant difference in TC/HDL ratio. In RA1 and RA2, TC and LDL negatively correlated with CRP (p=0.003, rho=-0.402 and p=0.041, rho=-0.28 respectively), and TC/HDL ratio and HDL showed no association with CRP.
Pts ACPA+ve were more likely to be smokers (27 vs. 19% ACPA–ve, p=0.016), have a past history of hypercholesterolaemia (25 vs. 15% ACPA-ve, p=0.029) and be receiving LLT (21 vs. 12% ACPA-ve, p=0.042). However, there was no significant difference in the lipid profile, even with adjustment for CRP and pts receiving LLT excluded.
There was no significant difference in HOMA-IR, QUICKI and NT-proBNP between RA1 and RA2 or according to ACPA status.
Conclusions Within this cohort of early IA CV RFs are prevalent, correlating with inflammation and not just a specific phenotype of RA. This supports the hypothesis that inflammation plays a key role in the known accelerated CV risk in RA, and effective treatment across the continuum is important. There may be an association between ACPA and lipid metabolism. Long-term follow-up is required to evaluate potential change in risk profile with effective disease modifying treatment.
Disclosure of Interest L.-A. Bissell: None Declared, A. Burska: None Declared, S. Horton: None Declared, H. Donica: None Declared, J. Freeston: None Declared, M. Buch Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, P. Emery Consultant for: Abbot, Pfizer, Roche, Chugai, BMS, UCB, MSD, J. Andrews: None Declared