Background Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease associated with an increased cardiovascular (CV) risk that is already present at the time of diagnosis. However, it is unclear at what point in the period before diagnosis of RA the CV risk increases. Therefore, we assessed the 10 year risk of CV morbidity and mortality in a cohort of subjects at risk for RA and analysed associations with anti-citrullinated protein antibody (ACPA) status and arthritis development.

Methods In a cohort of 594 consecutive arthralgia patients with positivity for rheumatoid factor (RF) and/or ACPA, demographics, medical history, medication use and comorbidities were assessed. Lipid profile was determined and blood pressure was measured in a subset of patients. The 10 year CV risk score according to the Dutch CV risk management guideline (Dutch Systematic Coronary Risk Evaluations (SCORE)) was calculated for patients of whom data were complete.

Results ACPA positive subjects (n=382) were younger (mean age 48.6 vs 51.6, p=0.003), more often smokers (31.8% vs 23.9%, p=0.045) and had lower cholesterol (mean level 5.2 vs 5.5, p=0.001) and HDL (mean level 1.1 vs 1.2, p=0.004) than ACPA negative subjects. Subjects who developed arthritis (n=205) had lower cholesterol (mean level 5.2 vs 5.4, p=0.008) and HDL levels (mean level 1.0 vs 1.2, p=0.001) and a higher TC/HDL ratio (median ratio 5.2 vs 4.8, p=0.047) compared to subjects who did not develop arthritis. Lower cholesterol (OR 1.24, CI 1.04–1.48), lower HDL (OR 2.01, CI 1.29–3.13) and higher TC/HDL ratio (OR 1.07, CI 1.000–1.138) predicted arthritis development.

The Dutch SCORE was calculated in 177 subjects (median 2, IQR 1–9). 76.4% had a low risk (SCORE <10%), 12.5% a medium risk (SCORE 10-<20%) and 11.4% had a high 10 year risk (SCORE >20%) of cardiovascular morbidity and mortality. The score was not associated with ACPA status or arthritis development.

Conclusions Dyslipidemia as known in RA patients with active disease was also present in seropositive arthralgia patients at risk for RA, and predicted development of RA. However, arthralgia subjects who developed arthritis did not have a higher CV risk score than those who did not develop arthritis. Also, despite differences in lipid profile and smoking, the CV risk score does not differ between ACPA positive and ACPA negative subjects at risk for RA. Overall, differences in lipid profile predict development of RA but were too small to have an effect on the 10 year risk of CV morbidity and mortality as calculated by the Dutch CV risk score.

Disclosure of Interest None declared