Abstract
Background: The Metabolic Score for Insulin Resistance (METS-IR) is a newly developed index that has been described to predict cardiovascular (CV) events. In this study, we calculated the METS-IR index in patients with rheumatoid arthritis (RA), a condition linked to an elevated CV risk. We then examined its relationship with disease characteristics and CV comorbidities, including disease activity, lipid profile, subclinical carotid atherosclerosis, and insulin resistance indices. Methods: A total of 515 RA patients were recruited. Disease-related characteristics and disease activity indices, including the Disease Activity Score (DAS28), the Clinical Disease Activity Index (CDAI), and the Simple Disease Activity Index (SDAI) were calculated. Additionally, the complete lipid profile, insulin resistance indices, metabolic syndrome criteria, and carotid ultrasound for intima-media thickness and carotid plaque detection were assessed. METS-IR was calculated. A multivariable linear regression analysis was performed to examine the associations between the disease characteristics and METS-IR. Results: METS-IR was positively correlated with age, body mass index, and traditional cardiovascular risk factors such as metabolic syndrome and insulin resistance indices. Carotid intima-media thickness-but not the presence of carotid plaque-was associated with significantly higher METS-IR values. Regarding disease-related characteristics, C-reactive protein and disease activity indices demonstrated a significant positive association with METS-IR after multivariable adjustment. Specifically, C-reactive protein was associated with higher METS-IR values (beta coefficient 0.2, 95% CI: 0.1-0.3, p < 0.001). All disease activity indices, except CDAI, showed a significant positive relationship with METS-IR. Conclusions: METS-IR is linked not only to CV risk factors but also, independently, to inflammatory disease activity in patients with RA. Its association with CV events in the general population and disease activity in RA highlights the significant role of inflammation in driving excessive cardiovascular risk in RA. This underscores the intricate relationship between metabolic dysfunction, systemic inflammation, and CV outcomes in RA.