Rheumatoid arthritis was associated with higher native T1 values (β 3.8 ms; 95% CI 0.8-6.8; p=0.013), with Mendelian randomization supporting a causal relationship for myocardial fibrosis.
Cohort (n=42,227)
Is rheumatoid arthritis associated with early myocardial changes detectable by CMR in individuals without overt coronary artery disease?
Rheumatoid arthritis is independently and potentially causally associated with diffuse myocardial fibrosis and oedema (higher native T1 signals) in individuals without overt CAD.
Mean Difference: 3.8 (95% CI 0.8–6.8)
p-value: p=0.013
Abstract Background Rheumatoid arthritis (RA) is an autoimmune inflammatory disease affecting 0.5-1% of adult population(1,2,3) and confers a 1.8-fold increased cardiovascular risk, comparable to diabetes(4). Persistent inflammation leads to diffuse myocardial fibrosis(5), contributing to cardiac dysfunction, though underpinning mechanisms remain unclear. Cardiovascular magnetic resonance (CMR) can sensitively detect myocardial fibrosis and oedema using T1 mapping and extracellular volume (ECV)(6), therefore offers a unique opportunity to detect early myocardial involvement(7,8), given RA’s often prolonged subclinical cardiac course. This study aims to explore the association between RA and CMR-derived myocardial abnormalities. Purpose To assess the association and potential causality between RA and CMR phenotypes in individuals without overt coronary artery disease (CAD). Methods This study used the data from the UK Biobank, a large population-based cohort study, which provides detailed information on demographics, lifestyle and medical history along with CMR data. We investigated the association between RA diagnosis and eight CMR-derived left heart phenotypes including chamber volumes, mass, strain, and tissue characterisation (native T1 mapping) using multivariable linear regression adjusted for age, sex, height, BMI, hypertension, diabetes, hyperlipidaemia, and smoking, after excluding individuals with prevalent CAD. Two-sample Mendelian Randomisation (MR) was conducted using published genome-wide association summary statistics of native T1 and RA, to explore the casual relationship. Results A total of 42,227 individuals (mean standard deviation age = 63.9 7.7 years, 53% female, RA n = 255) were included. In multivariable linear regression models, individuals with RA had higher native T1 values (β 95% CI = 3.8 0.8 to 6.8 ms, p = 0.013) (Figure 1). No significant associations were detected between RA and other CMR phenotypes. The MR analysis exploring the effect of RA on native T1 showed support for a positive causal association (MR-inverse variance weight IVW beta 95% CI = 0.009 0.0004 to 0.016, p = 0.039) (Figure 2). MR-Steiger test suggested that the assumption of RA causing myocardial fibrosis and oedema (higher native T1) was correct. Conclusion In this large population study, RA is independently associated with diffuse myocardial fibrosis and oedema (inflammation) indicated by higher native T1 signals after accounting for traditional cardiovascular risk factors in a cohort free from overt CAD. This association appears to be causal in nature based on the MR analysis. These findings highlight the role of non-traditional CV risk factors including systemic and local myocardial inflammation driven by RA in subclinical myocardial remodelling and underscore the value of CMR in early cardiac risk assessment in autoimmune rheumatic diseases.Figure 1 Figure 2
Nyi et al. (Thu,) conducted a cohort in Rheumatoid arthritis (n=42,227). Rheumatoid arthritis vs. Individuals without rheumatoid arthritis was evaluated on Native T1 values (β 3.8, 95% CI 0.8 to 6.8, p=0.013). Rheumatoid arthritis was associated with higher native T1 values (β 3.8 ms; 95% CI 0.8-6.8; p=0.013), with Mendelian randomization supporting a causal relationship for myocardial fibrosis.