The relationship between rheumatoid arthritis and cardiovascular risk: subclinical myocardial changes in the context of disease severity

Background

Rheumatoid arthritis (RA) is associated with substantially increased cardiovascular morbidity and mortality, independent of traditional risk factors. The underlying myocardial mechanisms contributing to this excess risk remain incompletely understood. Cardiovascular magnetic resonance (CMR) enables comprehensive, non-invasive assessment of myocardial structure, function, and tissue characteristics, allowing detection of subclinical cardiac involvement.

Objectives

To characterize myocardial structural, func

tio

nal, and tissue-level alterations using CMR in patients with RA without overt coronary artery disease, and to explore associations between CMR findings and RA disease severity.

Methods

In this mixed case–control study, 48 patients with long-standing, ACPA-positive RA and 34 age- and sex-matched healthy controls underwent comprehensive CMR. Patients with known ischemic heart disease or significant coronary calcification (Agatston score >500) were excluded. CMR assessment included biventricular volumes and function, feature-tracking strain analysis, native T1 and T2 mapping, late gadolinium enhancement, and stress perfusion imaging. Multivariable linear regression models adjusted for age, sex, hypertension, and diabetes were used to assess associations between RA, disease-related parameters (disease duration, DAS28), and CMR indices.

Results

Compared with controls, RA patients demonstrated significantly higher native T1 values (980 ± 34 vs. 955 ± 33 ms, p<0.01), reduced left ventricular global longitudinal strain (22 ± 2% vs. 24 ± 3%, p<0.01), increased left ventricular concentric remodeling, and lower left ventricular global function index. Right ventricular end-diastolic and end-systolic volume indices were also reduced in RA patients. In adjusted models, RA was independently associated with increased left ventricular mass index, higher mass-to-volume ratio, and elevated native T1 values. Within the RA cohort, longer disease duration was negatively associated with global longitudinal strain (β = −0.06, p<0.05), while higher DAS28 scores were associated with lower left ventricular ejection fraction (β = −4.11, p<0.05). No inducible ischemia was detected on stress perfusion imaging.

Conclusions

Patients with rheumatoid arthritis exhibit distinct subclinical myocardial remodeling characterized by diffuse fibrotic changes, impaired systolic deformation, and adverse ventricular remodeling, independent of overt coronary artery disease. The association between disease activity and myocardial dysfunction highlights the potential role of persistent inflammation in RA-related cardiovascular risk. CMR may provide a valuable tool for early cardiovascular risk stratification and monitoring in RA.