Background Rheumatoid arthritis (RA) is a multi-organ inflammatory disorder associated with high cardiovascular morbidity and mortality. Importantly, cardiac involvements are typically clinically silent, only manifesting as myocardial abnormalities after an extended subclinical phase. Myocardial abnormalities may arise from a number of distinct processes, including myocardial inflammation (myocarditis), and/or myocardial fibrosis, any of which may be active in RA.
Objectives We sought to assess cardiac involvement using a cardiac magnetic resonance imaging (CMR) approach and to determine its association with disease characteristics in RA patients without cardiac symptoms.
Methods Consecutive RA patients and controls without cardiac symptoms were enrolled. RA patients and control subjects with no history and/or clinical findings of systemic and pulmonary hypertension, coronary artery disease, valvular heart disease, atrial fibrillation, diabetes mellitus, and dyslipidemia underwent CMR. RA patients received conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) or biologic DMARDs (bDMARDs). Late gadolinium enhancement (LGE) was obtained for the assessment of myocardial fibrosis. Using a black-blood T2-weighted image (T2-WI), myocardial inflammation could be assessed. Left ventricular geometry was classified into four categories: concentric remodeling, concentric or eccentric hypertrophy, or normal. We compared the patients and controls in terms of prevalence of CMR abnormalities, and explored possible associations between CMR abnormalities and RA disease characteristics.
Results Sixty patients (mean age, 55.2±1.3 years; 85% female) and 20 controls (mean age 52.6±2.3 years; 86% female) were enrolled. Thirty RA patients received csDMARDs [25, methotrexate (MTX) (8.7±2.1mg); 5, other drugs)] and 30 RA patients received bDMARDs [(15, infliximab 3 mg/kg; 15, tocilizumab 8 mg/kg plus methotrexate (8.6±1.4 mg) mg/kg]. The control group showed no myocardial abnormalities. Twenty RA patients (33%) demonstrated myocardial abnormalities. T2-WI was seen in seven RA patients (11%). LGE was found in 19 RA patients (32%), six of whom also demonstrated T2-WI. Simplified Disease Activity Index (SDAI) scores were significantly higher in LGE-positive compared to LGE-negative (p=0.011). LGE was significantly associated with high NT-proBNP and eccentric hypertrophy (p=0.005, p=0.018, respectively). The use of bDMARDs was significantly associated with LGE-negative findings (p=0.0017). Other RA characteristics such as disease duration, autoantibody status, and cardiovascular risk factors were not significantly associated with myocardial abnormalities. After adjusting for confounding by age, RA duration, rheumatoid factor, and bDMARDs, the association of LGE with SDAI remained significant (p=0.023), in which the SDAI scores were, on average, 10.9 units higher in LGE-positive than in LGE-negative.
Conclusions Subclinical myocardial inflammation and fibrosis are common in active RA patients without cardiac manifestation. Abnormal CMR findings were associated with higher RA disease activity, suggesting a role for inflammation in the pathogenesis of myocardial involvement in RA.
Disclosure of Interest None declared