Background Rheumatoid arthritis (RA) patients are susceptible to development of heart failure (HF). Increased HF risk is not explained by increased prevalence of coronary heart disease (CHD) or traditional cardiovascular (CV) risk factors. Chronic inflammation is suggested to play an important role. In parallel with others (1, 2), we observed RA patients with active disease to have myocardial dysfunction and local myocardial late gadolinium enhancement (LGE) indicative of fibrosis or inflammation on cardiac magnetic resonance (cMR) (3).
Objectives In our patients (3), we here studied the effects of disease modifying anti-rheumatic drugs (DMARDs) on the myocardium over one-year period.
Methods Fifty-eight female patients with active RA (<70 years) and 22 fibromyalgia (FM) patients underwent cardiac magnetic resonance (cMR). Two RA groups existed: patients with untreated active early RA (ERA) starting conventional synthetic DMARDs (csDMARDs) or biological DMARDs (bDMARDs) and patients with chronic RA (CRA) who had inadequate response to csDMARDs and were candidates for bDMARDs. Patients with CHD, diabetes and smoking were excluded. CMR was performed to analyze LGE and ventricular function before and after one-year DMARD therapy
Results Of 30 ERA patients, each started csDMARDs (77% as combination), two started also bDMARD. Of 28 CRA patients, each started bDMARD (one monotherapy).
In RA patients, biventricular systo-diastolic function of the heart was impaired compared to FM (Table 2). Over the study-period, myocardial function improved (Table 2) and DAS28-CRP declined (3.5±1.1 vs 2.3±1.0; p<0.001). Only RA patients had LGE, with no improvement over time (67%).
Conclusions Myocardial function was impaired in RA patients with active RA compared to FM controls, although the latter group had worse classical CV risk factor profile. After one-year DMARD-treatment targeting to remission, myocardial function improved in parallel with decreasing RA activity. Inflammation seems to be deleterious to the myocardium. Tight control of RA activity may improve myocardial function.
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Acknowledgements Main funding: The Finnish Medical Foundation.
Disclosure of Interest None declared