Background Patients with rheumatoid arthritis (RA) have an increased risk of mortality compared to the general population, mainly due to an increased frequency of cardiovascular (CV) diseases (1). Furthermore, a twofold higher risk of sudden cardiac death, possibly due to cardiac arrhythmias (1). Inflammation and subsequent fibrosis of the conduction system may be responsible for conduction disturbances (CDs) and therefore anti-inflammatory treatment could possibly lower the risk of CDs and thus arrhythmias.
Objectives The aim of this study was to 1) investigate the prevalence of CDs at the time of RA diagnosis before start of disease-modifying antirheumatic drug (DMARD)-treatment 2) analyze the relationship between (changes in) inflammation markers, conduction times and traditional CV risk factors.
Methods In 482 DMARD-naive consecutive early RA patients electrocardiography (ECG), blood pressure measurements, and disease activity measurements (DAS28) were performed and lipid profile and C-reactive protein (CRP) were measured at baseline and after 1 year. With regression analyses, the relationship between CDs, blood pressure and cholesterol profile with CRP and DAS28 were analyzed.
Results Of the 482 patients 61 had a CD (12.7%, see graph). At baseline the mean symptom duration is 101 weeks, the median CRP was 7.0 (2.0-20.0) mmol/l and the mean DAS28 was 4.7 (1.4). There was no relation between CRP or DAS28 and the presence of CDs or the conduction times. However, there was a significant association between elevated CRP levels and heart rate (B: 6.253), systolic (B: 7.310) and diastolic blood pressure (B: 4.550). Similar associations were found for DAS28 levels. Elevated CRP and DAS28 levels also correlated inversely with the baseline lipid levels. After one year of treatment there was a significant decrease in CRP (3.0 mg/l (0.0-13.0)) and DAS28 (2.1 (1.5)), but this was not reflected in a significant improvement in conduction times. However, an improvement in CRP (or in DAS28) showed a decrease in heart rate compared to patients who did not improve (1.4 vs -4.4- beats/min), as well as an increase in total cholesterol (0.29 vs -0.09 mmol/l) and high-density-lipoprotein (HDL) cholesterol levels (0.22 vs 0.05 mmol/l). However, the TC:HDL ratio did not improve.
Conclusions In this cohort of early RA patients, the prevalence of CD is 13% and this appears to be equal to the general population (2-4). CDs were not associated with inflammation or disease activity, and disease treatment did not lead to improvement in conduction times. However, heart rate and cholesterol levels improved significantly upon treatment and the decreased heart rate could imply a lower mortality risk of 17% per 5 beats/min (5;6). Therefore, the current focus of CV risk management in early RA patients should be optimizing RA treatment and active management of traditional CV risk factors according to the latest guidelines. The ultimate effect of CDs in early RA patients on long-term survival remains to be determined.
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Disclosure of Interest None declared