Background Rheumatoid arthritis (RA) is a common autoimmune disease. Mortality is increased compared to the general population largely due to increased cardiovascular disease (CVD). Immune dysregulation and systemic inflammation are thought to be associated with this increased risk. CMR can provide an assessment of CVD, including myocardial and vascular morphology and function, but it is unknown which CMR measurements are most sensitive to detect early CVD. Objectives To determine CV manifestations of RA using CMR in newly diagnosed, treatment-naive patients compared with matched controls. Method Fifty-two RA patients fulfilling ACR/EULAR classification RA criteria, without CVD history, underwent CMR at 3.0T (Philips Achieva TX). They had symptoms for less than 1 year, had not yet received therapy with any disease modifying anti-rheumatic drugs, disease activity score (DAS28) ≥ 3.2 and at least one RA poor prognostic factor. 30 healthy controls were matched by age, sex and blood pressure. Standard balanced steady state free precession (SSFP) cine images were acquired and LV dimensions calculated. Strain analysis was performed by tissue-tagging using a spatial modulation of magnetization pulse sequence. For aortic distensibility (AD), multi-phase SSFP cine images (50 phases) were acquired in a plane transverse to the ascending aorta at the level of the pulmonary artery bifurcation. Aortic contours were drawn by manual planimetry of the endovascular–blood pool interface at the times of minimal and maximal distension. Native and 15 min post-contrast T1 maps were generated from mid-LV short axis using a modified 3,3,5 Look-Locker inversion sequence to calculate extra-cellular volume fraction (ECV). Results Participant characteristics are presented in Table 1. Aortic distensibility was reduced in RA patients compared to controls (mean±SD, 3.23 ± 1.6 10–3 mmHg-1 vs. 4.99 ± 1.8 10–3 mmHg-1, p = 0.001). Other measures of arterial stiffness including aortic stiffness index, compliance and strain showed differences with similar significance levels. Left ventricular remodelling was not different in the RA group compared with controls, but S’ was lower in RA (mean±SD, 0.99 ± 0.22 Seconds-1 vs. 1.13 ± 0.16 Seconds-1, p = 0.007) which may signify sub-clinical reduction in myocardial performance. Evidence for overt inflammation/fibrosis was seen in 4 patients with areas of focal non-ischaemic patterns of LGE, but native T1 and ECV was not different between the groups. See Table 2. Conclusion Early abnormal subclinical changes in vascular and myocardial function exist in newly diagnosed, treatment-naive RA patients, without overt changes in ventricular performance and geometry. The natural history of these observations and implications in the wider management of RA warrant further investigation.

/pdf/newly-diagnosed-treatment-naive-patients-with-rheumatoid-3sqwn9u750.pdf

Newly diagnosed, treatment-naive patients with rheumatoid arthritis have early abnormalities of vascular and myocardial function

Background Early aggressive treatment in RA equates to better long term outcomes, however targeting aggressive therapies including biologics to patients with the worse prognosis is critical to deliver acceptable risk/benefit ratios and health economic improvements. Such an approach requires prognostic biomarkers, whether the well recognised heterogeneity in synovial pathobiology in early RA translates to specific disease outcomes is currently unknown. Objectives The aim of this study was to investigate whether in a treatment naive early inflammatory arthritis cohort, baseline synovial pathotype significantly associates with disease outcome at 12 months. Methods 166 consecutive DMARD naive patients recruited as part of PEAC at Barts Health NHS Trust with synovial tissue suitable for analysis were included. At baseline patients were classified as RA (2010 ACR/EULAR criteria) or undifferentiated (UA). All patients underwent a baseline synovial biopsy of a clinically active joint along with collection of demographic data. Patients were subsequently treated with DMARD +/- steroid therapy with aim for low disease activity (DAS 2, CD20 1) and (iii) Lymphoid: (grade 2–3 CD20+ aggregates, CD20>2). Results 79% were classified as RA and 21% as UA. Mean disease duration was 9.27 months. 92% (153/166) patients had follow-up at 12months. 29% (44/153) of patients were classified as fibroid, 34% (52/166) as myeloid and 37% (57/166) as lymphoid. At baseline patients with a lymphoid pathotype had a significantly higher CRP and DAS28 and were significantly more likely to be sero positive for for RF and ACPA (p Conclusions Results demonstrate that in an early inflammatory arthritis cohort a lymphoid pathotype significantly associates with higher disease activity at baseline, sero positivity for RF and ACPA and a requirement for more aggressive therapy at 12 month. This supports a direct role for synovial lymphoid structures in disease pathogenesis and suggests a role as a prognostic biomarker facilitating early stratification of aggressive therapeutic intervention. Disclosure of Interest None declared

https://ard.bmj.com/content/annrheumdis/76/Suppl_2/238.1.full.pdf

THU0100 In early inflammatory arthritis a lymphoid pathotype signficantly associates with requirement for biologic therapy at 12 months follow up: results from the pathobiology of early arthritis cohort (PEAC)

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THU0100 In early inflammatory arthritis a lymphoid pathotype signficantly associates with requirement for biologic therapy at 12 months follow up: results from the pathobiology of early arthritis cohort (PEAC)