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THU0099 Cardiovascular MR (CMR) Evidence for Reduced LV Mass in Rheumatoid Arthritis (RA), Suggesting Pathology Other than Atherosclerosis for Heart Failure
  1. L.-A. Bissell1,2,
  2. B. Erhayiem3,
  3. E.M. Hensor1,2,
  4. G. Fent3,
  5. A. Burska1,2,
  6. H. Donica4,
  7. S. Plein3,
  8. M.H. Buch1,2,
  9. J.P. Greenwood3,
  10. J. Andrews1,2
  1. 1LIRMM, University of Leeds
  2. 2Nihr Lmbru
  3. 3LIGHT, University of Leeds, Leeds, United Kingdom
  4. 4Medical University of Lublin, Lublin, Poland


Background An increased risk of heart failure in RA exists1. Aetiology is unclear with some evidence that cardiomyopathy may occur early in RA, from pathology distinct to atherosclerosis3. Large well characterised CMR-RA studies to investigate pathogenesis are few2.

Objectives To evaluate sub-clinical CVD in an asymptomatic-CVD established RA cohort compared to healthy controls (HC), using reference standard CMR-measured outcomes & novel CMR-measures of carotid artery.

Methods 76 ACR1987 RA patients (pts) with dis.>5yrs, no CVD/diabetes, assessed for CV traditional risk factor (TRFs)/RA profile, pulse wave velocity (PWV), non-contrast 3T CMR (heart & carotids) reported by CMR-cardiologists, compared to 26 HC. Carotid measures inc. mean (MWT) & maximum (MxWT) wall thickness, wall (WVol) & luminal (LVol) volume & WVol-index (WVol-I, WVol/(WVol+LVol)). UVA variables (var.)=TRFs, BMI, waist/hip ratio (WHR), HOMA-IR, NTproBNP, dis. duration (ddur), 3vDAS28, ACPA, HAQ-DI, joint surgery hx, biologic use & PWV. MVA var.=age/sex/known associated (ass.) var./UVA r>0.3.

Results Mean (SD) age (yrs) of RA pts; 60 (9.2), 74% female; HC 52 (11.4), 54% female. Median (IQR) ddur 16.5 (10.7, 25.7)yrs, 81% ACPA+ve, DAS28CRP 2.59 (1.30, 3.33), 67% on biologic. There were no significant differences in lipids/glucose/HOMA-IR between RA/HC. Trend for higher NT-proBNP in RA seen. In MVA (inc. age/sex), increasing ddur ass. with NTproBNP (0.5% rise in NTproBNP per 1% increase in ddur, p0.034). RA pts (after adj. for age/sex/TRFs) had reduced LVmass/BSA, LVEF, native T1 values & increased strain (Mid-S') vs HC; no difference seen for LVEDV, LVESV, SV, LVmass/EDV, torsion or arterial stiffness (PWV/distensibility). No significant differences in carotid measures between RA/HC seen. In RA pts, 10yr JBS2 CV risk score correlated with WVol (r0.377 p=0.004) & LVol (r0.441 p=0.001). TRFs ass. with cardiac & carotid measures in RA.

Table 1.

CMR results

Conclusions CMR evidence for reduced LV mass in RA, suggesting pathology other than atherosclerosis as the cause of heart failure; perhaps microvascular dysfunction. TRFs, not RA features, are important determinants of CMR measures of subclinical CVD in RA.

  1. ArthRheum 2005;52:412–20

  2. EULAR 2015 OP0163

  3. A&R 2010:62v4

Disclosure of Interest None declared

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