Rapid Fire Abstracts
Chin Yit Soo, BSc, MB
Clinical research fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Chin Yit Soo, BSc, MB
Clinical research fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Laurence Duquenne, MD
Rheumatology registrar
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Lucy Thornton, MB
Rheumatology Registrar
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Thomas Anderton, MBChB
Clinical research fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Raluca Tomoaia, MD, PhD
Clinical Research Fellow
Leeds Institute of Cardiovascular and Metabolic Medicine, United Kingdom
May T. Lwin, MB
Clinical Research Fellow
University of Leeds, United Kingdom
Mehak Asad, MB
Clinical research fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Christel Kamani, MD, PhD
Consultant Cardiologist
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Amrit Chowdhary, MD
Cardiology Research Fellow
University of Leeds, United Kingdom
Sharmaine Thirunavukarasu, MbCHB
Cardiology Research Fellow
University of Leeds, United Kingdom
Henry Procter, MBChB
Cardiology research fellow
University of Leeds, United Kingdom
Sindhoora Kotha, BSc, MB
Cardiology Clinical Research Fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom, United Kingdom
Marilena Giannoudi, MRes(Hons), MSc, MRCP, FHEA
Cardiology Research Fellow
University of Leeds, United Kingdom
Eylem Levelt, PhD
Professor of Cardiology
The Baker Heart and Diabetes Institute , Australia
Lesley-Anne Bissell, PhD
Consultant Rheumatologist
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Paul Emery, MD
Professor of Rheumatology
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Benazir Saleem, PhD
Consultant Rheumatologist
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Richard Wakefield, PhD
Consultant Rheumatologist
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Kulveer Mankia, PhD
Consultant Rheumatologist
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, United Kingdom
Sven Plein, MD PhD
Professor of Cardiovascular Imaging
University of Leeds, United Kingdom
Nicholas Jex, PhD
Cardiology Research Fellow
University of Leeds, United Kingdom
Patients with rheumatoid arthritis (RA) display around 20% increased risk of heart failure, even after adjusting for traditional atherosclerotic risk factors. The reasons behind this are not fully understood. Analogous states of chronic inflammation such as type two diabetes have been shown to be associated with deleterious effects on myocardial metabolism and energetic depletion which predisposes to systolic dysfunction. The impact of RA on myocardial energetics and cardiac phenotype in individuals at risk of RA has yet to be established.
Using 31 Phosphorous magnetic resonance spectroscopy (31 P MRS) and cardiovascular magnetic resonance (CMR), we aimed to establish if myocardial energetics, measured as phosphocreatine (PCr) /ATP ratio and quantitative myocardial perfusion were reduced in individuals at risk with isolated anti-CCP positivity (CCP+ve) and those with refractory RA (RRA) compared to healthy volunteers (HV).
Methods:
A total of 42 age and sex matched participants were recruited (17 CCP+ve, 10 RRA and 15 HV). All subjects underwent 31 P MRS and comprehensive CMR protocol including volumetric analysis, quantitative myocardial perfusion and T1 mapping (Fig 1).
All scans were conducted on a Siemens 3 Tesla PRISMA MR system (Erlangen, Germany). Perfusion imaging used a free breathing, fast low angle shot (FLASH) magnetic resonance protocol with motion-corrected (MOCO) automated in-line perfusion mapping using the Gadgetron streaming software image reconstruction framework. Myocardial perfusion image reconstruction and processing was implemented using the Gadgetron software framework as previously described.
All 31P-MRS data were acquired with a non-gated 3D acquisition weighted CSI technique with 10 averages at the centre of K-space and ultrashort TE to minimise T2 effects and first order phase artefacts. 31P-MRS post processing analysis was performed using a custom Matlab software (Mathworks, Natick, Mass).
Results:
Cardiac geometry and function
Table-1 shows clinical and CMR / 31 P MRS data. Groups were matched for age, sex, BMI and systolic blood pressure. No significant difference was seen in NT-Pro BNP levels.
Bi-ventricular volumes, systolic function, maximal LV wall thickness and left atrial function were similar between groups.
Myocardial fibrosis
Native T1 values (HV: 1232±86, CCP: 1328±31, RRA: 1333±22, p= < 0.0001) were significantly increased in both CCP+ve and RRA groups. ECV (HV: 25±3, RRA: 31±6, p=0.03) and myocardial T2 (HV: 42±2, RRA: 47±5, p=0.02) were both significantly elevated in the RRA cohort.
Myocardial perfusion
No significant difference was observed in either stress myocardial blood flow (MBF) or myocardial perfusion reserve (MPR).
Myocardial energetics
PCr/ATP was significantly reduced in both CCP+ve and RRA groups compared to healthy controls (HV: 2.6 ±0.3, CCP: 1.8±0.3, RRA: 1.9±0.5, p=0.002,fig2).
Conclusion:
We report for the first time that both patients with refractory RA and those with isolated anti-CCP positivity demonstrate myocardial energetic impairment and elevated native myocardial T1 values compared to age, sex and BMI matched healthy controls.
The finding of increased energetic impairment and myocardial fibrosis in both those with established RA and those at risk of disease may provide a mechanistic insight to the increased incidence of heart failure in individuals with rheumatoid arthritis.
