Abstract Body (Do not enter title and authors here):
Background


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 predispose to systolic dysfunction. The impact of RA on myocardial energetics and cardiac phenotype in individuals at risk of RA has yet to be established.


Aims

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 30 age and sex matched participants were recruited (11 CCP+ve, 9 RRA and 10 HV). All subjects underwent ³¹ P MRS and comprehensive CMR protocol including volumetric analysis, quantitative myocardial perfusion and T1 mapping.


Results

Table-1 shows clinical and CMR / ³¹ P MRS data.
Groups were matched for age, sex, body mass index (BMI) and systolic blood pressure.
Left ventricular volumes, bi-ventricular systolic function, maximal LV wall thickness and left atrial function were similar between groups. Native T1 values and LV mass were increased in both CCP+ve and RRA versus controls.
PCr/ATP was significantly reduced in both CCP+ve and RRA groups compared to healthy controls.
No significant difference was observed in either stress myocardial blood flow (MBF) or myocardial perfusion reserve (MPR).





Conclusions

This is the first-time energetic impairment has been reported in both patients with anti-CCP positivity and refractory RA. Our findings also demonstrate increased LV mass and diffuse fibrosis in these groups compared to age, sex and BMI matched controls. These findings may provide a mechanistic insight to the increased incidence of heart failure in individuals with rheumatoid arthritis.