Abstract Background The mechanisms of cardiac involvement in immune mediated inflammatory diseases (IMID’s) remain incompletely understood1. Chronic systemic inflammation is thought to be the principal cause of cardiovascular manifestations, with variable expression in different IMIDs1. The time course and specific phenotype of cardiac involvement in different IMIDs is unknown. Methods We determined cardiovascular manifestations in early and late-stage rheumatoid arthritis (RA) and systemic sclerosis (SSc) using multi-parametric cardiovascular magnetic resonance (CMR) to determine the time- and disease-specific cardiovascular manifestation in two of the most common IMIDs. Ninety-eight participants were recruited – 11 early and 38 late SSc, 12 anti-cyclic citrullinated peptide antibody positive (CCP+ve) at risk of RA, 12 late RA, and 25 age and sex matched healthy volunteers (HV). All subjects underwent 31-Phosphorous-magnetic resonance spectroscopy (31P MRS) and comprehensive cardiac magnetic resonance (CMR) including volumetric analysis, quantitative myocardial perfusion, T1, T2 mapping, and late gadolinium enhancement (LGE) on a Siemens 3 Tesla PRISMA MR system. All 31P MRS data were acquired with a non-gated 3D acquisition weighted chemical shift imaging (CSI) technique. Results Myocardial energetics were abnormal with significantly reduced phosphocreatine/ATP (PCr/ATP) ratios in late SSc, anti-CCP+ve, and late RA (p=0.0002, fig1). Left ventricular (LV) volumes, systolic functions, left atrial (LA) volume and function were similar between groups (Table-1). RV volumes and ejection fractions were different but within normal ranges. Mean native T1 (p0.0001) and extra-cellular volume (ECV, p0.0001) were significantly increased in early and late SSc. Late gadolinium enhancement (LGE) was present in early SSc (33%), late SSc (29%), anti-CCP+ve (18%), and late RA (15%). Mean native T2 was significantly increased in early to late SSc and late RA (p=0.0001). Stress myocardial blood flow (MBF) was reduced significantly in late SSc (p=0.0148). Myocardial perfusion reserve (MPR) was significantly reduced in late SSc and late RA (p=0.0011). Increased CCP antibody titre correlated with reduced PCr/ATP. Conclusion Patients with SSc show evidence of myocardial inflammation, fibrosis as well as abnormal myocardial energetics and perfusion from an early disease stage, while patients at-risk of RA show no evidence of myocardial inflammation or fibrosis, but already exhibit abnormal myocardial energetics. In RA this progresses to reduced myocardial perfusion and increases in myocardial fibrosis and oedema in long-standing disease. These findings show that SSc is associated with earlier and more advanced cardiac involvement, while cardiac abnormalities in RA develop later with less inflammation and fibrosis. Myocardial energetics appear to be an early marker of CV involvement in both IMIDs and offers a potential new therapeutic target.
Soo et al. (Sat,) studied this question.