Background/Purpose: The prevalence of heart failure is increased 2-fold in RA; this is not explained by ischemic heart disease or other risk factors for heart failure.  We have previously shown that N-terminal pro-brain natriuretic peptide and high-sensitivity cardiac troponin-I are elevated in RA, suggesting subtle myocardial dysfunction or chronic myocyte injury. We hypothesized that in patients with RA without known heart disease, cardiac magnetic resonance imaging (CMR) would detect altered cardiac structure, function, and fibrosis.

Methods: We performed 1.5-T CMR in 59 patients with RA and 56 controls frequency-matched for age, race, and sex. CMR indices of structure, function, and fibrosis (late gadolinium enhancement (LGE), T1 values, extracellular volume fraction (ECV)) were compared between RA and control subjects using Mann-Whitney U tests and linear regression adjusting for age, race, and sex. Measurements were performed by CMR expert cardiologists blinded to disease or control status.

Results: Patients with RA had low to moderate disease activity (DAS28-CRP median [interquartile range] =3.16 [2.03, 4.05]. Indexed left ventricular (LV) mass, indexed LV end diastolic and systolic volumes, and left atrial size were not altered in RA. LV ejection fraction was also not significantly altered in RA. LGE was found in 2 patients with RA and 1 control subject; T1 mapping and ECV (measures of diffuse fibrosis) did not differ significantly between RA and control subjects (Table).

Conclusion: Contrary to a prior report, CMR measures of cardiac structure, function, and fibrosis were not significantly different in patients with well-controlled RA compared to a matched control group in the largest study to date.