Impaired myocardial perfusion in rheumatoid arthritis is associated with impaired strain, strain rate, disease activity and myocardial oedema: a cardiovascular magnetic resonance study
Piechnik, Stefan K.
Ntusi, Ntobeko A.
Matthews, Paul M.
Wordsworth, Paul B.
Francis, Jane M.
Ferreira, Vanessa M.
Background Rheumatoid arthritis (RA) commonly involves the cardiovascular system, and is associated with significant morbidity and mortality. Mechanisms of cardiovascular disease (CVD) involvement are not fully understood, but cardiovascular inflammation is thought to drive many of the CVD manifestations, including myocardial ischaemia. The clinical utility of CMR first-pass perfusion for assessment of myocardial ischaemia is well-established. The aim of this study was to assess whether RA patients without known epicardial coronary artery disease have evidence of myocardial hypoperfusion. Methods 55 RA patients (39 female, mean age 54 ± 11 years) with 55 matched controls (39 female, mean age 53 ± 10 years) were enrolled into the study. All patients with known cardiovascular disease were excluded. Study participants underwent CMR at 1.5T and the assessments included cine, tagging, T1 mapping, T2-weighted, perfusion, late gadolinium (0.15mmol/kg gadoteric acid - Dotarem®) imaging and ECV quantification. Comorbid status, disease activity index (DAS28-CRP) and duration of disease were recorded for each subject. Results RA patients and controls were well matched for age, sex and comorbidities (Table 1). There was no significant difference in LV size, mass and ejection fraction between RA patients and controls (Table 2). Peak systolic circumferential strain and peak diastolic strain rate were impaired in patients. Myocardial perfusion reserve index was 1.5 ± 0.3 and 1.9 ± 0.4 (p<0.001) in RA and controls, respectively. Non-segmental (circumferential) subendocardial perfusion defects were seen in 47% and none (p<0.001) of RA patients and controls studied. Impaired MPRI correlated with peak systolic strain (R -0.71, p<0.001) and peak diastolic strain rate (R 0.63, p<0.001) in RA (Figure 1). Further, abnormal MPRI was associated with DAS28-CRP (R -0.38, p=0.005) and volume fraction of T2 SI ratio (R -0.29, p=0.036) in RA.
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