Rheumatoid arthritis (RA) is a chronic inflammatory condition with elevated cardiovascular mortality but poorly understood pathophysiology. It has been suggested that autonomic dysfunction is evident in ≈60% of patients with RA, principally on the basis of reductions in heart rate variability derived indices of cardiac parasympathetic activity. Animal studies have shown that elevations in central and blood-borne concentrations of pro-inflammatory molecules can elevate sympathetic nerve activity (SNA) and reduce baroreflex sensitivity. Given these observations, in a recent study we sought to determine whether central sympathetic outflow is increased and baroreflex sensitivity is decreased in RA. Groups of age and sex-matched RA normotensive (n = 13), RA hypertensive (RA-HTN; n = 17), hypertensive (HTN; n = 16) and normotensive control (NC; n = 17) participants were recruited. Muscle SNA (microneurography), blood pressure and heart rate were assessed, and baroreflex sensitivity evaluated using sequential bolus infusions of sodium nitroprusside and phenylephrine (modified Oxford technique). We observed that compared to NC, muscle SNA was similarly elevated in RA, RA-HTN and HTN (burst frequency increased by ≈55%; p < 0.05). Sympathetic baroreflex sensitivity was not different between groups (p > 0.05), however cardiac baroreflex sensitivity was reduced in RA, RA-HTN, and HTN patients by ≈50% compared to NC (p < 0.05). These studies provide direct evidence for an elevation in central sympathetic outflow and reduction in cardiac baroreflex sensitivity RA, and it appears that this occurs independently of the presence of hypertension. This study was supported by a grant from Arthritis Research UK (196633).
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© 2015 Published by Elsevier Inc.