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Inflammation and cardiovascular autonomic dysfunction in rheumatoid arthritis: a bidirectional pathway leading to cardiovascular disease

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that affects the synovial joints, causing pain and loss of function. Interestingly, this inflammatory pattern also causes damage to the heart and vasculature, increasing the deleterious consequences of the disease. Indeed, cardiovascular disease (CVD) represents the primary cause of morbidity/mortality in RA. The increased rates of CVD in RA can be partially explained by the presence of traditional risk factors, such as diabetes, dyslipidaemia, hypertension and physical inactivity. However, recent studies have identified other factors that contribute to the pathophysiology of CVD in RA. Among them, impairment in autonomic cardiovascular regulation, otherwise known as cardiovascular autonomic dysfunction, has received growing attention over recent years (Adlan et al. 2017). Using mostly indirect methods, previous studies have presented equivocal information regarding the presence of autonomic dysfunction in RA patients. In order to address such limitations, Adlan et al. (2017) published a recent study in The Journal of Physiology, whereby they performed a comprehensive assessment of autonomic function in RA, including assessments of heart rate, cardiac and sympathetic baroreflex functions using the modified Oxford technique, and recordings of muscle sympathetic nerve activity using microneurography. In order to avoid the potential confounding effects of hypertension, the main outcomes of the study were compared between RA patients with and without hypertension, as well as between normotensive and hypertensive individuals without RA. Using this elegant design, they observed an increased heart rate, a reduction in cardiac baroreflex sensitivity, increased sympathetic activity and a preserved sympathetic baroreflex sensitivity in RA patients. Interestingly, these responses occurred independently of the presence of hypertension, and were correlated with inflammation and pain, highlighting the link between autonomic dysfunction and the typical symptoms of RA. The cross-sectional design of this study precludes causal inferences between inflammatory status and autonomic dysfunction in RA; however, information from previous studies does provide support for this concept (Tracey, 2002; Suzuki & Nakai, 2016). More specifically, influential reviews have discussed the bidirectional relationship between the immune system/ inflammation and the central nervous system (Tracey, 2002; Suzuki & Nakai, 2016). These authors propose that the central nervous system can regulate immune system function via two plausible mechanisms: receptor-specific proor antiinflammatory effects of noradrenaline (norepinephrine) released