Abstract
Background: Rheumatoid arthritis (RA) is an immune-mediated inflammatory disease. Antirheumatoid treatment reduces disease activity and inflammation, but not all patients respond to treatment. Autonomic dysfunction is common in RA leading to frequent cardiovascular complications. Yoga therapy may be useful in these patients, but there are little data on the effect of yoga on disease activity, inflammatory markers, and heart rate variability (HRV).
Objectives: This study assessed the effect of 12-week yoga therapy on disease activity, inflammatory markers, and HRV in patients with RA.
Materials and Methods: This randomized control trial was conducted on newly diagnosed RA patients attending outpatient services at the Department of Clinical Immunology, JIPMER. One hundred and sixty-six participants were randomized into two groups: the control group (CG) (n = 83) and yoga group (YG) (n = 83). Yoga therapy was administered to participants in the YG for 12 weeks, along with standard medical treatment. The CG received only standard medical treatment. Primary outcomes were disease activity score 28, interleukin-1α (IL-1α), IL-6, tumor necrosis factor-α (TNF-α), cortisol, and HRV parameters. All parameters were measured at baseline and after 12 weeks.
Results: Disease activity significantly decreased in both groups after 12 weeks, but it was reduced more in YG, which was statistically significant (p < 0.05). In both YG and CG, IL-1α, IL-6, TNF-α, and cortisol decreased after 12 weeks, but IL-1α and cortisol decreased more significantly in YG than in CG. Low-frequency component expressed as normalized unit (LFnu) and the low-frequency/high-frequency (LF-HF) ratio decreased significantly, and total power and HF component expressed as normalized unit (HFnu) increased significantly in the YG compared with CG.
Conclusion: Twelve-week yoga therapy, if given along with standard medical treatment, significantly reduces disease activity and improves sympathovagal balance in RA patients.
Introduction
Rheumatoid arthritis (RA) is common throughout the world with a prevalence of ∼0.5%–1%.1,2 In India, the prevalence is around 0.7%.3 RA is more common in women than men. Pharmacologic treatments have improved joint pain, swelling, inflammation, disease activity, and quality of life in the patients of RA. However, not all patients respond effectively to pharmacologic treatment.4
Incidences of cardiovascular (CV) morbidity and mortality have been reported to be higher in RA patients than in the general population.5,6 Cardiac autonomic neuropathy is one of the most common complications of RA and is associated with high mortality resulting from arrhythmia and myocardial infarction.7,8 In previous studies, CV autonomic dysfunction has been reported to be around 61%–75% in RA patients.9 Furthermore, there was overactivity of the sympathetic nervous system and underactivity of the parasympathetic nervous system.10 Some studies have reported that increased sympathetic activity stimulates the secretion of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and impacts inflammation.11–13 Other studies observed no such CV autonomic dysfunction in RA.14 There is paucity of data on the study of sympathetic and parasympathetic activity in RA patients. Heart rate variability (HRV) is the normal phenomenon of beat to beat variation in the cardiac cycle length observed in an innervated heart due to autonomic influences on the sinoatrial node.15,16 HRV is an established and accepted predictor of CV events17 and mortality.18,19
IL-1, IL-6, and TNF-α are the prime cytokines that drive the inflammatory process in RA.20 Other reports suggest that IL-1 and TNF-α regulate the expression of adhesion molecules in endothelial cells leading to endothelial dysfunction and an increase in CV atherosclerosis and CV disease events.21 Furthermore, IL-1 and TNF-α stimulate the recruitment of neutrophils into the joints leading to joint damage.22
