Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.
Influence of Autonomic Nervous Modulation on Rheumatoid Arthritis.
Malysheva, Olga, Baum, Petra, Esber, Anke, Baerwald, Christoph G.
Growing evidence supports the hypothesis that alteration of the interaction between the autonomic nervous system (ANS) and the immune system contributes to the pathogenesis of rheumatoid arthritis (RA). To further characterize neuroimmune interactions common variants of the beta2-adrenergic receptors (beta2R) and functional stress pattern responses were studied in RA patients and controls.
An allele-specific polymerase chain reaction was used to determine the common variants of the beta2R at position 16, 27, and 164 in patients with RA (n = 310) and ethnically matched healthy controls (n = 305). In a subgroup of RA patients (n = 100) the autonomic response upon various standardized stressors was performed by utilizing the heart rate variability (HRV) test (ProSciCard III, Version 2.2a, Medi-Syst GmbH, Germany) and compared to 40 age and sex matched osteoarthritis patients. HRV measures including frequency domain analysis (employing rapid processing of a 5 minute ECG rhythm strip) yielding measures of parasympathetic and sympathetic activity as well as the total power of ANS influence on various parameters: high frequency (HF), low frequency (LF), and very low frequency index of HRV and square root of the mean of the squares of successive R-R interval differences (RMSSD).
There was a highly significant distortion in the distribution of beta2R polymorphisms at codon 16 between RA patients and controls. Arginine (Arg) at codon 16 was present in 278 RA patients (89.7 %) compared to 202 controls (66.2%; OR 4.43, 95 % CI 2.81 to 7.02, p = 0.00001). Interestingly, HRV at baseline in RA patients was characterized by reduced power of the ANS in general as well as a decreased parasympathetic activity compared to OA patients (HRV index: 7.81 ±0.3 vs. 9.23 ± 0.6, p < 0.05; RMSSD: 25.46 ± 1.2 ms vs. 33.84 ± 3.2 ms, p < 0.03). Otherwise, sympathetic stress response was reduced under the mental stress test (MST) in RA patients compared to OA patients (LF HRV: 1.69 ± 0.21 Hz vs. 3.05 ± 1.0 Hz, and LF/HF HRV: 1.1 ± 0.09 vs. 1.34 ± 0.06, p < 0.05, respectively). Stratifying RA patients for the genetic at position 16 revealed a statistically significant decrease of parasympathetic activity, in particular for the deep breathing test, in patients with homozygosity for Glycine (Gly) 16 compared to RA patients with heterozygosity (Arg16Gly). However, RA patients with homozygosity for Glycine 16 showed a normalisation of the sympathetic reactivity upon MST. Interestingly, all patients exhibiting parasympathetic hyperactivity at baseline (RMSSD >50 ms) were in remission (DAS 1.4 ± 0.4).
Polymorphisms of the beta2AR contribute to the genetic background of RA and is associated with disturbed functional autonomic stress reactivity in RA patients. In particular parasympathetic reactivity might be used as an indicator of RA remission. Further studies are warranted to determine the role of the ANS in the disease process of RA.
To cite this abstract, please use the following information:
Malysheva, Olga, Baum, Petra, Esber, Anke, Baerwald, Christoph G.; Influence of Autonomic Nervous Modulation on Rheumatoid Arthritis. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1691