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Autonomic function and rheumatoid arthritis: a systematic review.
Ahmed M Adlan1, Gregory Y H Lip2, Julian F R Paton3
1College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2 TT, UK.
Seminars in Arthritis and Rheumatism
|August 26, 2014
Summary
Autonomic nervous system (ANS) dysfunction is common in rheumatoid arthritis (RA), affecting about 60% of patients. This dysfunction involves impaired cardiovascular reflexes and altered heart rate variability, but a direct link to inflammation remains unclear.
Area of Science:
- Cardiovascular Health
- Rheumatology
- Neuroimmunology
Background:
- Rheumatoid arthritis (RA) is linked to higher mortality, particularly cardiovascular.
- The immune and autonomic nervous systems (ANS) play key roles in cardiovascular disease development.
- Understanding ANS function in RA is crucial for managing cardiovascular risks.
Purpose of the Study:
- To systematically review the prevalence and nature of ANS dysfunction in RA patients.
- To investigate the potential causal relationship between inflammation and ANS dysfunction in RA.
Main Methods:
- Systematic literature review of studies assessing autonomic function in RA patients.
- Databases searched include MEDLINE, Central, and Cochrane Library.
- Included studies utilized various methods like cardiovascular reflex tests (CCTs) and heart rate variability (HRV).
Main Results:
- ANS dysfunction was reported in approximately 60% of RA patients (median prevalence).
- Common findings include impaired cardiovascular reflexes and altered HRV, suggesting reduced parasympathetic and elevated sympathetic activity.
- A link between increased inflammation and ANS dysfunction was observed in some studies, but causality could not be established.
Conclusions:
- Autonomic nervous system dysfunction is highly prevalent in rheumatoid arthritis patients.
- The primary pattern involves impaired cardiovascular reflexes and altered heart rate variability.
- Current evidence is insufficient to confirm a causal relationship between inflammation and ANS dysfunction in RA.
