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Abnormal autonomic cardiovascular control in ankylosing spondylitis
E Toussirot1, M Bahjaoui-Bouhaddi, J C Poncet
1Department of Rheumatology, Centre Hospitalier Universitaire J Minjoz, Boulevard Fleming, 25030 Besançon Cédex, France.
Annals of the Rheumatic Diseases
|July 27, 1999
Summary
Ankylosing spondylitis patients show reduced parasympathetic activity and impaired baroreflex function, particularly in those with active disease. This autonomic nervous system dysfunction may link inflammation to cardiac issues in ankylosing spondylitis.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Research
- Rheumatology
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory disease.
- Cardiovascular complications are a concern in AS patients.
- The role of the autonomic nervous system (ANS) in AS is not fully understood.
Purpose of the Study:
- To assess the contribution of the autonomic nervous system to cardiovascular adjustments in AS patients.
- To investigate potential links between ANS dysfunction, disease activity, and cardiac involvement in AS.
Main Methods:
- Evaluated heart rate (HR) responses to deep breathing (E/I ratio) and standing (30/15 ratio) in 18 AS patients and 13 controls.
- Measured cardiac baroreflex slope, blood pressure, and plasma catecholamines.
- Assessed AS disease activity using erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and BASDAI score.
Main Results:
- AS patients exhibited a progressive decrease in blood pressure upon standing.
- The 30/15 ratio and baroreflex slope were significantly lower in AS patients compared to controls.
- Higher HR and a trend towards altered inflammatory markers were observed in AS patients with higher disease activity (BASDAI > 5).
Conclusions:
- AS patients demonstrate altered autonomic nervous system function, characterized by decreased parasympathetic activity and impaired baroreflex sensitivity.
- These autonomic changes correlate with disease activity and inflammation levels.
- Autonomic dysfunction may contribute to cardiac involvement in ankylosing spondylitis.