Abstract
Behçet’s disease (BD) is a chronic multi-system disease presenting with recurrent oral and genital ulceration, and relapsing uveitis. Heart rate recovery (HRR) after exercise is a marker of parasympathetic activity. A delayed recovery of systolic blood pressure (SBP) after exercise might reflect sympathetic hyperactivity. The analysis of variations in heart rate has also been used to determine the balance between sympathetic and vagal nerve activities in the heart. Our objective was to determine HRR, the SBP response to exercise and heart rate variability (HRV) in patients with BD in the absence of neurological involvement. The study population consisted of 32 patients with BD and 30 healthy controls who were matched with respect to age, sex, and physical activity. Heart rate recovery was calculated as the difference between heart rate at peak exercise and heart rate at 1, 2, and 3 min of recovery. Blood pressure recovery indexes were determined by dividing the systolic blood pressure at 2 and 3 min in recovery to the systolic blood pressure at peak exercise. In patients with BD, mean HRR at 1 min (HRR1) were not significantly different than that of controls (21 ± 7 vs 20 ± 7 bpm, p = 0.50). Although, resting mean SBP of patients with BD was higher than controls (121 ± 13 vs 115 ± 12 mmHg, p = 0.039), the SBP recovery indices of the patients with BD at 2 and 3 min were similar to those of controls (0.84 ± 0.07 vs 0.84 ± 0.09, p = 0.89 and 0.78 ± 0.09 vs 0.78 ± 0.08, p = 0.93, respectively). Both time domain and frequency domain parameters of patients with BD were similar to that of controls. This study shows that the patients with BD have normal HRR1 and normal SBP response to exercise and normal HRV. These findings might suggest unaltered autonomic neural control of the cardiovascular system in this disorder in the absence of neurological involvement.
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Erol, T., Tekin, A., Tufan, M. et al. Autonomic neural control of the cardiovascular system in patients with Behçet’s disease in the absence of neurological involvement. Clin Rheumatol 31, 1499–1504 (2012). https://doi.org/10.1007/s10067-012-2045-x
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DOI: https://doi.org/10.1007/s10067-012-2045-x