Aberrances in Autonomic Cardiovascular Regulation in Fibromyalgia Syndrome and Their Relevance for Clinical Pain Reports

Objective: To investigate autonomic cardiovascular regulation in fibromyalgia syndrome (FMS). Methods: In 35 patients and 29 healthy controls, electrocardiography, impedance cardiography, and finger continuous blood pressure measurements were conducted. Assessed parameters comprised blood pressure, R-R interval (RRI), heart rate variability, baroreflex sensitivity (BRS), stroke volume, and left ventricular ejection time (LVET). To evaluate cardiovascular autonomic reactivity to mental stress, parameters were obtained at rest and during an arithmetic task. As an estimate of clinical pain severity, participants completed the McGill Pain Inventory. Results: Patients exhibited lower power in all heart rate variability frequency bands (p < .05), lower BRS (7113 +/- 3.45 versus 10.73 +/- 5.72 ms/mmHg), as well as reduced stroke volume, LVET, and RRI (p < .05). Stress-induced modulations were less pronounced in BRS, LVET, blood pressure, and RRI (all p < .05). Across the whole sample and in both subgroups, BRS (r = -.40) and blood pressure (r = -.39) correlated negatively with pain severity. Conclusions: The data suggest that autonomic cardiovascular regulation in FMS is impaired in terms of reduced sympathetic and parasympathetic influences, as well as baroreflex malfunctioning. Furthermore, autonomic cardiovascular adjustment to acute stress is blunted. The inverse association between BRS and pain severity reflects the well-documented pain inhibition through the baroreceptor system. On account of this and the reduced baroreflex function in FMS, one may assume deficient ascending pain inhibition arising from the cardiovascular system, which may contribute to hyperalgesia that is characteristic of the disorder.