PMID- 36151442 OWN - NLM STAT- MEDLINE DCOM- 20230222 LR - 20230222 IS - 1434-9949 (Electronic) IS - 0770-3198 (Linking) VI - 42 IP - 3 DP - 2023 Mar TI - Coexistence of fibromyalgia syndrome and inflammatory rheumatic diseases, and autonomic cardiovascular system involvement in fibromyalgia syndrome. PG - 645-652 LID - 10.1007/s10067-022-06385-8 [doi] AB - The spectrum of symptoms represented by fibromyalgia syndrome (FMS) has a profound effect on daily activities and impairs the quality of life. A considerable proportion of patients with inflammatory rheumatic diseases (IRDs) fulfill the FMS criteria, which can complicate the diagnosis, treatment, and follow-ups of IRD. In addition, the coexistence of FMS may cause unnecessary laboratory and radiological assessments. Several mechanisms have been proposed that may have a role in the etiopathogenesis of FMS, one of which is autonomic dysregulation. In studies evaluating cardiac autonomic dysfunction based on heart rate variability (HRV), there has been found to be a decrease in HRV and dominance of the sympathetic nervous system. Autonomic reactivity reflects modulations of several functions to overcome the existing state and conditions. Blunted autonomic reactivity has been found in some FMS patients, which makes it difficult for these patients to respond appropriately to unexpected stress sources that occur during daily living activities. Baroreceptor signals have an inhibitory influence on the central nervous system, and these impulses cause pain suppression. From this perspective, there are studies that have suggested the involvement of diminished baroreflex sensitivity in the etiology of FMS. The risk of endothelial dysfunction and increased arterial stiffness have been shown to occur in FMS patients due to autonomic dysfunction, sympathetic nervous system dominance, chronic stress, and pain. There is also evidence linking FMS with the risk of atrial and ventricular arrhythmias. Considering all these cardiovascular autonomic dysfunctions, tests that can confirm abnormalities should be performed when suspicion arises. There is a need for specific pharmacological and non-pharmacological treatment alternatives to be identified for subgroups of patients with cardiovascular system abnormalities. Key points * The frequency of FMS accompanying inflammatory rheumatic diseases is considerable and this coexistence leads to troubles in evaluating treatment response and determining appropriate medical treatment options in inflammatory rheumatic diseases. * Various cardiovascular autonomic abnormalities have been described in FMS patients. Among these, the most emphasized are autonomic dysfunction, the disruption of the balance between the sympathetic-parasympathetic nervous systems, blunted autonomic reactivity to acute stress, changes in baroreflex sensitivity, increased arterial stiffness, and electrophysiological alterations. * Autonomic cardiovascular dysfunction may be involved in the complex etiopathogenesis of the fibromyalgia syndrome and may trigger at least some symptoms. CI - (c) 2022. The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR). FAU - Kocyigit, Burhan Fatih AU - Kocyigit BF AUID- ORCID: 0000-0002-6065-8002 AD - Faculty of Medicine, Department of Physical Medicine and Rehabilitation, Kahramanmaras Sutcu Imam University, Kahramanmaras, Turkey. bfk2701@hotmail.com. FAU - Akyol, Ahmet AU - Akyol A AUID- ORCID: 0000-0002-8953-5196 AD - Physiotherapy and Rehabilitation Application and Research Center, Hasan Kalyoncu University, Gaziantep, Turkey. LA - eng PT - Journal Article PT - Review DEP - 20220923 PL - Germany TA - Clin Rheumatol JT - Clinical rheumatology JID - 8211469 SB - IM MH - Humans MH - *Fibromyalgia MH - Quality of Life MH - *Cardiovascular System MH - Heart/diagnostic imaging MH - Pain/complications MH - Heart Rate/physiology MH - *Rheumatic Fever OTO - NOTNLM OT - Autonomic nervous system OT - Cardiovascular abnormality OT - Dysautonomia OT - Fibromyalgia OT - Rheumatic diseases EDAT- 2022/09/24 06:00 MHDA- 2023/02/22 06:00 CRDT- 2022/09/23 23:37 PHST- 2022/08/13 00:00 [received] PHST- 2022/09/20 00:00 [accepted] PHST- 2022/09/16 00:00 [revised] PHST- 2022/09/24 06:00 [pubmed] PHST- 2023/02/22 06:00 [medline] PHST- 2022/09/23 23:37 [entrez] AID - 10.1007/s10067-022-06385-8 [pii] AID - 10.1007/s10067-022-06385-8 [doi] PST - ppublish SO - Clin Rheumatol. 2023 Mar;42(3):645-652. doi: 10.1007/s10067-022-06385-8. Epub 2022 Sep 23.