Abnormal gastric myoelectrical activity in postural tachycardia syndrome
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Postural tachycardia syndrome (PoTS) is an important cause of orthostatic intolerance resulting from cardiovascular autonomic dysfunction. In addition to postural symptoms, PoTS patients may have allied features, including gastrointestinal (GI) symptoms, which have not yet been thoroughly investigated. We evaluated gastric myoelectrical activity in PoTS patients.
Using cutaneous electrogastrography (EGG), we recorded gastric myoelectrical activity before and after standard liquid meal ingestion in 15 PoTS patients (age 27 ± 4 years); including 7 with and 8 without GI symptoms, and in 11 healthy individuals (age 23 ± 7 years). We performed spectral analysis of EGG recordings to obtain the dominant frequency of gastric pacemaker rhythm (DF), instability coefficient of DF (ICDF), and low (LFR%), normal (NFR%), and high (HFR%) range power percentages of the total power.
Instability coefficient of DF, an index of variability of gastric pacemaker rhythm, was significantly elevated both pre- and post-prandially (30–45 min after the meal) in the PoTS group (8.8 ± 6, 10.0 ± 8 %) compared with controls (4.0 ± 3, 4.0 ± 3 %; both p < 0.05). Patients with GI symptoms had significantly higher post-prandial ICDF (15.0 ± 5 %) than those without GI symptoms (5.6 ± 4 %; p < 0.05). There were no significant differences in DF, LFR%, NFR% and HFR% before and after the meal between the PoTS and control groups, or between PoTS patients with and without GI symptoms.
Our study revealed increased variability of gastric pacemaker rhythm in PoTS, and these findings might be related to pathophysiology of functional GI symptoms in PoTS.
- Abnormal gastric myoelectrical activity in postural tachycardia syndrome
Clinical Autonomic Research
Volume 23, Issue 2 , pp 73-80
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- Orthostatic intolerance
- Autonomic nervous system
- Gastric motility
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- Author Affiliations
- 1. Department of Medicine, Autonomic and Neurovascular Medicine Unit, Imperial College London, 2nd Floor QEQM Wing, St. Mary’s Hospital, Praed Street, London, W2 1NY, UK
- 2. Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK
- 3. Autonomic Unit National Hospital for Neurology & Neurosurgery Queen Square/ Division of Clinical Neurology Institute of Neurology, University College London, London, UK
- 4. Department of Neurology, Chiba University School of Medicine, Chiba, Japan