reported a high prevalence of impaired sudomotor function in the POTS patients who reported GI symptoms suggesting that abnormal post-ganglionic sympathetic function could play a role in the pathophysiology of these GI abnormalities. In four of these studies that measured gastric motility, they found that 43% prevalence of rapid gastric emptying and 20% prevalence of delayed gastric emptying. Pooled data from 352 patients recruited from 6 different studies, showed 21-80% prevalence of nausea, vomiting, and abdominal pain. Multiple studies have reported the presence of alterations in the gastrointestinal motility. Furthermore, large meals or high carbohydrate meals exacerbates the feelings of palpitations, weakness, and fatigue in these patients. In addition to the cardiovascular symptoms, patients with POTS experience significant gastrointestinal symptoms namely nausea, bloating, diarrhea or even severe constipation. Of note, there is overlapping in the pathophysiology of POTS with patients having more than one etiology. Depending on the mechanism involved different POTS phenotype has been described: (i) hypovolemic POTS (ii) neuropathic POTS and (iii) POTS associated with Ehlers-Danlos and joint hypermobility syndrome (EDS/JHS). The later could induce an exaggerated fluid shift upon standing from thorax to lower body. The orthostatic tachycardia could be a compensatory phenomenon to hypovolemia, impaired sympathetic-mediated vasoconstriction or increased vascular compliance. In POTS patients, multiple mechanisms have been proposed to explain the exaggerated increase in heart rate. These changes cause unloading of the arterial baroreceptors and increase in sympathetic activity, vasoconstriction and restoration of stroke volume and cardiac output. Upright posture-induced a fluid shift of approximately 700 mL of blood from the upper thorax to the splanchnic circulation and lower extremities, which result in decrease in venous return to the heart, ventricular filling, and stroke volume. Under normal conditions, the assumption of upright posture does not result in major changes in blood pressure due to the integration of complex autonomic, circulatory and neurohumoral responses. The pathophysiology of POTS is complex, and are related to abnormal cardiovascular autonomic adaptation to postural changes.
POTS is estimated to affect up to 3 million persons in the United States and is considered a syndrome rather than a single disease. These symptoms are associated with a rapid increase in heart rate (≥30 bpm) that occur within 10 minutes upon standing. It is characterized by chronic (>6 months) orthostatic intolerance symptoms (palpitation, lightheadedness, blurred vision and mental clouding) triggered by assuming an upright posture and that improved upon recumbency. Postural Tachycardia Syndrome (POTS) is a disabling condition that mostly affects young women in their reproductive age. As a long-term goal, this study can lead us to understand the pathophysiology of common co-morbidities in patients with POTS to provide new treatment approaches and prevention strategies. Furthermore, we will determine differences in these outcomes in POTS patients with and without evidence of postganglionic sympathetic fiber neuropathy. The focus of the present proposal is to determine glucose homeostasis, GI motility, and their association with GI and cardiovascular symptoms in POTS patients versus healthy controls. Sympathetic fiber regulate motor and the postprandial GI peptides secretion. Current evidence suggesting that abnormal post-ganglionic sympathetic function could play a role in the pathophysiology of these GI abnormalities. Patients with POTS experience significant gastrointestinal symptoms. POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME AND GASTROINTESTINAL SYMPTOMS: Contribution of Gastrointestinal Peptides
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