POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME AND GASTROINTESTINAL SYMPTOMS: Contribution of Gastrointestinal Peptides

Postural Tachycardia Syndrome (POTS) is a disabling condition that mostly affects young women in their reproductive age. 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. These symptoms are associated with a rapid increase in heart rate (≥30 bpm) that occur within 10 minutes upon standing. POTS is estimated to affect up to 3 million persons in the United States and is considered a syndrome rather than a single disease.

The pathophysiology of POTS is complex, and are related to abnormal cardiovascular autonomic adaptation to postural changes. 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. 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. These changes cause unloading of the arterial baroreceptors and increase in sympathetic activity, vasoconstriction and restoration of stroke volume and cardiac output.

In POTS patients, multiple mechanisms have been proposed to explain the exaggerated increase in heart rate. The orthostatic tachycardia could be a compensatory phenomenon to hypovolemia, impaired sympathetic-mediated vasoconstriction or increased vascular compliance. The later could induce an exaggerated fluid shift upon standing from thorax to lower body. 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). Of note, there is overlapping in the pathophysiology of POTS with patients having more than one etiology.

In addition to the cardiovascular symptoms, patients with POTS experience significant gastrointestinal symptoms namely nausea, bloating, diarrhea or even severe constipation. Furthermore, large meals or high carbohydrate meals exacerbates the feelings of palpitations, weakness, and fatigue in these patients.

Multiple studies have reported the presence of alterations in the gastrointestinal motility. Pooled data from 352 patients recruited from 6 different studies, showed 21-80% prevalence of nausea, vomiting, and abdominal pain. 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. Furthermore, Al-Shekhlee et al. 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.