Effect of Food Intake on Hemodynamic Parameters during the Tilt-Table Test in Patients with Postural Orthostatic Tachycardia Syndrome

Abstract

Background and Purpose The aim of this study was to determine the effect of food intake on the heart rate (HR) in postural orthostatic tachycardia syndrome (POTS). Methods The following five-phase protocol was applied to 41 subjects who had a sustained HR increment of ≥30 beats/min within 10 min of standing in an initial tilt-table test: 1) 10-min supine phase, 2) 10-min 70°-tilted phase, 3) ingestion of 400 mL of Nutridrink Multi Fibre®, 4) 45-min supine phase, and 5) 10-min 70°-tilted phase. Subjects were divided into four groups: A) difference in HR for standing vs. supine (ΔHR) before the meal of ≥30 beats/min ( n =13), B) ΔHR <30 beats/min before the meal but ≥30 beats/min after the meal ( n =12), and C) ΔHR <30 beats/min both before and after the meal ( n =16). Group D consisted of 10 healthy subjects. Results Before the meal, ΔHR was significantly higher in group A than in all of the other groups, and in group B than in group D ( p <0.001). After the meal, ΔHR was significantly higher in groups A and B ( p <0.001 and p <0.0001, respectively). When we pooled patients (according to their symptoms) from group A and B into a POTS group and from group C and D into a non-POTS group, an increase in HR of 25 beats/min before the meal had a sensitivity of 92.0% and a specificity of 80.8%. After the meal, an increase in HR of 30 beats/min had a sensitivity of 96.0% and a specificity of 96.2%. Conclusions Food intake can significantly alter the results of the tilt-table test and so should be taken into account when diagnosing POTS.

Heart rate and heart rate variability comparison between postural orthostatic tachycardia syndrome versus healthy participants; a systematic review and meta-analysis

“…Blood circulation, blood pressure, and adequate tissue perfusion are closely coordinated with the autonomic nervous system in that, body postural changes will result in smaller and bearable changes in hemodynamics [1]. Inadequate blood volume, dysfunctional autonomic nervous system and sometimes, old-age and postprandial status, can result in altered hemodynamics when raising to the upright position (Orthostasis) [1, 2]. The altered hemodynamics results in a variety of symptoms collectively known as orthostatic intolerance (OI).…”

“…Among others, the autonomic nervous function is one of the key players in maintaining hemodynamics and preventing POTS. Sympathetic denervation in lower extremities, preserved cardiac innervation and increased sympathetic activities (hyper-adrenergic state) have been shown to be sole etiologies of POTS [2, 3, 6, 8]. Other postulated theories include Cardiovascular deconditioning, abnormal venous function with reduced venous return, baroreflex abnormalities, hypovolemia and genetic abnormalities [4, 7].…”

Heart rate and heart rate variability comparison between postural orthostatic tachycardia syndrome versus healthy participants; a systematic review and meta-analysis.

“…Blood circulation, blood pressure and adequate tissue perfusion are closely coordinated with autonomic nervous system in that, body postural changes will result in smaller and bearable changes in hemodynamics (1). Inadequate blood volume, dysfunctional autonomic nervous system and sometimes, old-age and postprandial status, can result into altered hemodynamics when raising to upright position (Orthostasis) (1,2). The altered hemodynamics result into a variety of symptoms collectively known as orthostatic intolerance (OI).…”

“…Among others, Autonomic nervous function, is one of key players in maintaining hemodynamics and preventing POTS. Sympathetic denervation in lower extremities, preserved cardiac innervation and increased sympathetic activities (hyper-adrenergic state) have been shown to be sole etiologies of POTS (2,3,6,8). Other postulated theories include Cardiovascular deconditioning, abnormal venous function with reduced venous return, baroreflex abnormalities, hypovolemia and genetic 4 abnormalities (4, 7).…”

Heart rate and heart rate variability comparison between postural orthostatic tachycardia syndrome versus healthy participants; a systematic review and meta-analysis.

“…Among others, Autonomic nervous function, is one of key players in maintaining hemodynamics and preventing POTS. Sympathetic denervation in lower extremities, preserved cardiac innervation and increased sympathetic activities (hyper-adrenergic state) have been shown to be sole etiologies of POTS (2,3,6,8). Other postulated theories include Cardiovascular deconditioning, abnormal venous function with reduced venous return, baroreflex abnormalities, hypovolemia and genetic abnormalities (4,7).…”