Decreased sympathetic inhibition in gastroesophageal reflux disease

Abstract

This study was undertaken to evaluate autonomic nervous system function in patients with gastroesophageal reflux disease. Based on clinical criteria, 28 consecutive patients with no history of heart, metabolic, or neurologic disease (mean age 41 y, range 20-62 y) reporting with upper gastrointestinal symptoms typical of gastroesophageal reflux underwent esophageal manometry, ambulatory 24-hour pH study with electrocardiographic monitoring, power spectral analysis of heart rate variability, and cardiovascular tests. Twelve healthy subjects served as controls. A positive result of prolonged esophageal pH study (pH in the distal esophagus less than 4, lasting more than 4.2% of recording time) was observed in 21 patients (reflux group); seven patients were categorized in the nonreflux group. No patient showed arrhythmias or any correlation between heart rate variability changes during electrocardiographic monitoring and episodes of reflux (pH less than 4, lasting more than 5 minutes). A decrease of sympathetic function occurred only in the reflux group (p <0.05) supported by the lower increase of systolic/diastolic blood pressure at sustained handgrip. No other cardiovascular tests showed statistically significant differences in the control or nonreflux groups. Total time reflux showed an inverse correlation with sympathetic function in the reflux group (r = -0.415, p <0.028). We concluded that there is some evidence for a slightly decreased sympathetic function in patients with gastroesophageal reflux disease that is inversely correlated with total time reflux. In these patients, decreased sympathetic function may cause dysfunction of intrinsic inhibitory control with increased transient spontaneous lower-esophageal sphincter relaxations, thus resulting in gastroesophageal reflux disease.

Cardiac autonomic dysfunction in patients with gastroesophageal reflux disease

“…Some reports also found a decreased sympathetic function or a generalized autonomic decline in patients with GERD [13,14] . Campo et al [13] outlined that there is some evidence for a slightly decreased sympathetic function in patients with GERD that is inversely correlated with total time reflux. However, decreased sympathetic function may cause dysfunction of intrinsic inhibitory control with increased transient spontaneous lower esophageal sphincter relaxations, resulting in GERD.…”

“…The principal mechanism of gastroesophageal reflux is mediated through afferent stimuli from the gastric fundus to the sensory nucleus in the medulla and then through the efferent signals for transient lower esophageal sphincter relaxation. The observed autonomic dysfunction is supposed to cause intrinsic inhibitory reflex disturbances, abnormal fundal accommodation and gastric emptying, and consequently, an increased number of transient lower esophageal sphincter relaxations [13] . Some reports also found a decreased sympathetic function or a generalized autonomic decline in patients with GERD [13,14] .…”

“…The observed autonomic dysfunction is supposed to cause intrinsic inhibitory reflex disturbances, abnormal fundal accommodation and gastric emptying, and consequently, an increased number of transient lower esophageal sphincter relaxations [13] . Some reports also found a decreased sympathetic function or a generalized autonomic decline in patients with GERD [13,14] . Campo et al [13] outlined that there is some evidence for a slightly decreased sympathetic function in patients with GERD that is inversely correlated with total time reflux.…”

Cardiovascular response to sustained handgrip test in gastroesophageal reflux disease patients

“…A significant lower DBP response to SHT was found when ERD patients were compared with non-reflux patients (NERD). 17 However, other studies done by Elewa et al and Milovanovic et al found no significant differences in DBP response to Sustained Handgrip test in patients with GERD than in control group. 18,19 The probable reason of the present findings is due to the decreased sympathetic activity.…”

“…The loss of this adrenergic or vagal nonadrenergic modulation may provide excessive or uncoordinated motor responses. 17 The observed autonomic dysfunction may probably cause intrinsic inhibitory reflex disturbances, abnormal fundal accommodation and gastric emptying, and consequently an increased number of transient lower esophageal sphincter relaxations (TLESRs) resulting in GERD.…”