Abnormal Esophagocardiac Inhibitory Reflex in Patients with Diffuse Esophageal Spasm

Bortolotti, Mauro; Sarti, Paolo; Brunelli, Federico; Mazza, M.; Barbara, L

doi:10.1159/000201281

Cited by 14 publications

(10 citation statements)

References 17 publications

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“…It is feasible that long‐standing acid sensitivity could play a role in provoking the altered esophageal motility in patients with MVP. Other work has shown that the onset of cardiac arrhythmia may be associated with esophageal dysmotility and that coronary artery spasm can be precipitated by infusion of acid into the distal esophagus, suggesting the possibility of a cardio‐esophageal neural reflex that may also explain how abnormalities of the cardiac valves result in dysmotility 24,25 . Clearly, at the present time, explanations of the pathophysiology of the association between MVP and esophageal dysmotility are little more than plausible speculation.…”

Section: Discussionmentioning

confidence: 79%

Esophageal dysmotility and acid sensitivity in patients with mitral valve prolapse and chest pain

Hammett

Hansen

Lorang

et al. 2003

Diseases of the Esophagus

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Mitral valve prolapse (MVP) patients often experience non-cardiac chest pain. The aims of this study were to determine, in patients with non-cardiac chest pain: (i) whether esophageal dysmotility is more common in patients with MVP than in patients without MVP; and (ii) if acid sensitivity is an important cause of the chest pain in MVP patients. Esophageal manometry and acid perfusion testing were performed in 277 consecutive patients with non-cardiac chest pain. Patients with MVP (13 female, one male; mean age 49 years) were more likely (P = 0.01) to have esophageal dysmotility, while acid perfusion was less likely (P < 0.05) to provoke their chest pain, than in patients without MVP. The most common esophageal motor abnormalities detected in patients with and without MVP were diffuse esophageal spasm (prevalence, 57%) and non-specific motor disorder (prevalence, 9%), respectively. This study, the first large prospective series examining possible esophageal sensorimotor correlates of chest pain in MVP patients, demonstrates that in the absence of a cardiac cause for chest pain, a specific esophageal motility disorder should be excluded, rather than assuming the chest pain is likely to be due to acid sensitivity.

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Section: Discussionmentioning

confidence: 79%

Esophageal dysmotility and acid sensitivity in patients with mitral valve prolapse and chest pain

Hammett

Hansen

Lorang

et al. 2003

Diseases of the Esophagus

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Section: Introductionmentioning

confidence: 99%

“…The esophagus and heart are linked by a variety of reflexes initiated at esophageal receptors and ending in the coronary vessels 1 and the specific impulse‐generating and ‐conducting system 2 , 3 . Stimulation of esophageal mechanoreceptors induces an esophagocardiac inhibitory reflex that is more intense than normal in some motor disorders 3 and may cause cardiac hypokinetic arrhythmias, similar to those observed in swallow syncope 4 , 5 or during esophageal manipulations 2 , 6 . As this phenomenon may be reproduced by inflating a balloon into the esophagus 2 , 5 and because one of the most frequently performed tests for the diagnosis of the esophageal origin of non‐cardiac chest pain (NCCP) is the intraesophageal balloon distension, 7 , 8 it seemed appropriate to investigate the presence of this esophagocardiac reflex in patients undergoing this test, particularly as one of the esophageal disorders found in patients with an angina‐like chest pain is diffuse spasm, 9–11 which shows a higher than normal decrease of cardiac frequency during balloon inflation 3 .…”

Section: Introductionmentioning

confidence: 99%

Abnormal esophagocardiac reflex in patients with non-cardiac chest pain

2001

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As the mechanoreceptor stimulation of the esophagus activates an esophagocardiac inhibitory reflex, with possible cardiac hypokinetic arrhythmias, we investigated whether patients with non-cardiac chest pain have this reflex, which could represent a source of risk in predisposed individuals during the intraesophageal balloon distension test. Electrocardiogram readings were recorded in nine patients with non-cardiac chest pain (group A), the esophageal origin of which was diagnosed with cardiac and esophageal examinations, in 10 patients with hyperkinetic esophageal motor disorders without chest pain (group B), and in eight normal subjects used as controls (group C), after swallowing solid boluses and during intraesophageal balloon inflation at 100 mmHg for 10 s. The percent variation of the R-R interval from its mean basal value to its highest value observed after stimulation was calculated. Solid swallows induced an increase in heart rate followed by a decrease that was significantly higher in group B than group C, while group A was not significantly different from group C. Balloon inflation induced a significant decrease in heart rate in all groups, but in group A the degree of decrease was significantly lower than in groups B and C. In conclusion, esophageal wall distension, either as a result of solid bolus or balloon inflation, elicits an inhibitory esophagocardiac reflex that is higher than normal in patients with hyperkinetic esophageal motor disorders without pain and lower than normal in patients with non-cardiac chest pain of esophageal origin, who, consequently, have nothing to fear from this procedure.

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“…Deglutition · Syncope · Dysphagia · Achalasia · AV block von Ohnmachtsanfällen und Reduktion von therapiebedingten Begleiterkrankungen möglich [1,2,3,4,6]. Komorbiditäten können weitere therapeutische Maßnahmen erforderlich machen, beispielsweise die Versorgung mit einer perkutanen endoskopischen Gastrostomie-Sonde (PEG; [2,3]).…”

Section: Introductionunclassified

“…Komorbiditäten können weitere therapeutische Maßnahmen erforderlich machen, beispielsweise die Versorgung mit einer perkutanen endoskopischen Gastrostomie-Sonde (PEG; [2,3]). …”

Section: Introductionunclassified