Search

Purpose of Review: In this manuscript, we aim to review the proposed mechanisms of the pathophysiology of functional heartburn (FH) and functional chest pain (FCP) as well as highlight the different neuromodulatory therapies available to providers and the evidence for each of them. Recent Findings: Understanding the basis for the symptoms that patients are presenting with is essential when evaluating patients with possible esophageal motility disorders or gastroesophageal reflux disease. Objective testing to understand these conditions is a key component to that understanding. Patients undergoing evaluation for heartburn or chest pain, following cardiac evaluation, often require a combination of endoscopy, esophageal manometry, and pH testing. Treatment for FH or FCP often involves some combination of neuromodulatory pharmacologic or behavioral therapies based on their understood pathophysiology. Summary: When a diagnosis of functional heartburn or functional chest pain is reached, it is important for the managing provider to understand the available therapeutic options. Often, treatment requires management with neuromodulation. [ABSTRACT FROM AUTHOR]

Noncardiac chest pain is a challenging condition often encountered by primary care providers, emergency medicine physicians, and gastroenterologists. It is frequently accompanied by persistent symptoms, diagnostic uncertainty, decreased quality of life, and high health care burden. Gastroesophageal reflux disease is the most common esophageal cause followed by functional chest pain, and at least half of patients with noncardiac chest pain have psychiatric comorbidities such as anxiety or depression. Management is focused on identification of an underlying cause to target treatment and address psychiatric comorbidities. This article discusses the evaluation and management of the common gastrointestinal causes of noncardiac chest pain. [ABSTRACT FROM AUTHOR]

Background Functional chest pain (FCP) is characterized by the presence of chest pain of presumed esophageal origin, but with a negative workup on routine investigations, including ruling out gastroesophageal reflux disease (GERD). Antidepressants are frequently prescribed to treat FCP and are presumed to act as neuromodulators of visceral hypersensitivity. However, there is little evidence of their efficacy in patients with FCP. We retrospectively assessed the efficacy of citalopram or amitriptyline vs. no treatment in patients with FCP. Methods Esophageal diseases, including GERD, eosinophilic esophagitis and major esophageal motility disorders, were excluded. Thus, patients with established FCP according to Rome IV criteria were included in the study. Then, patients treated for at least 3 months with citalopram 20 mg, amitriptyline 50 mg, or observation were selected. The primary endpoint was complete disappearance or significant amelioration of symptoms at the end of treatment. Results Over a 5-year period, 102 patients (74 female; mean age 49±10 years) were diagnosed with FCP and were recognized to have received once daily citalopram (n=32), amitriptyline (n=34), or no treatment (n=36). After a 3-month follow up, improvement in chest pain was reported by 16 (47.1%) patients treated with citalopram, 18 (56.3%) patients treated with amitriptyline, and 4 (11.1%) patients without treatment (P=0.02 and 0.01 for no treatment vs. citalopram and amitriptyline therapy, respectively). Conclusion Both citalopram and amitriptyline are effective pharmacological options in the symptomatic relief of almost 50% patients with well characterized FCP. [ABSTRACT FROM AUTHOR]

Noncardiac chest pain is a challenging condition often encountered by primary care providers, emergency medicine physicians, and gastroenterologists. It is frequently accompanied by persistent symptoms, diagnostic uncertainty, decreased quality of life, and high health care burden. Gastroesophageal reflux disease is the most common esophageal cause followed by functional chest pain, and at least half of patients with noncardiac chest pain have psychiatric comorbidities such as anxiety or depression. Management is focused on identification of an underlying cause to target treatment and address psychiatric comorbidities. This article discusses the evaluation and management of the common gastrointestinal causes of noncardiac chest pain., (Copyright © 2024, Gastro-Hep Communications, Inc.)

Background and aim. Noncardiac chest pain (NCCP) is a medical condition described as acute, recurrent, or chronic chest pain, that is difficult to distinguish from ischemic heart pain, when the cardiac source has been excluded. Noncardiac chest pain represents a challenging clinical situation in gastroenterology practice, requiring sometimes a high amount of clinical investigation for a specific diagnostic. In some cases, the etiology is represented by esophageal diseases. This review aims to present the updated knowledge of the esophageal origin of NCCP. Methods. A search was performed in the main databases containing medical publications. The following search terms were used: noncardiac chest pain, esophageal chest pain (ECP), pathophysiology, noncardiac chest pain etiology, gastroesophageal reflux disease (GERD), motility esophagus disorders, functional chest pain. Observational studies were included. Studies that described only cardiac chest pain were excluded. Results. Noncardiac chest pain requires precise recognition of signs, symptoms and diagnostic testing in clinical practice. Due to financial constraints on subsequent care, an accurate algorithm based on clinical noncardiac chest pain guidelines should be followed. Esophageal chest pain represents a challenging diagnosis. Conclusions. Noncardiac chest pain is a prevalent and alarming symptom. Esophageal chest pain etiology should be considered once a cardiac source has been excluded. [ABSTRACT FROM AUTHOR]

Introduction: Non-cardiac chest pain (NCCP) is mainly related to oesophageal disease, and in spite of being a common condition in Mexico, information regarding it is scarce. Aim: To assess the clinical characteristics and health-related quality of life of patients with NCCP of presumed oesophageal origin. Material and methods: Patients with NCCP of presumed oesophageal origin with no previous treatment were included in the study. Associated symptoms were assessed and upper gastrointestinal endoscopy and 24-hour oesophageal pH monitoring were performed to diagnose gastroesophageal reflux disease, while oesophageal manometry was used to determine oesophageal motility disorders. The SF-36 Health-Related Quality of Life (HR-QoL) questionnaire was completed and its results compared to a control group without oesophageal symptoms. Results: The study included 33 patients, of which 61% were women, and the mean age was 46.1 (± 11.6) years. Causes of NCCP were gastroesophageal reflux disease in 48%, achalasia in 34%, and functional chest pain in 18%. The average progression time for chest pain was 24 (2-240) months, with ≤3 events/week in 52% of the patients. The most frequent accompanying symptoms were: regurgitation (81%), dysphagia (72%) and heartburn (66%). Patients with NCCP show deterioration in HR-QoL compared to the control group (P = .01), regardless of chest pain aetiology. The most affected areas were general perception of health, emotional issues, and mental health sub-scale (P > 0.05). Conclusions: In our population, patients with NCCP show deterioration in HR-QoL regardless of the aetiology, frequency, and accompanying symptoms.

Non-cardiogenic chest pain (NCCP) is defined as a pain indistinguishable from that caused by cardiac ischemia, after excluding this cause. NCCP is very frequent and its clinical management represents a great challenge for the gastroenterologist. The most common causes are gastroesophageal reflux disease (GERD), esophageal motility disorders and functional chest pain (FCP). The treatment should be aimed at correcting or alleviating the underlying cause. New diagnostic and therapeutic methods have appeared in recent years to improve the clinical management of this condition. Proton pump inhibitor (PPI), upper digestive endoscopy, wireless pH capsule, and esophageal pH-impedanciometry are the methods used to identify NCCP caused by GERD. High resolution esophageal manometry is the main tool to identify esophageal motor disorder with NCCP after GERD has been excluded. The negative diagnostic evaluation suggests that the cause is functional (DTF). Conventional treatments for GERD and esophageal motor disorders have proven useful in patients with NCCP when these causes are identified. In patients with DTF, therapy with neuromodulators has shown the best results. The psychological comorbidity is very frequent in all patients with NCCP and this should always be evaluated at the time of diagnosis and considered within the therapeutic plan. The purpose of this review is to discuss the current diagnosis and treatment of NCCP. [ABSTRACT FROM AUTHOR]

Background: Patients with non-cardiac chest pain (NCCP) are referred for esophageal motility testing and pH monitoring since gastroesophageal reflux disease (GERD) and esophageal motility disorders are frequently encountered in these patients. Our aim was to determine the prevalence and distribution of these disorders and to identify predictors of abnormal esophageal function testing. Methods: We performed a retrospective study of NCCP patients who presented after a negative cardiac evaluation and underwent esophageal manometry, esophageal pH monitoring and upper endoscopy from January 2010 to January 2017. Key results: In a total of 177 patients, esophageal motility disorders were diagnosed in 31% and GERD in 35% of the patients. The most common diagnoses were ineffective esophageal motility (IEM) in 14.1%, jackhammer esophagus in 6.8%, diffuse esophageal spasm in 5.1% and achalasia in 2.3% patients. Older age [for every 5-year increment, odds ratio (OR) 1.2 (95% confidence intervals (CI) 1.00-1.3) p = .047] and dysphagia [OR 3.8 (95% CI, 1.9-7.5) p < .001] were predictors of esophageal motility disorders. Older age [for every 5-year increment, OR 1.2 (95% CI, 1.01-1.3) p = .032] was predictive of GERD. Abnormal esophageal testing was associated with male gender [OR 2.2 (95% CI, 1.04-4.6) p = .039], older age [for every 5-year increment, OR 1.2 (95% CI, 1.03-1.3) p = .016] and Caucasian race [OR 3.1 (95% CI, 1.1-8.7) p < .029]. Conclusions: Approximately two thirds of patients presenting with NCCP have GERD or esophageal motility disorders. Esophageal function testing in NCCP should be considered in older patients, men, Caucasians and those presenting with dysphagia. [ABSTRACT FROM AUTHOR]

Noncardiac chest pain is associated with poor quality of life and high care expenditure. The majority of noncardiac chest pain is either gastresophageal reflux disease related or due to esophageal motility disorders, and the rest are considered functional chest pain (FCP) due to central and peripheral hypersensitivity. Current treatment of FCP improves 40-50% of patients. Cannabinoid receptors 1 (CB1) and 2 (CB2) modulate release of neurotransmitters; CB1 is located in the esophageal epithelium and reduces excitatory enteric transmission and potentially could reduce esophageal hypersensitivity. We performed a prospective study to evaluate its effects on pain threshold, frequency, and intensity in FCP. Subjects with FCP received dronabinol (5 mg, twice daily; n = 7; average age, 44 years; mean body mass index, 26.7) or placebo (n = 6; average age, 42 years; mean body mass index, 25.9) for 28 days (4 weeks). Chest pain, general health, and anxiety/depression questionnaires were assessed at baseline and at 4 weeks. Subjects underwent an esophageal balloon distention test prior to treatment and on last day of the study. Dronabinol increased pain thresholds significantly (3.0 vs. 1.0; P = 0.03) and reduced pain intensity and odynophagia compared to placebo (0.18 vs. 0.01 and 0.12 vs. 0.01, respectively, P = 0.04). Depression and anxiety scores did not differ between the groups at baseline or after treatment. No significant adverse effects were observed. In this novel study, dronabinol increased pain threshold and reduced frequency and intensity of pain in FCP. Further, large scale studies are needed to substantiate these findings. [ABSTRACT FROM AUTHOR]

Chest pain that is not explained by reflux disease or cardiac, musculoskeletal, mucosal, or motor esophageal abnormalities is classified as functional chest pain (FCP). Although several mechanisms are involved, esophageal hypersensitivity plays a major role and it could be considered a biomarker for FCP. Psychologic comorbidity such as anxiety, neuroticism, depression, and somatization is common. When the diagnosis of FCP is suspected, patients should undergo evaluation with esophageal motility testing, endoscopy, 24-h esophageal pH monitoring, and in some cases, sensory tests. Once the diagnosis of FCP has been established, treatment options rely on controlling patients' symptoms. Medical treatment has focused predominantly on medications that target pain, such as antidepressants and other pain neuromodulators. Non-pharmacologic interventions with complementary behavioral treatments, such as cognitive behavioral therapy, biofeedback, and hypnosis, have recently been recognized as useful in FCP patients. The latest findings on the evaluation and treatment of FCP are outlined herein. [ABSTRACT FROM AUTHOR]

After excluding a cardiac cause, potent anti-reflux therapy should be administered to patients with non-cardiac chest pain since gastroesophageal reflux disease (GERD) is the most common underlying mechanism of this disorder. If GERD is an unlikely cause of patient's symptoms, an esophageal motor disorder should be excluded. Spastic motility disorders can be treated with a smooth muscle relaxant (such as calcium channel blocker, nitrate, or phosphodiesterase 5 inhibitors). Alternatively, spastic motility disorders may respond to anti-spasmodics, pain modulators, botulinum toxin injection into the distal esophagus, and/or surgery. Patients with functional chest pain have recently seen an expanded treatment armamentarium including medications such as trazadone, tricyclic anti-depressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, pregabalin, and/or ramelteon. [ABSTRACT FROM AUTHOR]

Highlights: [•] Central hyperexcitability is believed to play a role in functional chest pain. [•] Microstructural reorganization of the pain neuromatrix was assessed. [•] Microstructural changes were not present in functional chest pain patients. [•] This challenges the hypothesis that visceral hypersensitivity is due to central changes. [Copyright &y& Elsevier]

Background Esophageal intubation is a widely utilized technique for a diverse array of physiological studies, activating a complex physiological response mediated, in part, by the autonomic nervous system ( ANS). In order to determine the optimal time period after intubation when physiological observations should be recorded, it is important to know the duration of, and factors that influence, this ANS response, in both health and disease. Methods Fifty healthy subjects (27 males, median age 31.9 years, range 20-53 years) and 20 patients with Rome III defined functional chest pain (nine male, median age of 38.7 years, range 28-59 years) had personality traits and anxiety measured. Subjects had heart rate ( HR), blood pressure ( BP), sympathetic (cardiac sympathetic index, CSI), and parasympathetic nervous system (cardiac vagal tone, CVT) parameters measured at baseline and in response to per nasum intubation with an esophageal catheter. CSI/ CVT recovery was measured following esophageal intubation. Key Results In all subjects, esophageal intubation caused an elevation in HR, BP, CSI, and skin conductance response ( SCR; all p < 0.0001) but concomitant CVT and cardiac sensitivity to the baroreflex ( CSB) withdrawal (all p < 0.04). Multiple linear regression analysis demonstrated that longer CVT recovery times were independently associated with higher neuroticism (p < 0.001). Patients had prolonged CSI and CVT recovery times in comparison to healthy subjects (112.5 s vs 46.5 s, p = 0.0001 and 549 s vs 223.5 s, p = 0.0001, respectively). Conclusions & Inferences Esophageal intubation activates a flight/flight ANS response. Future studies should allow for at least 10 min of recovery time. Consideration should be given to psychological traits and disease status as these can influence recovery. [ABSTRACT FROM AUTHOR]

Background and Aims: High-dose proton pump inhibitor (PPI) treatment leads to relatively little symptomatic improvement in patients with functional chest pain (FCP). This study was to evaluate the use of smooth muscle segmental changes in esophageal contraction as measured by topographical plots of high resolution manometry (HRM) as predictive factors of the response to high-dose PPI treatment in FCP patients. Methods: Thirty patients diagnosed with FCP were treated with rabeprazole 20 mg twice daily for 2 weeks and classified as positive and negative responders based on symptom intensity score. HRM topographical plots were analyzed for segment lengths, maximal wave amplitudes, and pressure volumes of the proximal and distal smooth muscle segments. Results: A positive response was observed in 23.3% of the patients. While the pressure volume of the proximal segment was significantly higher in the positive responders than the negative responders (900.4 ± 91.5 mm Hg/cm per s vs. 780.5 ± 133.3 mm Hg/cm per s, P = 0.017), the pressure volume of the distal segment was significantly lower in the positive responders (1914.0 ± 159.8 mm Hg/cm per s vs. 2140.5 ± 276.2 mm Hg/cm per s, P = 0.014). A prominent shifting in pressure volume to the distal segment was observed in the negative responders compared with the positive responders (segmental ratio of pressure volume (SRPV): 2.9 ± 0.5 vs. 2.1 ± 0.1, P < 0.001), and 2.39 was found to be the SRPV that best differentiated positive and negative responders. Conclusions: A low SRPV was associated with a positive response to high-dose PPI treatment in patients with FCP. [ABSTRACT FROM AUTHOR]

Background Functional chest pain is commonly reproduced by bag distension in the esophageal body. It is unknown whether such pain is primarily associated with mechanical stress and strain (force-deformation) or with changes in mucosal perfusion. Methods Fourteen patients (6M, 8F, average age 55.9 years) underwent ramp bag distension before and after injection of 20 mg butylscopolamine bromide (BS) using a novel bag catheter incorporating endosonography and laser Doppler perfusion monitoring. Healthy subjects served as controls. Mucosal perfusion was evaluated and stress and strain were computed and related to the sensation. Key Results The symptom score increased with bag volume ( P < 0.001). Volume as a function of pressure was higher in patients than in controls ( P < 0.001), both before and during BS. The stress-strain relationship was exponential and indicated a stiffer esophageal wall in patients especially before BS ( P < 0.01). The stress-strain curves indicate increased muscle tone in the functional chest pain patients. The perfusion decreased with increasing symptom score from visual analog scale 1-7 during BS. The decrease was on average 18.9% in patients and 19.7% in controls ( P = ns). Multiple regression analysis from distensions during BS showed that the discomfort/pain sensations depended on stress and strain ( P < 0.001) and with stress as the largest contributor. Perfusion did not contribute. Conclusions & Inferences Pain evoked by bag distension in patients with functional chest pain is stress-dependent rather than dependent on mucosal perfusion. Furthermore, the esophagus of the patients was characterized by more pronounced muscle tone during the distensions. [ABSTRACT FROM AUTHOR]

Visceral hypersensitivity plays a key role in the pathogenesis of esophageal functional disorders such as functional heartburn and chest pain of presumed esophageal origin (noncardiac chest pain). About 80% of patients with unexplained noncardiac chest pain exhibit lower esophageal sensory thresholds when compared to controls during esophageal sensory testing (ie, esophageal barostat, impedance planimetry). Such information has led to prescription of peripherally and/or centrally acting therapies for the management of these patients. This review summarizes and highlights recent and significant findings regarding the pathophysiology, evaluation, and treatment of the hypersensitive esophagus, a central factor in functional esophageal disorders. [ABSTRACT FROM AUTHOR]

Background There is limited and conflicting data regarding the role of esophageal hypersensitivity in the pathogenesis of functional chest pain (FCP). We examined esophageal sensori-motor properties, mechanics, and symptoms in subjects with FCP. Methods Esophageal balloon distension test was performed using impedance planimetry in 189 (m/f = 57/132) consecutive subjects with non-cardiac, non-reflux chest pain, and 36 (m/f = 16/20) healthy controls. The biomechanical and sensory properties of subjects with and without esophageal hypersensitivity were compared with controls. The frequency, intensity, and duration of chest pain were assessed. Key Results One hundred and forty-three (75%) subjects had esophageal hypersensitivity and 46 (25%) had normal sensitivity. Typical chest pain was reproduced in 105/143 (74%) subjects. Subjects with hypersensitivity demonstrated larger cross-sectional area ( P < 0.001), decreased esophageal wall strain ( P < 0.001) and distensibility ( P < 0.001), and lower thresholds for perception ( P < 0.01), discomfort ( P < 0.01), and pain ( P < 0.01) compared to those without hypersensitivity or healthy controls. Chest pain scores (mean ± SD) for frequency, intensity and duration were 2.5 ± 0.3, 2.2 ± 0.2, and 2.2 ± 0.2, respectively, and were similar between the two patient groups. Conclusions & Inferences Seventy-five per cent of subjects with FCP demonstrate esophageal hypersensitivity. Visceral hyperalgesia and sensori-motor dysfunction of the esophagus play a key role in the pathogenesis of chest pain. [ABSTRACT FROM AUTHOR]

Noncardiac chest pain is an angina-type discomfort without indication of ischemia. Diagnosis can be difficult because of its heterogeneous nature. Classification varies by specialty; gastroenterology uses the terminology gastroesophageal reflux disease related versus non-gastroesophageal reflux disease related. Other disciplines recognize noncardiac chest pain etiologies as having gastrointestinal, musculoskeletal, psychiatric, or pulmonary/other as underlying etiologies. Diagnostics yield a specific cause for effective treatment, which is aimed at the underlying etiology, but it is not always possible. Some patients with noncardiac chest pain have comorbidities and ongoing pain that lead to decreased quality of life and continued health care use., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Introduction: Non-cardiac chest pain (NCCP) is mainly related to oesophageal disease, and in spite of being a common condition in Mexico, information regarding it is scarce., Aim: To assess the clinical characteristics and health-related quality of life of patients with NCCP of presumed oesophageal origin., Material and Methods: Patients with NCCP of presumed oesophageal origin with no previous treatment were included in the study. Associated symptoms were assessed and upper gastrointestinal endoscopy and 24-hour oesophageal pH monitoring were performed to diagnose gastroesophageal reflux disease, while oesophageal manometry was used to determine oesophageal motility disorders. The SF-36 Health-Related Quality of Life (HR-QoL) questionnaire was completed and its results compared to a control group without oesophageal symptoms., Results: The study included 33 patients, of which 61% were women, and the mean age was 46.1 (±11.6) years. Causes of NCCP were gastroesophageal reflux disease in 48%, achalasia in 34%, and functional chest pain in 18%. The average progression time for chest pain was 24 (2-240) months, with ≤ 3 events/week in 52% of the patients. The most frequent accompanying symptoms were: regurgitation (81%), dysphagia (72%) and heartburn (66%). Patients with NCCP show deterioration in HR-QoL compared to the control group (P=.01), regardless of chest pain aetiology. The most affected areas were general perception of health, emotional issues, and mental health sub-scale (P>0.05)., Conclusions: In our population, patients with NCCP show deterioration in HR-QoL regardless of the aetiology, frequency, and accompanying symptoms., (Published by Masson Doyma México S.A.)

Aim: To investigate the efficacy of amitriptyline with proton pump inhibitor (PPI) for the treatment of functional chest pain (FCP)., Methods: This was a randomized, open-label trial investigating the addition of low dose amitriptyline (10 mg at bedtime) to a conventional dose of rabeprazole (20 mg/d) (group A, n = 20) vs a double-dose of rabeprazole (20 mg twice daily) (group B, n = 20) for patients with FCP whose symptoms were refractory to PPI. The primary efficacy endpoints were assessed by global symptom score assessment and the total number of individuals with > 50% improvement in their symptom score., Results: The between-group difference in global symptom scores was statistically significant during the last week of treatment (overall mean difference; 3.75 ± 0.31 vs 4.35 ± 0.29, the between-group difference; P < 0.001). Furthermore, 70.6% of patients in group A had their symptoms improve by > 50%, whereas only 26.3% of patients in group B had a similar treatment response (70.6% vs 26.3%, P = 0.008). Specifically, patients in group A had a significantly greater improvement in the domains of body pain and general health perception than did patients in group B (52.37 ± 17.00 vs 41.32 ± 12.34, P = 0.031 and 47.95 ± 18.58 vs 31.84 ± 16.84, P = 0.01, respectively)., Conclusion: Adding amitriptyline to a PPI was more effective than a double-dose of PPI in patients with FCP refractory to a conventional dose of PPI.