Chest Pain Of Esophageal Origin Research Articles

The Role of Psychological Factors in Noncardiac Chest Pain of Esophageal Origin.

Noncardiac chest pain (NCCP) of esophageal origin is a challenging clinical problem of diverse etiology that affects more than 80 million Americans yearly. We assess the prevalence and impact of psychological disorders on NCCP of esophageal origin, describe possible mechanisms associated with this condition, and review psychological therapy options. Online search using PubMed and Medline from January 1, 1966, to April 30, 2023. Psychological disorders have been reported in up to 79% of patients with NCCP of esophageal origin. Several psychological disturbances have been identified with this condition, including depression, anxiety, panic disorder, phobias, and obsessive-compulsive and somatoform disorders. It is unclear whether the psychological disorders trigger the chest pain or vice versa. Multiple psychological mechanisms have been linked to chest pain and may contribute to its pathogenesis and severity. These mechanisms include cardiophobia, poor coping strategies, negative social problem solving, stress and perceived control, hypervigilance to cardiopulmonary sensations, altered pain perception, and alexithymia. Psychological therapies for NCCP of esophageal origin include cognitive behavioral therapy, hypnotherapy, physical and relaxation training, breathing retraining, and alternative medicine. Among the therapeutic options, cognitive behavioral therapy has been shown to be an effective treatment for NCCP of esophageal origin. This review raises awareness about the high prevalence of psychological disorders in NCCP of esophageal origin and highlights the need for clinical trials and trained therapists to address the management of this taxing clinical problem.

Protocolo diagnóstico del dolor torácico esofágico

Chest pain of oesophageal origin has similar characteristics to angina. A proper differential diagnosis should therefore be established at the start. This disease is a prevalent disorder that has no impact on patient mortality but entails a high use of healthcare resources. The oesophageal causes of chest pain include gastro-oesophageal reflux (GOR), oesophageal motility disorders and oesophageal hypersensitivity. It is estimated that more than half of the cases of chest pain of noncardiac origin have their origin in GOR. Anxiety and depression frequently coexist in these patients, which modulates the perception of disease severity.

Evaluation of esophageal high-resolution manometry combined with 24-hour pH monitor in detecting endoscopy-negative chest pain of esophageal origin

Objective To investigate esophageal high-resolution manometry （HRM） combined with 24-hour pH monitor in detecting endoscopy-negative chest pain of esophageal origin. Methods Test results of esophageal HRM combined with 24-hour pH monitor from 40 patients with recurring chest pain of esophageal origin were retrospectively analyzed. Results In 40 patients, 27 （67. 5% ） were diagnosed as gastroesophageal reflux disease with an average DeMeester scores at 18.3 ± 3.4, including 19 patients with esophageal body dismotility and 11 with reduced lower esophageal sphincter pressure （LESP） at a mean reduction of 5.7 mm Hg. There were 6 cases （ 15.0% ） of achalasia, in which 1 （2. 5% ） was type Ⅰ and 5 （ 12. 5% ） was type Ⅱ , with an average relaxation ratio of lower esophageal sphincter （RRLES） at （ 30. 1 ± 2. 3 ） %. There were 4 cases of diffuse esophageal spasm （DES）, with an average contraction frontal velocity （CFV） of 12. 3 ± 2. 4 cm.s^- 1 and abnormal contraction waves in esophageal body, spontaneous synchronous contraction waves were observed in 3 of 4 patients LESP increased in 1 patient with DES and remained normal in other 3. RRLES decreased in 2 cases with DES and remained normal in other 2. There were 2 cases （5. 0% ） of nutcracker esophagus, with an average distal contractile integral at 6745.5 ± 175.2 mm Hg.cm^-1 .s^-1 and an average CFV at4. 3 ±0. 4 cm.s^-1. There was 1 case （2. 5% ） with absence of esophageal peristalsis, with a low LESP at 2 mmHg and DeMeester scores at 38. 3. The patient was finally diagnosed as systemic sclerosis according to esophageal biopsy and other auxiliary examination. Conclusion HRM combined with 24-hour pH monitor is valuable in detecting endoscopy-negative chest pain of esophageal origin. Key words: Chest pain; Esophageal high-resolution manometry; Ambulatory esophageal pHmonitoring; Diagnosis

Experimental human pain models in gastro-esophageal reflux disease and unexplained chest pain

Methods related to experimental human pain research aim at activating different nociceptors, evoke pain from different organs and activate specific pathways and mechanisms. The different possibilities for using mechanical, electrical, thermal and chemical methods in visceral pain research are discussed with emphasis of combinations (e.g., the multimodal approach). The methods have been used widely in assessment of pain mechanisms in the esophagus and have contributed to our understanding of the symptoms reported in these patients. Hence abnormal activation and plastic changes of central pain pathways seem to play a major role in the symptoms in some patients with gastro-esophageal reflux disease and in patients with functional chest pain of esophageal origin. These findings may lead to an alternative approach for treatment in patients that does not respond to conventional medical or surgical therapy.

Chest pain of esophageal origin

Chest pain of esophageal origin

Chest pain of esophageal origin

Chest pain of esophageal origin is the most common atypical/extraesophageal manifestation of gastroesophageal reflux disease (GERD). We are increasingly recognizing the important role of the cardiologist in making the diagnosis. Studies continue to focus on the mechanisms of pain in this challenging group of patients. Factors that determine the development and persistence of visceral hypersensitivity are currently under investigation. Invasive diagnostic studies have been replaced by therapeutic trials or empirical therapies. Proton pump inhibitors have been demonstrated to be the most effective treatment for GERD-related noncardiac chest pain (NCCP). Pain modulators remain the primary therapy for non-GERD-related NCCP. Sertraline is the first selective serotonin reuptake inhibitor to demonstrate a significant improvement in chest pain symptoms.

Chest pain of esophageal origin

Chest pain of esophageal origin is the most common atypical/extraesophageal manifestation of gastroesophageal reflux disease (GERD). We are increasingly recognizing the important role of the cardiologist in making the diagnosis. Studies continue to focus on the mechanisms of pain in this challenging group of patients. Factors that determine the development and persistence of visceral hypersensitivity are currently under investigation. Invasive diagnostic studies have been replaced by therapeutic trials or empirical therapies. Proton pump inhibitors have been demonstrated to be the most effective treatment for GERD-related noncardiac chest pain (NCCP). Pain modulators remain the primary therapy for non-GERD-related NCCP. Sertraline is the first selective serotonin reuptake inhibitor to demonstrate a significant improvement in chest pain symptoms.

Functional chest pain of esophageal origin: hyperalgesia or motor dysfunction

OBJECTIVE: Many patients with functional (noncardiac) chest pain exhibit both hypersensitivity and motor dysfunction of the esophageal wall. We aimed to determine whether the sensory or motor dysfunction plays an important role in the pathogenesis of chest pain. METHODS: We performed graded balloon distentions of the esophagus using impedance planimetry in 16 consecutive patients with chest pain and otherwise normal cardiac and esophageal evaluations and in 13 healthy controls. In those patients who experienced chest pain with balloon distention, the test was repeated after atropine was given. Sensory and biomechanical parameters were measured. RESULTS: Balloon distention reproduced typical chest pain in 13/16 patients (81%) and at lower ( p < 0.01) sensory thresholds than controls. Pain was reproduced in all 13 patients and at lower ( p < 0.05) sensory thresholds after atropine. Also, after atropine, the esophageal cross-sectional area and wall tension increased ( p < 0.05), the tension/strain association shifted to the right ( p < 0.05), and reactivity decreased ( p < 0.002) relative to results before atropine or in healthy controls ( i.e., the esophageal wall relaxed and became more deformable). CONCLUSIONS: Even after relaxing the esophageal wall, most patients experienced chest pain and at lower sensory thresholds. Hence, hyperalgesia rather than motor dysfunction appears to be the predominant mechanism for functional chest pain of esophageal origin.

Functional chest pain of esophageal origin: hyperalgesia or motor dysfunction.

Many patients with functional (noncardiac) chest pain exhibit both hypersensitivity and motor dysfunction of the esophageal wall. We aimed to determine whether the sensory or motor dysfunction plays an important role in the pathogenesis of chest pain. We performed graded balloon distentions of the esophagus using impedance planimetry in 16 consecutive patients with chest pain and otherwise normal cardiac and esophageal evaluations and in 13 healthy controls. In those patients who experienced chest pain with balloon distention, the test was repeated after atropine was given. Sensory and biomechanical parameters were measured. Balloon distention reproduced typical chest pain in 13/16 patients (81%) and at lower (p < 0.01) sensory thresholds than controls. Pain was reproduced in all 13 patients and at lower (p < 0.05) sensory thresholds after atropine. Also, after atropine, the esophageal cross-sectional area and wall tension increased (p < 0.05), the tension/strain association shifted to the right (p < 0.05), and reactivity decreased (p < 0.002) relative to results before atropine or in healthy controls (i.e., the esophageal wall relaxed and became more deformable). Even after relaxing the esophageal wall, most patients experienced chest pain and at lower sensory thresholds. Hence, hyperalgesia rather than motor dysfunction appears to be the predominant mechanism for functional chest pain of esophageal origin.

Chest pain of esophageal origin

Chest pain of esophageal origin or noncardiac chest pain is reported by at least a fifth of the general population. Recent literature focused on further understanding mechanisms of chest pain in subset of patients with functional chest pain of presumed esophageal origin. Studies have demonstrated concurrent visceral and somatic pain hypersensitivity, and amplified secondary allodynia, in patients with noncardiac chest pain (NCCP), suggesting central sensitization. Other studies have demonstrated abnormal cerebral processing of intraesophageal stimuli. However, gastroesophageal reflux disease (GERD) has remained the most common esophageal cause of NCCP. The introduction of the proton pump inhibitor test, a highly sensitive and cost-effective diagnostic strategy, simplified our diagnostic approach toward patients with GERD-related NCCP. For patients with positive proton-pump-inhibitor test results, long-term treatment with antireflux medication is warranted. For patients with non-GERD-related NCCP, pain modulators remain the cornerstone of therapy.

Abnormal esophagocardiac reflex in patients with non-cardiac chest pain.

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.

Chest pain of esophageal origin

Patients with unexplained chest pain remain a difficult and perplexing challenge for the gastroenterologist. Despite exclusion of a cardiac origin many patients remain disabled by pain. In these, a diligent search for an esophageal cause-gastroesophageal reflux disease, motility abnormalities, or esophageal hypersensitivity using all available diagnostic (therapeutic) tools-results in a positive outcome. Appropriate use of a diagnostic trial of therapy, ambulatory pH monitoring and/or esophageal manometry, necessitates understanding of the respective benefits. The recent literature examines the value of a short course of high-dose proton pump inhibitors in establishing a diagnosis of gastroesophageal reflux disease-associated chest pain, the use of tricyclic antidepressants, and behavioral therapy in the management of these difficult patients with nonreflux, noncardiac chest pain.

Chest pain of esophageal origin

The treatment of patients with unexplained chest pain is difficult and challenging. After a cardiac etiology has been ruled out, a diligent search for an esophageal etiology-gastroesophageal reflux disease, motility abnormalities, or esophageal hypersensitivity-should be undertaken with judicious use of a diagnostic (therapeutic) trial of therapy, ambulatory pH monitoring, or esophageal manometry. The recent literature discusses the use of high-dose omeprazole in diagnosing and treating chest pain associated with gastroesophageal reflux disease, correlates abnormal ambulatory pH monitoring with response to omeprazole, and provides additional insights into the pathogenesis of esophageal chest pain.

Noncardiac Chest Pain of Esophageal Origin.

Cardiac and musculoskeletal disease should be excluded before considering an esophageal etiology for chest pain. Acid reflux is a common cause of chest pain and should be identified and treated. A therapeutic trial should consist of a proton pump inhibitor (omeprazole 20 mg or lanzoprazole 30 mg) given one or two times per day for at least 6 to 8 weeks. An alternative is to use an ambulatory pH study to confirm reflux. Also, if the patient fails the initial treatment, reflux should be confirmed with pH testing before increasing the dose of proton pump inhibitor or considering combination or surgical therapy. Esophageal manometry should be considered in patients with chest pain and dysphagia. It is also reasonable to perform manometry before a pH study since manometric localization of the lower esophageal sphincter (LES) is needed to ensure accurate pH probe placement. Only after manometric confirmation of a spastic esophageal motility disorder should patients be treated for esophageal spasm. In these patients, it is reasonable to try a long-acting formulation of a calcium-channel blocker or nitrate. Patients with chest pain who have a negative cardiac evaluation and who do not have reflux may have an abnormality in esophageal or cardiac sensation. These patients should be treated with a trial of an antidepressant and considered for referral to a mental health practitioner. All medication trials should continue at least 6 to 8 weeks to avoid a placebo effect and to allow adequate time for a therapeutic response.

Chest pain of esophageal origin

One third to one half of patients presenting with chest pain have no evidence of coronary artery disease and are characterized as having non-cardiac chest pain. In a large subset of these patients, the esophagus can be the source of the symptoms. This paper summarizes recent progress in our understanding of chest pain of esophageal origin. The value of esophageal diagnostic evaluation in patients with chest pain and normal coronary arteries remains controversial. Symptomatic gastroesophagel reflux is the most common cause of chest pain of esophageal origin. The use of impedance planimetry has provided a better insight in the mechanisms underlying hypersensitivity to esophageal balloon distension. The high prevalence and likely role of panic disorder in patients with chest pain of non -cardica origin has been confirmed. Further investigations towards factors underlying atypical chest pain should include not only a gastrointestinal but also a psychological work-up. Finally, recent reports indicate the contribution of the esophagus to chest pain events in patients with known coronary artery disease.

The diagnostic value of oesophageal radionuclide transit in patients admitted for but without acute myocardial infarction.

The use of radionuclide transit (RT) as a screening test for chest pain of oesophageal origin has been debated. The aim of this study was to determine the value of RT as a screening test for oesophageal disorders in comparison with oesophageal manometry in patients admitted with acute chest pain but without acute myocardial infarction (non-AMI patients), and to assess the frequency of oesophageal disease present in these patients. A total of 222 non-AMI patients entered the study. An extensive examination programme comprised noninvasive cardiac studies, pulmonary studies, a careful physical examination of the musculoskeletal system, and oesophago-gastric examinations including endoscopy, pH monitoring of the oesophagus and a Bernstein test. In 91% of the patients one or more diagnoses were obtained. Based on clinical and laboratory data a 'consensus' diagnosis was made. With manometry as the reference RT had a poor sensitivity (35%) but an acceptable specificity (82%). With the consensus diagnosis as the gold standard the sensitivities of both manometry and RT were poor (29%), whereas the specificity of RT, but not of manometry, was very high (97%). Gastrointestinal diagnoses were found in 57% of the patients. In conclusion, none of the applied oesophageal examinations are valuable as single screening tests. Both RT and manometry have low sensitivities. RT may be used as a cheap, noninvasive and rapid supplementary examination. When positive, it strongly supports further invasive studies of the oesophagus in non-AMI patients with unexplained chest pain.

Esophageal visceral pain sensitivity: effects of TENS and correlation with manometric findings.

Increased esophageal visceral sensitivity has been suggested to be an important factor in the development of esophageal chest pain. Transcutaneous electrical nerve stimulation (TENS) has been found effective in the treatment of visceral heart pain in severe angina pectoris, but its effect on esophageal pain perception is not known. In this study, we used the method of graded intraesophageal balloon distension to study the effects of TENS on esophageal motility and pain sensitivity. In addition, we explored the relationship between manometric findings and esophageal susceptibility to pain. TENS reduced symptoms during balloon distension significantly and decreased peristaltic velocity. Increased visceral perception was positively correlated to the amplitude and duration of the esophageal peristalsis. This study suggests a correlation between increased peristaltic waves and visceral perception in the esophagus. TENS appears to reduce esophageal pain sensitivity and thus may be a useful treatment for noncardiac chest pain of esophageal origin.

Chest pain of esophageal origin and nonobstructive dysphagia

In patients with angina-like noncardiac chest pain and dysphagia occurring in the absence of structural esophageal lesions, disordered esophageal function may be the cause of the symptoms. Specialized esophageal function tests are often required to detect these. This paper summarizes the recently reported new findings on diagnosis, pathophysiology, and treatment of noncardiac chest pain and nonobstructive dysphagia.

ESOPHAGEAL EMERGENCIES

Esophageal disorders are commonly seen in the emergency department. Dysphagia (difficulty swallowing) should always be taken seriously and should never be considered a functional complaint, whereas odynophagia (painful swallowing) is usually caused by an inflammatory process. This article addresses dysphagia/odynophagia, as well as esophagitis, neoplasms, gastroesophageal reflux disease, esophageal trauma, and the often difficult differentiation of chest pain of esophageal origin.

Chest pain of esophageal origin

Chest pain of esophageal origin