Esophageal motor disorders in patients evaluated for dysphagia and/or noncardiac chest pain

During the period January, 1983–October, 1990, 429 subjects were referred for functional evaluation of dysphagia and/or noncardiac chest pain. Of these, 304 (70.8%) were shown to have some kind of esophageal motor abnormality. The most frequent motor abnormality of the esophagus was represented by nonspecific motor disorders (31%), followed by achalasia (13%), whereas the other dysfunctions accounted for a smaller percentage. In particular, diffuse esophageal spasm was shown to be quite rare. It is concluded that esophageal manometry may provide a high diagnostic yield in patients presenting with dysphagia and/or noncardiac chest pain.     

Esophageal perception and noncardiac chest pain

Symptoms arising from the esophagus are produced generally in one of two ways: through stimulation of chemosensitive-nociceptors (eg, through excess esophageal exposure to refluxed gastric acid or the resulting inflammation arising in acid-damaged tissue) or through stimulation of mechanosensitive nociceptors (eg, through repeated deformation or distension of the esophageal wall resulting from peristaltic or lower esophageal sphincter dysfunction). These symptoms are usually attributed in most patients to such well recognized conditions as reflux esophagitis, achalasia,etc. that subsequently result in the delivery of specific and effective treatment.However, a subset of patients exists in which the etiology of "similar-sounding symptoms" remains obscure and their responses to standard specific treatments poor. Now recognized as among this group of patients are those with visceral hypersensitivity. Visceral hypersensitivity is not itself a disease but a definable aberrant sensory response (allodynia or hyper-algesia) to end-organ stimulation. Such an aberrant sensory response is neither specific for nor limited to the esophagus, and the etiopathogenesis for its development within this organ is unknown. Nonetheless, esophageal symptoms as a manifestation of visceral hypersensitivity are increasingly recognized and worthy of attention because they identify a disorder that responds to treatment aimed at the end organ's nociceptors or their neuroanatomic pathways within the CNS.     

Follow-up of patients with noncardiac chest pain

Noncardiac chest pain may be a debilitating symptom. The utility of esophageal testing to enhance patient quality of life has been inconclusive. The purpose of this study was to evaluate prospectively the impact of esophageal testing on patient well-being. Fifty-five patients undergoing esophageal testing were available for follow-up. Seventeen (31%) patients were classified in group 1: considered to have the esophagus as a likely etiology because of positive testing; 14 (25%) in group 2: possible contribution of the esophagus to symptoms; and 24 (44%) in group 3: unlikely esophageal etiology with negative testing. Thirty-four patients continued to be symptomatic at follow-up (median 112 days). The change in pain intensity from pretesting to follow-up was significant only for group 3 (P=0.001). There was a decline in hospital utilization in all three groups. (Emergency room visitsP=0.004 group 1, hospital admissionsP=0.02, group 3). Group 1 and 2 patients tended to miss less work, social functions, and activities. Group 3 continued to stay in bed and avoid normal functions. Nine of 34 (26%) patients who were symptomatic at follow-up identified the esophagus as the source of symptoms. In all, 42% of group 1, 29% of group 2, and 18% of group 3 patients considered the esophagus to be the source of their symptoms. We conclude that esophageal testing does not always prevent the persistence of symptoms and that patients have misperceptions about testing results on follow-up.This work was presented in part at the American Gastroenterological Association, New Orleans, Louisiana, May 1991.     

Systematic esophageal evaluation of patients with noncardiac chest pain

We prospectively studied 73 patients with angina-like chest pain severe enough to warrant admission to a coronary care unit over a five-month period. Thirty-four patients (47%) were found to have coronary artery disease as the cause of their symptoms, based on exercise testing, stress radionuclide imaging, or cardiac catheterization. The remaining 39 patients had normal cardiac findings and then underwent videoesophagography, radionuclide esophageal transit study, and esophageal manometry. Thirty-three of the 39 underwent acid perfusion testing (modified Bernstein's test). The findings at esophageal manometry were abnormal in 29 (74%) of 39. Manometric diagnoses were "nutcracker esophagus" in 17 (59%), nonspecific esophageal motility disorders in nine (31%), diffuse esophageal spasm in two (7%), and achalasia in one (3%). Bernstein's test reproduced symptoms in only 12%. The sensitivity of videoesophagography in detecting esophageal motility disorders was 66%, and that of radionuclide esophageal transit was 79%. The positive predictive values were 86% and 85%, respectively.     

Oesophageal manometry during eating in the investigation of patients with chest pain or dysphagia.

Dysphagia is a frequent cause of referral for oesophageal manometry although the motor response to eating is not routinely studied. We examined symptoms and oesophageal motor patterns in response to eating bread in 30 patients with either gastro-oesophageal reflux (n = 20), or normal oesophageal function tests (n = 10). No patient experienced symptoms while swallowing water but one complained of heartburn and one developed symptomatic oesophageal 'spasm' during eating. In eight further patients, pain or dysphagia which occurred with swallowing bread was associated with aperistalsis. Comparing asymptomatic and symptomatic periods, there was a slight increase in mean swallow frequency from 7.5 (0.79) (SEM) to 9.0 (1.17) swallows per minute (NS; n = 10). The mean number of aperistalsis swallows increased from 4.5 (0.96) per minute to 6.2 (1.30) (p less than 0.01; n = 10). Aperistalsis during symptoms was mainly caused by non-conducted swallows rather than synchronous contractions (mean 5.8 (1.45) per minute compared with 1.2 (0.44]. Aperistalsis can be produced by rapid swallowing in the normal oesophagus through 'deglutitive inhibition'. These results suggest that some patients experience dysphagia associated with aperistalsis perhaps as a response to increased frequency of swallowing. Functional abnormalities of this nature will not be detected by conventional oesophageal manometry.     

Diagnosis of noncardiac chest pain in older patients

Barium swallow and gallbladder study may reveal esophageal or gastric cancer, esophageal or duodenal ulcer, or gallstones. If serious GI tract disorders such as these are ruled out, the next step is to seek an esophageal source of recurring chest pain. Intraesophageal acid infusion and edrophonium chloride (Tensilon) stimulation can be used in the office to reproduce chest pain secondary to an esophageal disorder. With either test, reproduction of the patient's typical chest pain is positive. About one-third of patients seen in our laboratory with noncardiac chest pain have a positive response.     

The cost-effectiveness of the omeprazole test in patients with noncardiac chest pain.

PURPOSE: Recent evidence suggests that an empiric trial of omeprazole (the "omeprazole test") is sensitive and specific for diagnosing gastroesophageal reflux disease (GERD) as the cause of noncardiac chest pain. Our objective was to examine the clinical, economic, and policy implications of alternative diagnostic strategies for patients with noncardiac chest pain. METHODS: Decision analysis was used to evaluate the clinical and economic outcomes of two diagnostic strategies that begin with the omeprazole test (60 mg daily for 7 days) followed sequentially by invasive testing utilizing endoscopy, ambulatory 24-hour esophageal pH monitoring, and esophageal manometry as necessary, compared with two traditional strategies involving sequential invasive diagnostic tests. Cost estimates were based on Medicare reimbursement and the Red Book of average wholesale drug prices. Probability estimates were derived from a systematic review of the medical literature. RESULTS: The average cost per patient for the four diagnostic strategies varied from $1,859 to $2,313. Strategies utilizing the initial omeprazole test resulted in 84% of patients being symptom free at 1 year, compared with 73% to 74% for the strategies that began with invasive tests. The strategy of the omeprazole test, followed if necessary by ambulatory pH monitoring, then manometry, and then endoscopy, was both most effective and least expensive. It led to an 11% improvement in diagnostic accuracy and a 43% reduction in the use of invasive diagnostic tests, thus yielding an average cost savings of $454 per patient, compared with the strategy of beginning with endoscopy, then pH monitoring, and then manometry. CONCLUSIONS: Among patients with noncardiac chest pain, diagnostic strategies that begin with the omeprazole test result in reduced costs, improved diagnostic certainty, and a greater proportion of symptom-free patients at 1 year than do traditional strategies that begin with invasive diagnostic tests.     

Esophageal manometrics in patients with angina-like chest pain

Fifty-eight patients with angina-like chest pain had esophageal manometric testing. Forty-three had no evidence of coronary artery disease at the time of referral or at subsequent contact; 15 patients were proven to have coronary artery disease. High-amplitude contraction waves were the most frequently found manometric abnormality (15 patients). Less frequent were increased duration of contractions, achalasia, and diffuse esophageal spasm; the latter was present in only 3 patients. An approach to the interpretation of information obtained during manometry is presented. Using this approach, the esophagus was strongly implicated as the cause of the pain in 20 patients and was suspect in 18 others. Seven patients had results that exonerated the esophagus, and in the 13 remaining individuals, the esophagus was probably not the offending organ.     

The psychological aspects of noncardiac chest pain

There is some evidence to support a psychosocial link to GERD,although it is a weak one. The little research that has been done in this area is, in general, poor and inconclusive. Better designed studies must be done.The elements that seem to offer the best possibilities for research in GERD are the psychological variables involved in care seeking and the variations between care seekers and non-care seekers. In addition, research on psychosocial predictors of response to proton pump inhibitors, prokinetic agents, and antidepressants and other pain-modulating drugs need to be better understood.The psychosocial link to NCCP is stronger with regard to panic disorder,but much research needs to be done. Despite the paucity of well done,rigorously controlled studies in NCCP patients, that there is a high prevalence of psychiatric disturbance in this group. Parental health and childhood trauma are intriguing areas for further research, particularly in light of the connection between abuse and IBS and other functional GI disorders.Finally, panic disorder has been established as an important comorbidity of NCCP. It also merits more research, particularly into the pathophysiology that may link these two disorders.     

High amplitude, peristaltic esophageal contractions associated with chest pain and/or dysphagia.

Esophageal manometric tracings obtained using low-compliance pneumohydraulic infusion systems were reviewed from patients with symptoms of chest pain and/or dysphagia. Using this sytem, we report on 7 symptomatic patients with markedly increased esophageal peristaltic amplitude. Maximal peristaltic amplitude for these 7 patients (225-430 mmHg) was greater than for normals (75-175 mmHg). Mean peristaltic amplitude for the 7 was 170 mmHg, which was greater than for normals (81 +/- 30 mmHg, mean +/- 2 SD). This finding is believed to reflect the sensitivity of currently available manometric systems. It may be possible with these techniques to define more clearly the bulk of presumed esophageal dysfunction, which is at present poorly characterized. The relationship of clinical symptoms to abnormal esophageal motility is often less than optimal and may result from an inability to define "normal" or from inadequacies of currently available techniques. Our observations of a subset of symptomatic patients having peristaltic contractions with amplitudes exceeding the normal range seem to characterize one form of esophageal motility defect. This abnormality was seen more frequently than diffuse esophageal spasm in our laboratory.     

Randomized trial of sertraline in patients with unexplained chest pain of noncardiac origin

BACKGROUND: Between 10% and 30% of patients with symptoms similar to angina and sufficient to justify cardiac catheterization are found to have normal coronary angiograms. Treatment of patients with chest pain with no apparent cardiac cause is a major clinical problem. Our hypothesis was that sertraline would reduce the severity of pain in patients with chest pain of noncardiac origin. METHODS AND RESULTS: This was a single-site, double-blind, placebo-controlled study of the efficacy, tolerability, and safety of sertraline in the treatment of noncardiac chest pain in outpatients. Thirty patients were enrolled in the study. After 1 week of single-blind placebo washout, patients were randomly assigned in a double-blind fashion either to drug or placebo. The Beck Depression Inventory was administered at baseline and at completion of study. Daily pain diaries (visual analogue scale, rating pain on a scale of 1 to 10) were selfadministered and evaluated at baseline and at follow-up visits. Statistical measures were performed with an intention-to-treat approach. Patients who received sertraline over the course of the study showed a statistically significant reduction in pain compared with those who were receiving placebo. CONCLUSIONS: The use of sertraline in patients with noncardiac chest pain produced clinically significant reduction of daily pain. These results suggest the need for further studies of the efficacy and tolerability of sertraline and other selective serotonin reuptake inhibitors in the long-term management of noncardiac chest pain.     

Diagnosis and treatment of noncardiac chest pain

Chest pain is common: one in four of the population have an episode annually. Of those who present to hospital, nearly two-thirds have noncardiac chest pain. More than half of these cases might have gastroesophageal reflux disease. Opinion differs over what is the most appropriate application of current investigatory methods. Evidence suggests that, once cardiac disease is ruled unlikely, empiric use of a proton pump inhibitor is an option; if acid suppression fails, detailed investigations as clinically indicated can be considered. A range of esophageal investigations is available, including 24-hour or 48-hour esophageal pH testing and esophageal manometry, as well as provocative tests, but there is no consensus as to which methods are the most useful. Psychiatric evaluation is not routine, but psychiatric or psychological disorders are common. Musculoskeletal disorders are also common, but are frequently overlooked. It is possible to subject patients to a comprehensive set of investigations before empiric therapy, but recent studies have failed to demonstrate an improved outcome using this exhaustive approach. A new tactic is required, with less attention spent on absolute diagnostic accuracy and more emphasis on optimizing the long-term clinical outcome in patients with noncardiac chest pain. It is possible that the targeted use of multiple drug trials in a policy of 'therapy as investigation' might be a superior methodology.     

非心源性胸痛患者心理异常与症状间的关系

目的调查非心源性胸痛（NCCP）患者的心理精神因素异常状况，探讨它们与症状程度间的关系。方法对87例NCCP患者和健康对照组90人进行问卷调查，内容包括Zung焦虑自评量表（SAS）、Zung抑郁自评量表（SDS）、症状评分表，进行分析比较。结果1、NCCP患者焦虑、抑郁的发生率明显高于健康对照组（P〈0．005），平均焦虑、抑郁程度高于对照组（P〈0．001）。2、NCCP患者的症状积分与焦虑评分、抑郁评分呈正相关（P〈0．001）。结论焦虑和抑郁在NCCP发病机制中具有重要地位。     

Treatment of noncardiac chest pain of psychological origin

Opinion statement Psychiatric comorbidity is not an uncommon phenomenon in patients with noncardiac chest pain (NCCP). Panic disorder seems to be the most important psychiatric comorbidity for a number of reasons. First, it is the most common psychiatric disorder associated with NCCP. Second, panic disorder is a highly treatable condition that can produce dramatic improvement of NCCP when treatment is appropriate. Finally, the treatment of psychiatric comorbidity, whether panic disorder or other psychiatric disorders, can pay significant dividends in terms of improving the patient’s overall well-being and adaptation to illness, even if his/her chest pain symptoms are not alleviated. Adopting a biopsychosocial model to intervene on the stress of these patients’ experience is a key concept that can make NCCP a much less formidable challenge for the gastroenterologist.     

Exercise testing in patients with chest pain to sumatriptan

Objectives: In order to assess whether chest pain attributed to sumatriptan is associated with abnormalities on cardiac exercise testing, we performed a case-control study.Subjects: Cases were selected as consumers of sumatriptan who reported sumatriptan associated chest pain. A reference group was selected randomly from consumers of sumatriptan with the same GP as the case, who reported no chest pain after use of sumatriptan. If possible, controls were matched for age (within 5-year groups) and gender.Outcomes: In a total of 74 cases and 55 controls symptom-limited exercise tests were performed. Besides a small difference in age, there were no differences in basic characteristics between cases and controls. Three cases had ST-depression on ECG during exercise. However, none of the variables measured during exercise testing differed significantly between cases and controls.Conclusions: The prevalence of abnormal exercise tests in patients with sumatriptan-induced chest pain is low, and not statistically different from patients without chest pain after intake of sumatriptan. Routine performance of exercise testing in patients with sumatriptan-associated chest pain is not recommended.     

Determinants of high-sensitivity troponin T among patients with a noncardiac cause of chest pain

BackgroundIt is unknown to what extent noncardiac causes, including renal dysfunction, may contribute to high-sensitivity cardiac troponin T levels.MethodsIn an observational international multicenter study, we enrolled consecutive patients presenting with acute chest pain to the emergency department. Of 1181 patients enrolled, 572 were adjudicated by 2 independent cardiologists to have a noncardiac cause of chest pain. Multiple linear regression analyses were used to determine the important predictors of log-transformed high-sensitivity cardiac troponin T. Kaplan-Meier curve was used to assess the prognostic significance of high-sensitivity cardiac troponin T > 0.014 μg/L (99th percentile).ResultsA total of 88 patients (15%) had high-sensitivity cardiac troponin T > 0.014 μg/L. Less than 50% of cardiac troponins could be explained by known cardiac or noncardiac diseases. In decreasing order of importance, age, estimated glomerular filtration rate, hypertension, previous myocardial infarction, and chronic kidney disease (adjusted r² 0.44) emerged as significant factors in linear regression analysis to predict high-sensitivity cardiac troponin T. High-sensitivity cardiac troponin T was best explained by a linear curve with age as ≤ 0.014 μg/L. Patients with high-sensitivity cardiac troponin T levels > 0.014 μg/L were at increased risk for all-cause mortality (hazard ratio 3.0; 95% confidence interval, 0.8-10.6; P = .02) during follow-up.ConclusionAmong the known covariates, age and not renal dysfunction is the most important determinant of high-sensitivity cardiac troponin T. Because known cardiac and noncardiac factors, including renal dysfunction, explain less than 50% of high-sensitivity cardiac troponin T levels among patients with a noncardiac cause of chest pain, unknown or underestimated cardiac involvement during the acute presenting condition seems to be the major cause of elevated high-sensitivity cardiac troponin T.