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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angina-like chest pain in patients with coronary arteriography raises difficult diagnostic problems. The pain may be due to microvascular angina (or syndrome X). It is postulated that during the typical angina of these patients, the ST segment shifts on exercise electrocardiogram and the abnormal electrophysiologic tests on cardiac catheterisation are due to a decreased coronary flow reserve related to microvascular abnormalities. Angina-like chest pain may also be of oesophageal origin. Gastro-oesophageal reflux and oesophageal motility disorders are the two commonest oesophageal abnormalities held responsible for the pain. Recent observations suggest that sensitivity of the oesophagus to several stimuli may be another important cause of chest pain of oesophageal origin. This condition is called irritable oesophagus. Twenty-four hour pH- and pressure-recording is at present the best way to reach a specific diagnosis about the nature of the oesophageal abnormality.
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PMID:Gastro-oesophageal reflux disease, an important cause of angina-like chest pain. 269 37

Using 24 hour pH monitoring as a reference standard, the usefulness of the acid perfusion (AP) test in predicting gastro-oesophageal reflux disease (GORD) was assessed in 71 non-cardiac chest pain (NCCP) patients and 23 endoscopic oesophagitis patients. Of the 71 NCCP patients, 35 had a positive AP test (of whom 20 had an abnormal 24 hour pH) and 36 had a negative AP test (of whom 14 had an abnormal 24 hour pH study). Thus, the sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of the AP test in this group was 59%, 59%, 57%, and 61%, respectively. The corresponding values in the oesophagitis group were 85%, 67%, 94%, and 40%. In the NCCP group when heartburn alone was used as the positive criterion the PPV rose to 74%. When chest pain with or without heartburn was used, however, the PPV dropped to 38%. A 'symptom index' was used to define the number of chest pain episodes that were caused by acid reflux. Only 48% of AP test positive patients had demonstrable acid mediated chest pain. In the NCCP population with a normal oesophageal examination (1) AP test reproduction of chest pain is poorly predictive of GORD; (2) AP test reproduction of heartburn is more predictive of GORD but does not ensure that the chest pain is caused by GORD; (3) a negative AP test does not exclude GORD and (4) only 48% of AP test positive patients have demonstrable acid mediated chest pain. The ambulatory 24 hour pH test may have rendered the AP test obsolete in the assessment of GORD as the cause of NCCP.
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PMID:Acid perfusion test: does it have a role in the assessment of non cardiac chest pain? 261 93

Oesophageal function was assessed in 52 patients with angina pectoris whose coronary angiograms were completely normal and in 21 patients with angina pectoris who had significant coronary artery disease. During a standard oesophageal manometric study, abnormalities were found in 23 (44%) patients with normal coronary angiograms but in only 2 (10%) patients with coronary artery disease (p less than 0.01). Twenty-four (46%) patients with normal coronary angiograms were found to have gastro-oesophageal reflux disease during 24-hour oesophageal pH monitoring. Of the 52 patients with normal coronary angiograms, 19 (37%) had gastro-oesophageal reflux disease and abnormal oesophageal motility, 5 (10%) had gastro-oesophageal reflux disease alone, and 7 (13%) had oesophageal motility disorder alone. The use of provocation procedures, including intravenous edrophonium during oesophageal manometry and treadmill exercise testing during pH monitoring, enabled the oesophageal abnormality to be demonstrated simultaneously with chest pain in 25 of these 31 patients. Typical angina pectoris, coincident with abnormal oesophageal motility, was precipitated in a subgroup of patients who had been shown to have oesophageal manometric abnormalities and gastro-oesophageal reflux disease by the infusion of hydrochloric acid into the oesophagus; both the chest pain and manometric abnormality resolved following the oral administration of antacid.
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PMID:Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease. 276 42

The clinical relevance of a system of ambulatory 24-hour oesophageal pressure and pH recording with automated data analysis was investigated in 33 unselected patients with non-cardiac chest pain. After conventional manometry with edrophonium (Tensilon) provocation, 24-hour oesophageal pH and pressure monitoring was performed. In 17 patients conventional manometry, edrophonium provocation and 24-hour pH recording revealed an oesophageal origin of the symptoms: 6 patients had oesophageal motility disorders, 3 were positive responders to edrophonium and 8 had chest pain associated with gastro-oesophageal reflux. In none of the patients who had a pain attack during prolonged oesophageal pressure recording, was a new motility disorder detected.
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PMID:[The value of ambulatory 24-hour esophageal manometry in the diagnosis of retrosternal pain of non-cardiac origin]. 281 4

Various oesophageal manometric disorders have been associated with chest pain or dysphagia. The classic motility disorders are achalasia and diffuse oesophageal spasm. In achalasia, a disorder of aperistalsis in the oesophageal body and incomplete relaxation of the lower oesophageal sphincter, either surgical myotomy or pneumatic dilatation is an effective approach, although some investigators have suggested a role for pharmacological therapy. For the treatment of diffuse oesophageal spasm, a disorder of non-peristaltic motor activity in the oesophagus, various pharmacological approaches with nitrates, anticholinergics, and calcium antagonists have been used. In the presence of associated lower oesophageal sphincter dysfunction, bouginage or pneumatic dilatation may be indicated. Long oesophagomyotomy should be considered for those patients who fail to respond to these measures. Recent manometric techniques have led to the identification of patients with chest pain or dysphagia who have abnormalities of increased contractile amplitude ('nutcracker' oesophagus) or duration. An association with gastro-oesophageal reflux or with psychiatric disturbance has been suggested. Treatment directed towards these factors is indicated and may be supplemented by pharmacological intervention, e.g. by calcium antagonists or anticholinergics.
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PMID:Primary oesophageal motility disorders. Current therapeutic concepts. 286 26

Investigations of the oesophagus were undertaken in 50 consecutive patients who presented with recurrent chest pain thought to be non-cardiac in origin after cardiological assessment. An oesophageal disorder was demonstrated in 60%, gastro-oesophageal reflux and diffuse oesophageal spasm being the two commonest entities. However, routine contrast radiology and upper gastrointestinal endoscopy revealed abnormalities in only a minority of patients. Patients with non-cardiac chest pain of uncertain origin should initially undergo endoscopy. If no major abnormalities are detected radionuclide oesophageal transit studies, oesophageal manometry, and ambulatory monitoring of oesophageal pH should be carried out.
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PMID:The oesophagus as a cause of recurrent chest pain: which patients should be investigated and which tests should be used? 286 13

The diagnostic yield of routine esophageal manometrics in evaluating noncardiac chest pain is low. To determine if bethanechol stimulation would increase the diagnostic yield, we examined 87 patients with chest pain but no gastroesophageal reflux, 47 patients with gastroesophageal reflux but no chest pain, and 20 normal subjects. All subjects underwent standard esophageal manometrics before and after two doses of 50 micrograms/kg body wt bethanechol administered subcutaneously 15 min apart. Mean amplitude and duration of contractions and percentage of abnormal contractions were measured in the distal 7 cm of the esophageal body. Pathologic manometric parameters were defined as mean +/- 2 SD of values obtained in normal patients. Patients with chest pain had pathological responses for amplitude of contraction, duration of contraction, and percentage of abnormal contractions of 31%, 14%, and 22%, respectively, in the basal period. This increased to 43%, 66%, and 40%, respectively, after the first dose of bethanechol and to 53%, 85%, and 82% after the second dose of bethanechol. Chest pain was reproduced with new manometric abnormalities in 46% of patients after the first dose of bethanechol and in 77% after the second dose. Our conclusions are that: sequential bethanechol administration significantly increases the diagnostic yield of standard esophageal manometrics in the evaluation of noncardiac chest pain and duration of contraction after pharmacologic provocation with bethanechol is the best parameter to segregate patients with chest pain from normal subjects and gastroesophageal reflux patients.
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PMID:Bethanechol increases the diagnostic yield in patients with esophageal chest pain. 287 16

Symptomatic gastroesophageal reflux occurs daily in an estimated 7% of adults and weekly or monthly in 29%. Untreated it can lead to esophageal erosions, ulceration and stricture formation. The pathogenesis is often multifactorial: defects in the function of the lower esophageal sphincter, esophageal clearance mechanisms and gastric emptying combine to produce frequent lengthy periods during which the lower esophagus is bathed in regurgitated acid. In most patients reflux disease is easily recognized as recurrent heartburn, regurgitation or dysphagia, or a combination. When acute chest pain or respiratory illness is the primary presenting complaint the patient needs particularly careful investigation to determine whether the symptoms are due to a primary cardiac or respiratory condition, are secondary to gastroesophageal reflux alone or represent a combination of disorders. Endoscopy with biopsy and long-term pH monitoring are the most reliable ways of determining whether reflux disease is present. Additional investigations, such as exercise testing, cardiac catheterization or inhalation challenge, may be needed in patients with cardiac or respiratory symptoms. Treatment should follow a stepped-care approach and in most patients should begin with changes in lifestyle, including dietary manipulation, reducing alcohol and cigarette consumption, and raising the head of the bed, together with appropriate use of antacids or alginate-antacid combinations. H2-receptor antagonists and agents to improve both gastric emptying and the tone of the lower esophageal sphincter may be added in sequence. Most patients will respond well to this regimen. Surgery should be considered only for those with intractable symptoms or with complications (e.g., stricture formation, bleeding, development of dysplastic epithelium in those with Barrett's esophagus, or secondary pulmonary disease that does not respond to medical management). It is successful in 85% of well-selected patients and has few complications.
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PMID:Gastroesophageal reflux: clinical presentations, diagnosis and management. 287 69

33 patients with angina-like chest pain of oesophageal origin were investigated. In 8 (24%) the pain proved to be related to oesophageal motor disorders unaccompanied by gastro-oesophageal reflux; in 12 (36%) acid reflux contributed to chest pain; but in the remaining 13 (40%) identical chest pain episodes were due to various mechanisms including reflux without motor disorders, motor disorders without reflux, motor disorders without reflux but with positive acid-perfusion test, and acid reflux without motility disorders but with positive edrophonium-stimulation test. These data strongly suggest that the mechanism of pain in these patients is related to irritability of the oesophagus.
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PMID:The irritable oesophagus--a frequent cause of angina-like pain. 288 70

Calcium-channel blocking agents can relieve anginal and chest pain associated with hypermotility of the esophagus. Although calcium-channel antagonists differ in their effects on the esophageal body and the lower esophageal sphincter, reduction of lower esophageal sphincter pressure theoretically could result in gastroesophageal reflux and pain. This pain may be difficult to differentiate from chest pain of cardiac origin. An association between calcium-channel blocking agents and chest pain is speculative at this time. However, the possibility of such an effect should be considered by clinicians in the total management of patients. Future clinical studies are warranted to address the issue of the incidence of such an effect and to define more precisely the potential interrelationship among the calcium-channel antagonists, their efficacy in relieving cardiac pain, and their potential liability in inducing chest pain of noncardiac origin.
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PMID:Calcium-channel blocking agents and chest pain. 304 91


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