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

The study was carried out on 18 patients with angina pectoris in whom the usual treatment with nitroderivatives and/or Ca-antagonists did not improve or prevent the angina-like chest pain in the absence of unstable angina. The patients underwent the following oesophageal examinations: X-ray, endoscopy-biopsy, manometry, acid perfusion test and 24-hour oesophageal pH ambulatory monitoring, the latter two being made in association with dynamic ECG. The presence of coronary insufficiency had been previously determined by means of ECG and scintigraphic stress tests and, when necessary, coronary arteriography was performed. In 10/18 patients severe oesophageal motor disorders were observed, the most frequent being diffuse oesophageal spasm. In the entire group the lower oesophageal sphincter basal tone was significantly lower than normal. In 14/18 patients a pathologic gastroesophageal reflux was detected: in 2 of these patients a temporal correlation between pain attacks and episodes of gastroesophageal reflux were observed in the absence of ECG modifications. Acid perfusion test induced the angina-like chest pain in another 2 patients without ECG modifications. In conclusion, the angina-like chest pain of these patients is not due to a failure of the antianginal therapy in relieving the coronary insufficiency, but is most probably related to gastroesophageal reflux. This oesophageal disorder may be considered a side effect caused by prolonged therapy with nitroderivatives and Ca-antagonists. In fact, these drugs decrease the lower oesophageal sphincter tone which is the main barrier against the reflux of gastric contents into the oesophagus so favoring gastroesophageal reflux and related disorders, including oesophageal pain.
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PMID:"Oesophageal angina" in patients with angina pectoris: a possible side effect of chronic therapy with nitroderivates and Ca-antagonists. 139 24

This study investigates 113 consecutive patients with gastro-oesophageal reflux disease before and after fundoplication and crural repair with respect to symptomatic improvement of chest pain, angina pectoris, exercise-linked chest pain, meal-linked chest pain, dyspnea, and air hunger, and any correlation between these items and smoking habits. The patients were followed by identical questionnaires completed at the time of oesophageal manometric examination prior to operation and from 6 months up to more than 5 years after operation. There was a highly significant reduction in all kinds of chest pain including angina pectoris, and of dyspnea at follow-up independent of smoking habits. However, air hunger was not significantly reduced. The present results suggest that gastro-oesophageal reflux disease should be taken into consideration in the symptomatic diagnosis of angina pectoris.
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PMID:Remission of angina pectoris and dyspnea by fundoplication in gastro-oesophageal reflux disease. 148 38

Recurrent chest pain in patients with normal coronary arteries is a difficult clinical problem. Although long-term studies have shown that these patients have an excellent prognosis in terms of cardiac morbidity and mortality, many patients remain physically debilitated and continue to visit emergency departments. Recent information suggests that microvascular angina, esophageal disorders (including reflux disease and dysmotility), and panic disorder may be important causes of pain in such patients. It is particularly important to consider the diagnosis of gastroesophageal reflux disease, which is easier to diagnose and treat than most other causes of recurrent chest pain.
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PMID:Chest pain in patients with normal coronary arteries. A new look at potential causes. 157 28

Patients with unexplained chest pain represent a major clinical dilemma for primary-care physicians, gastroenterologists, and cardiologists. References to this prevalent clinical problem date to more than 150 years ago; confusion about its pathophysiology has resulted in the use of a variety of descriptive terms such as "noncardiac," "atypical," and "angiographically negative" chest pain. Since none of these terms applies to all cases, the description "chest pain of undetermined origin" may be preferable. Because the esophagus has a similar location and innervation as the heart, an esophageal source for unexplained chest pain syndromes has been frequently suggested. Recent studies have emphasized the importance of gastroesophageal reflux as a likely component of esophageal pain. Moreover, "irritable esophagus" is an emerging concept that implies a generalized alteration in esophageal pain threshold, that is, abnormal nociception. The potential effects of stress or altered psychological states in this phenomenon must be considered, and the role of "panic attacks" in the production of pain in these patients needs to be clarified. In addition, stress may produce altered esophageal motility and lead to manometric abnormalities such as the "nutcracker esophagus" or a hypertensive lower esophageal sphincter. Finally, the precise contribution of the heart in producing pain in patients with normal coronary angiograms remains unclear because the precise role of microvascular angina has yet to be clarified.
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PMID:Chest pain of undetermined origin: overview of pathophysiology. 159 59

Identifying the cause of recurrent chest pain may be difficult. Significant coronary artery disease must be excluded before patients can be assured that their symptoms are truly "noncardiac." A normal coronary angiogram is the most definitive test but this may not preclude the presence of a new "fly in the ointment," i.e., microvascular angina. Musculoskeletal pain syndromes, psychological problems, and esophageal disorders, including both esophageal motility disorders and gastroesophageal reflux disease, are the most common causes of noncardiac chest pain. Nearly 30% of these patients will have an esophageal motility disorder, although its clinical relevance in the asymptomatic patient is controversial. Simple, inexpensive, provocation tests (most commonly edrophonium, bethanechol, and/or balloon distention) have been developed to recreate motility-related chest pain in the laboratory. These tests can identify the esophagus as the source of pain, but in most cases they do not direct therapy. Other disadvantages of provocation tests include the lack of a gold standard reference point, side effects, and the need for placebo because of a subjective end point. Recently, ambulatory esophageal pH and pressure monitoring have been used to define precisely the cause of esophageal chest pain. These systems can record multiple episodes of pain for up to 24 hours in an outpatient setting and have shown that gastroesophageal reflux (rather than motility disorders) is the most common esophageal cause of pain. However, these studies also suggest that many episodes of chest pain do not have an identifiable esophageal cause. Furthermore, this equipment is expensive, uncomfortable, may alter normal activity, and is not useful in patients having infrequent pain episodes. Psychological disturbances should be carefully sought in any patient with noncardiac chest pain: Many patients have anxiety, depression, or panic attacks that may complicate or contribute to their reported symptoms. It is questionable if these patients need additional testing. Rather, the challenge of the future is to prove that the multitude of tests aid in the overall treatment and outcome of patients with noncardiac chest pain.
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PMID:Overview of diagnostic testing for chest pain of unknown origin. 159 63

The esophageal origin of angina-like noncardiac chest pain can be identified with certainty only when spontaneous chest pain episodes are associated with gastroesophageal reflux, abnormal esophageal motility, or both. Since noncardiac chest pain typically occurs infrequently, prolonged monitoring is required to establish such an association. Ambulatory esophageal monitoring offers the additional advantages of studying the patient in everyday life and avoiding hospital admission. Although the amplification and storage of 24-hour signals in a portable recorder no longer poses technical problems, the complexity of the analysis of the recorded signals should not be underestimated. For noncardiac chest pain, the most relevant part of the analysis is the association between chest pain episodes and the recorded esophageal signals. To determine whether contraction amplitude or duration during chest pain episodes is abnormal, their measurements are compared with baseline values from the same patient. Fully automated analysis by computer is feasible and, since it avoids observer bias, preferable. The yield of 24-hour monitoring in noncardiac chest pain reported by different groups of investigators varies considerably. Motor abnormalities have been identified as the cause of chest pain in 4.5-18% of patients studied, and reflux in 4.5-25%. In addition, some patients had both dysmotility- and reflux-related pain episodes. As expected, the yield of the technique is higher in patients with frequent pain episodes. In patients who do not experience pain during 24-hour monitoring, the technique cannot provide a firm diagnosis of pain of esophageal origin. Recently, a much higher yield of 24-hour monitoring was reported in patients with noncardiac chest pain admitted to a coronary-care unit. A total of 76% of these patients were found to have either reflux- or dysmotility-related chest pain. Despite its relatively low yield, the addition of esophageal pressure monitoring to ambulatory pH monitoring is worthwhile and probably also cost-effective in patients with frequent episodes of unexplained chest pain.
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PMID:Ambulatory esophageal monitoring in noncardiac chest pain. 159 69

During the session on diagnostic testing, various diagnostic tests used to identify the cause of chest pain were discussed. This critique of diagnostic assessments of the complex etiology of chest pain is presented as a contribution toward further investigation and clarification of this difficult clinical syndrome. The first step in the evaluation process is to exclude coronary artery disease. Patients with angina and normal coronary artery flow may have atypical disease, such as microvascular angina or syndrome X. The precise relationship between these disorders and esophageal disease or gastroesophageal reflux, as well as their possible involvement in chest pain of undetermined origin, requires further definition. A limitation of esophageal provocation tests is that they may identify the esophagus as the source of pain without determining the specific esophageal disorder that causes the pain. Problems associated with 24-hour pH and pressure monitoring include (a) poor correlation between reflux episodes and heartburn symptoms, (b) the lack of a good functioning swallowing signal, and (c) the huge amount of data that must be analyzed, along with shortcomings in computer-aided analysis. Nevertheless, the various available diagnostic tests can provide important information to the clinician.
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PMID:Critique of the session on diagnostic testing. 159 70

35 patients with angina-like chest pain underwent esophageal manometry after a coronary artery disease had been ruled out by angiography. Furthermore, patients after gastric or esophageal surgery, with pathologic upper gastrointestinal endoscopy or with pathologic gastroesophageal reflux as seen on 24-hour-pH-metry were excluded from this study. 29 out of 35 patients (83%) had a normal manometric study, six patients (17%) had a motility disorder; five of these showed an unspecific dismotility pattern and were asymptomatic while the study was done; only one patient presented with esophageal spasm. Since only this latter patient was symptomatic while the study was done, a correlation between symptoms and this motility disorder seems likely. --If pathologic gastroesophageal reflux has been ruled out, esophageal manometry can establish a diagnosis in only 3% of patients with angina-like chest pain without esophageal symptoms (dysphagia, odynophagia, heartburn or regurgitation). We conclude that this complicated examination should not be done in these patients.
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PMID:[Esophageal motility disorders with thoracic pain of unknown origin]. 188 9

Recurring substernal chest pain is an important clinical problem, causing anxiety for patients and their physicians because of the fear of possible cardiac disease. The differential diagnosis includes coronary artery disease, oesophageal disorders such as acid reflux disease and motility disturbances, musculoskeletal problems, psychological disorders including panic attacks, and a new 'fly in the ointment'--microvascular angina. History alone usually cannot distinguish cardiac from non-cardiac chest pain. After exclusion of significant coronary artery disease, attention must be turned to oesophageal disorders, which may be seen in as many as 50% of these patients. Oesophageal motility disorders, particularly the nutcracker oesophagus, are common, but the relationship between pain and abnormal contraction pressures is not well established. Provocative tests such as edrophonium (Tensilon) and balloon distension help to identify the oesophagus as the source of chest pain but do not direct therapy. Recent studies with ambulatory oesophageal monitoring suggest that gastro-oesophageal reflux may be a more common cause of chest pain than motility disorders. This is an important finding as acid reflux is a treatable problem, while therapies for motility disorders may only worsen reflux disease. The recent observation that oesophageal disorders are frequently associated and interact with psychological disorders such as anxiety, depression, somatization and panic attacks complicates the evaluation and understanding of chest pain. How these various abnormalities may be linked is an unresolved issue. Increased central nervous system stimulation and altered visceral and/or central pain sensitivity could be the common factors. It is hoped that further research into these areas will lead to new understandings of and possible solutions to the complex problem of non-cardiac chest pain.
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PMID:Investigation and management of non-cardiac chest pain. 191 53

Angina-like chest pain, caused by alterations of esophageal function, is an increasingly common occurrence confronting cardiologists: advances in pathogenetic knowledge and in diagnostic possibilities in this field have in fact shed light on the prevalence of esophageal angina, which is present in approximately 60% of patients with angiographically intact coronaries (11% of anginal patients overall). Classically, esophageal chest pain is attributed to alterations of motility or to mucosal disease (pathologic gastro-esophageal reflux of the acid, mixed or alkaline type): this last cause prevails quantitatively. Little is known of the nociceptive mechanisms triggered by these alterations: as far as mucous disease is concerned, activation of the chemosensitive receptors has been postulated, while esophageal mechanoreceptors may be activated, in the course of a motor disorder, by distension of the wall. A recently proposed additional mechanism consists in the induction of parietal esophageal ischemia by chemical or mechanical injury: it is a fascinating and potentially resolvable mechanism, which however requires further investigation. Moreover, elements of psychological nature are also involved in the genesis of esophageal pain. A diagnosis of esophageal angina, heavily conditioned by obvious considerations of prognostic order, must necessarily aim for "certainty". Prolonged monitoring of the endoluminal pH and the adoption of provocative tests, in the course of pH monitoring and manometry, play an important role in achieving this aim (ergometric test, distension induced with a balloon, edrophonium, electrostimulation, seem most effective). A promising outlook is supported by the recent introduction of prolonged manometry. Finally, diagnostic attitude must necessarily abandon its limited specialistic horizon to consider the patient's profile in its entirety.
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PMID:[Esophageal angina]. 206 70


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