Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease

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.     

Temporal relationships between episodes of non-cardiac chest pain and abnormal oesophageal function.

Analysis of the association between symptoms and abnormal oesophageal function is a central part of 24 hour oesophageal pressure and pH recording in patients with non-cardiac chest pain. Such studies have used different time windows including a period after the onset of pain. Since stress and pain can induce oesophageal motor abnormalities and transient lower oesophageal sphincter relaxations, a proportion of the motor abnormalities and the reflux episodes observed after the onset of pain may be a consequence rather than the cause of that pain. This study aimed to assess this possibility in patients with chest pain that was presumed to be of oesophageal origin by comparing the results of analysis using time windows before and after the onset of pain. Forty eight patients experienced a total of 166 spontaneous chest pain episodes during 24 hour ambulatory monitoring. A time window beginning two minutes before and ending at the onset of pain (-2/0) was compared with a window beginning at the onset of pain and ending two minutes afterwards (0/+2). The percentage of episodes related to reflux, abnormal oesophageal motility, or neither were 22.9%, 24.7%, and 52.4% in the -2/0 time window and 9.0%, 22.3%, and 68.7% in the 0/+2 time window, respectively. However, 11 of the 37 episodes associated with abnormal motility in the 0/+2 time window were preceded by a reflux episode, and 19 of these 37 episodes had abnormal motility in the -2/0 time window. Consequently, in only seven of the 166 chest pain episodes (4.2%) in two patients were the findings consistent with secondary oesophageal motor disorders provoked by pain. Likewise, only six of the 166 chest pain episodes (3.6%) were consistent with reflux provoked by pain. These findings indicate that in patients with non-cardiac chest pain, gastro-oesophageal reflux and oesophageal motor abnormalities are rarely a consequence of the pain.     

Gastro-oesophageal reflux and severity of pulmonary disease in cystic fibrosis

The correlation between oesophageal dysfunction (OD), pathologic gastro-oesophageal reflux (GOR), and severity of pulmonary disease was studied in 12 patients with cystic fibrosis (CF). They were interviewed about symptoms of OD and underwent 24-h pH recording in the oesophagus, oesophageal manometry combined with reflux provocation tests, the acid perfusion test, the acid clearance test, lung function tests, and scoring of the chest radiograph. Six of the 12 patients reported symptoms of OD. Abnormal GOR, as shown by 24-h pH monitoring of the oesophagus, was found in eight of them. Altogether 9 of the 12 participants had at least one pathologic oesophagus test result. Results of radiologic examinations of the oesophagus, performed in six patients, were pathologic. The four patients with the best chest radiograph scores and the best lung function had significantly less signs and symptoms of OD and GOR than the other eight patients. We conclude that OD, GOR, and pulmonary disease covariate in CF.     

24 hour ambulatory oesophageal motility monitoring: how should motility data be analysed?

Ambulatory oesophageal motility/pH monitoring permits accurate detection of oesophageal events during spontaneous chest pain episodes. Opinions differ, however, about the methods to review the extensive motility data and the definition of abnormal motility changes. We studied 30 patients (18 women, age 46 years) with suspected oesophageal chest pain using a portable recording system attached to a 4.5 mm catheter with pressure transducers 3 and 8 cm and pH probe 5 cm above the lower oesophageal sphincter (LOS). An event marker was triggered by the patient for chest pain. In the patient's diary, pain was recorded on a scale of increasing severity 1-10. Two methods of analysis were used to assess 24 hour motility data. The 24 hour technique sampled five minute asymptomatic baselines throughout the study to define the patient's normal range of oesophageal motility. The second technique used only the 10 minute period immediately before each chest pain episode as the asymptomatic baseline. Chest pain episodes were defined as abnormal if associated with pH less than 4 or motility changes not present during the asymptomatic baseline analysis: 135 chest pain episodes were recorded. The method of motility analysis significantly (p less than 0.01) changed the number of chest pain episodes associated with abnormal motility: 24 hour technique - 14 episodes (10%) versus a 2.5-fold increase with the 10 minute baseline technique - 33 episodes (24%). Acid related pain episodes were similar in both groups - 13%. The majority of chest pain episodes had no association with abnormal motility or acid reflux. Increasing chest pain severity was inversely correlated with the presence of abnormal oesophageal events. We conclude that limited analysis of 24 hour motility data may over diagnose motility related chest pain events and lead to inappropriate medical or surgical therapy.     

Angina-like chest pain of oesophageal origin

Angina-like chest pain of non-cardiac origin is a major diagnostic and therapeutic problem. The oesophagus is frequently suspected to be the cause of the chest pain in these patients. However, a positive statement for the oesophageal origin of the pain can only be made when during manometry or pH-monitoring the familiar pain attack appears to be accompanied by reflux, severe motor disorders or a combination of both. Due to the intermittent nature of the pain this is only rarely the case during short-listing conventional examinations. Provocation tests have been used to induce the familiar chest pain. The Bernstein acid perfusion test and the edrophonium test yield the best results. Prolonged (24-hour) ambulatory recording of intra-oesophageal pressure and pH to increase the chances of recording chest pain concomitantly with an episode of reflux and/or motor disorders appears to be the most sensitive and also the most physiological test. It is the only test that provides reliable information on the underlying mechanism of the pain, especially in patients with the syndrome of irritable oesophagus, thus contributing in establishing the appropriate therapy for these patients.     

Nutcracker oesophagus: Association with chest pain and dysphagia controlling for gastro-oesophageal reflux

BACKGROUND: The association between nutcracker oesophagus, gastro-oesophageal reflux and their symptoms is controversial. AIM: To evaluate the association of nutcracker oesophagus with chest pain and dysphagia controlling for gastro-oesophageal reflux. METHODS: From a database of 935 consecutive patients investigated with oesophageal manometry and pH-metry, we selected all patients with nutcracker oesophagus including diffuse and segmental patterns. Patients with normal oesophageal peristalsis served as controls. Symptoms assessment, manometry testing and 24h oesophageal pH monitoring off acid-suppressive medications were performed following a standardized protocol. The associations between nutcracker oesophagus and symptoms were assessed by logistic regression analysis. RESULTS: Nutcracker oesophagus was found in 60 patients (6.4%), of which 30 had diffuse nutcracker oesophagus and 30 had segmental nutcracker oesophagus. The control group was composed by 656 patients with normal oesophageal peristalsis. Diffuse nutcracker oesophagus was associated with chest pain (odds ratio 4.3; 95% CI 1.9-9.9; P<0.0001) and dysphagia (odds ratio 5.3; 95% CI 2.3-12.2; P<0.0001), whereas segmental nutcracker oesophagus was associated with chest pain (odds ratio 2.8; 95% CI 1.1-6.9; P=0.026), controlling for total oesophageal acid exposure, age, sex and lower oesophageal sphincter (LOS) pressure. CONCLUSION: This study suggests that both diffuse and segmental nutcracker oesophagus should be regarded as meaningful abnormalities and not mere manometric curiosities.     

Acid perfusion test: does it have a role in the assessment of non cardiac chest pain?

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.     

Analysis of 24-hour esophageal pressure and pH data in unselected patients with noncardiac chest pain

Fourty-four unselected patients with noncardiac chest pain were studied using conventional manometry with additional edrophonium provocation and 24-hour ambulatory esophageal pH and pressure recording with a system developed by our group. New, fully automated techniques of statistical analysis of the complete set of esophageal pressure and pH signals were used to examine the temporal relation between pain, esophageal motility disturbances, and gastroesophageal reflux. The analysis used the 97.5th percentile of amplitude and duration of all esophageal contractions in each patient as well as a chi 2 test of the distribution of contraction types to determine whether a pain episode was related to abnormal motility or not. The edrophonium test results were positive in 2 patients. Only 25 patients (56.8%) had at least one pain episode (total, 111 episodes) during 24-hour recording. Thirty-three percent of the pain episodes were related to reflux and 23.4% to abnormal motility, and 43.2% were not related to an esophageal function disturbance. In the patient-oriented analysis in this study, it was required for a positive correlation that the symptom index (percentage of related pain episodes) was higher than 75%. It was found that the pain was related to reflux in 2 patients (4.6%), to reflux and motor abnormalities in 4 (9.2%), and to motor abnormalities in 2 patients (4.6%). In 36 patients (81.8%), no relation with an esophageal abnormality could be established, either because the patients had no pain during the 24-hour study, or because the pain seemed unrelated to reflux or abnormal motility.     

Pressure events surrounding oesophageal acid reflux episodes and acid clearance in ambulant healthy volunteers.

Previous studies of the mechanisms that precipitate acid reflux episodes and acid clearance have used unphysiological, short term hospital based data. A new 24 hour pH and motility recording system combined with computerised data analysis have been used to study naturally occurring acid reflux episodes in healthy ambulant volunteers. A variety of events that produced recognisable transdiaphragmatic pressure patterns were associated with acid reflux episodes (particularly belching). Peristaltic waves were the predominant contractions leading to oesophageal acid clearance and were the commonest contraction type during reflux episodes. Peristaltic wave parameters (amplitude, velocity, frequency, and percentage proportion) varied during different periods of the 24 hour recording. This study has produced new information about 24 hour oesophageal function and naturally occurring acid reflux which will provide a basis for comparison with patients with gastro-oesophageal reflux disease.     

Oesophageal motility, luminal pH, and electrocardiographic-ST segment analysis during spontaneous episodes of angina like chest pain.

The relation between oesophageal motility, luminal pH, and spontaneous pain events in 47 patients with recurrent angina like pain and normal coronary arteries was investigated. Preliminary investigation by conventional station pull through manometry (SPTM), was followed by a 24 hour period of ambulatory oesophageal motility and luminal pH monitoring. Computerised analysis of motility and pH data recorded during chest pain was then compared with pre-elected control samples taken before and after symptoms. Concurrent real time electrocardiographic (ECG)-ST segment analysis was performed to catalogue any ECG-STT wave changes indicative of myocardial ischaemia. SPTM showed a high group percentage incidence of simultaneous contractions (mean (SD) 11.1 (2.3)%) and a raised lower oesophageal sphincter tone (57.4 (15.2) mm Hg). During ambulatory monitoring, 35 patients experienced one or more episode of angina, providing a total of 59 pain events, although no significant change in group motility and reflux parameters peculiar to episodes of chest pain were found. Ischaemic ECG changes were detected in 10 (21%) patients, but were accompanied by pain in only two. Independent analysis of the ECG traces corresponding to these purported ischaemic ECG events determined them unequivocal in three patients and probable in a further two. No apparent correlation was noted, however, between these ECG events and corresponding patterns of motility or reflux.     

Investigation and management of non-cardiac chest pain

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.     

Fate of Nissen fundoplication after 20 years. A clinical, endoscopical, and functional analysis.

Of 46 patients who had Nissen fundoplication for proved gastro-oesophageal reflux, 25 were available for follow up after a median of 20 years, 15 had died of unrelated causes, and six could not be traced. All 25 patients in the follow up study were personally interviewed: 21 consented to an endoscopy, 14 to 24 hour recording of oesophageal pH and manometry, and 15 to radionuclide transit test. Repeat fundoplication for recurrent reflux was performed in two cases during the study. Heartburn and regurgitation were significantly lessened (p < 0.005), but the incidence of dysphagia was slightly increased. Endoscopy showed six of 21 fundic wraps to be defective. Erosive oesophagitis was seen in two patients, and Barrett's oesophagus (histologically confirmed) in one of them and six other patients. Total reflux time was abnormal in four of 14 patients. No patient with an intact fundic wrap seen on endoscopy, only two of seven with Barrett's oesophagus, and one of four with abnormal reflux had oesophagitis. Fundoplication in itself did not affect oesophageal motility or transit, provided that the wrap was intact. It is concluded that Nissen fundoplication gave a reasonably good longterm effect in chronic reflux disease, with the stage of the fundic wrap as the main determinant of outcome.     

Esophageal motility in cases of chest pain with normal coronarography

The aim of this study was to assess the incidence of oesophageal abnormalities and to determine their nature in patients with retrosternal chest pain and normal coronary angiography with a negative coronary spasm provocation test. Oesophageal manometry was carried out in all cases with or without a spasm provocation (usually alkalosis) test. Forty consecutive patients were studied: 19 men (47.7 +/- 10.0 years) and 21 women (54.7 +/- 7.5 years). A history of gastro-intestinal disorder was obtained in 57 p. 100 of cases (hiatal hernia and/or gastro-oesophageal reflux, biliary lithiasis and/or cholecystectomy, gastritis). Seventeen patients had broad based powerful oesophageal contractions which are an established cause of pain; they were recorded under basal conditions in 5 cases and after a provocation test in 12 cases. Two patients had a megaoesophagus without giant waves. Thirteen patients had manometric signs of reflux (malposition and hypotonia of the lower oesophageal sphincter) of whom 7 had giant waves on provocation. In addition, three patients experienced pain during gastro-oesophageal reflux (1 case) or hypotonia of the lower oesophageal sphincter (2 cases). In all, a very probable oesophageal origin of the chest pain was demonstrated in 22 patients (55 p. 100 of cases).     

Audit of the role of oesophageal manometry in clinical practice.

This oesophageal laboratory serves a population of 1.5 million. The study aimed to review referral patterns and assess the cost effectiveness of oesophageal manometry in clinical practice. All 276 consecutive manometry studies performed between 1988 and 1991 were reviewed. Reasons for referral in the 268 first referrals were: dysphagia 50.4%, non-cardiac chest pain 23.1%, gastro-oesophageal reflux disease 14.2%, connective tissue disease 11.2%, and 'other' 1.1%. Manometry was normal in 49.3%, showed achalasia in 17.9%, diffuse oesophageal spasm in 13.4%, connective tissue disease in 7.8%, hypertensive lower oesophageal sphincter in 4.5%, nutcracker oesophagus in 2.6%, and 'other' in 4.5%. A positive diagnosis was significantly more common if dysphagia was the reason for referral (65.9% v 35.3%, p < 0.01). A positive diagnosis was established in 60% of patients referred with connective tissue disease, 30.6% with non-cardiac chest pain, and 21.1% with gastro-oesophageal reflux disease. A positive diagnosis was significantly more common in connective tissue disease when symptoms were present (85% v 10%, p < 0.05). Management was changed in 48.9% of all patients because of manometry findings. The cost of each oesophageal manometry study was calculated to be 63.00 pounds: every change in patient management cost 129.00 pounds. In conclusion, oesophageal manometry changed management in over 20% of patients with non-cardiac chest pain or gastro-oesophageal reflux disease and in over 60% of those with dysphagia. It is, therefore, a useful and cost effective test in patients with these symptoms.     

Comparison of esophageal manometry,provocative testing,and ambulatory monitoring in patients with unexplained chest pain

Prolonged ambulatory esophageal pH and pressure monitors are being developed to evaluate noncardiac chest pain. This new technology needs comparison with conventional esophageal tests before determining which studies are most useful in diagnosing and treating esophageal chest pain. Therefore, we studied 45 patients with esophageal manometry, acid perfusion and edrophonium tests, and 24 hr pH and pressure monitoring. Manometry was abnormal in 20 patients (44%) with nutcracker esophagus, the most common motility disorder. Fifteen (33%) had positive acid perfusion test and 24 (55%) positive edrophonium test. During ambulatory monitoring, all patients experienced chest pain with a total of 202 individual events: 32 events (15%) secondary to acid reflux, 15 (7%) secondary to motility abnormalities, 7 (3%) to both pH and pressure changes, and 149 events (74%) occurred in the absence of any abnormal pH or motility changes. Patients with normal manometry were significantly (P less than 0.01) more likely to have acid reflux chest pain events than did nutcracker patients, who had an equal frequency of pH and motility events. A positive acid perfusion test was significantly associated with abnormal pressure events (P = 0.02; odds ratio 5.95), while a positive edrophonium test more likely predicted acid reflux chest pain during 24-hr monitoring (P = 0.007; odds ratio 7.25). Therefore, abnormal manometry and positive provocative tests point to the esophagus as the likely source of chest pain. However, ambulatory pH and pressure monitoring are required to accurately define the relationship between chest pain and acid reflux or motility disorders.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of the magnitude of gastro-oesophageal reflux in Barrett's oesophagus.

A manometric study to determine the role of gastro-oesophageal reflux in Barrett's oesophagus was performed on 20 patients with Barrett's oesophagus and 53 patients with reflux oesophagitis without Barrett's oesophagus (25 with mild oesophagitis and 28 with severe oesophagitis). For the same reason, the 20 patients with Barrett's oesophagus also underwent 24 hour continuous oesophageal pH monitoring, and the results obtained were compared with those of 20 oesophagitis patients without Barrett's oesophagus (10 with mild oesophagitis and 10 with severe oesophagitis). The manometric results show that the motor changes found in the Barrett's group are specific but similar to the motor dysfunction associated with reflux oesophagitis. Motor anomalies are probably related more to the inflammatory process in the oesophageal wall than to the metaplastic changes themselves. The pH monitoring results show that while reflux in the Barrett's oesophagus patients was greater overall than in the oesophagitis group without Barrett's oesophagus, the changes are similar when the results are compared with the severe oesophagitis group. In conclusion there are other factors besides gastro-oesophageal reflux involved in the pathogenesis of Barrett's oesophagus.     

ECG record during changes in oesophageal pH.

Seventeen patients with non-cardiac chest pain were investigated by simultaneous ambulatory 24 hour ECG and oesophageal pH monitoring. While 11 patients lowered their oesophageal pH below 4 for a significant percentage, (3.4%) of recorded time and experienced chest pain, no simultaneous ECG changes occurred. In 10 patients chest pain was reproduced by an oesophageal acid perfusion test (Bernstein test). No changes in ECG record during the test were shown. We conclude that although reflux oesophageal pain may be difficult to differentiate from cardiac pain, clinically oesophageal pH changes do not produce any ECG changes.     

Reflux-associated nutcracker oesophagus in a 49-year-old patient with non-cardiac chest pain (NCCP)

A 49-year-old woman was admitted to our department because of intermittent left-sided chest pain for the past 2 years. The patient reported an increasing frequency and duration of the symptoms which were independent from food intake, medication or physical exercises. A cardiac cause of the chest pain was excluded before admittance to our hospital. The initially performed upper endoscopy revealed a small oesophageal hiatal hernia but no signs of acute or chronic inflammation. Basal oesophageal manometry and pH monitoring confirmed the presence of a nutcracker oesophagus, defined by high-amplitude contractions of the distal oesophagus, in combination with a gastro-oesophageal reflux disease. The patient was treated with high-dose pantoprazole for 8 weeks before re-examination. Interestingly, the symptoms completely disappeared upon medication and the relief of the chest pain was accompanied by normalisation of the nutcracker oesophagus pattern. Thus, our observation provides evidence for a causative role of acid reflux in the pathophysiology of the nutcracker oesophagus and, in addition, suggests that effective acid suppression might be a useful therapeutic tool to deal with this painful motility disorder of the oesophagus.     

Presence of bile in the oesophagus is associated with less effective oesophageal motility

BACKGROUND/AIMS: Reflux of bile to the oesophagus has been shown to be of importance in the development of gastro-oesophageal reflux disease. This study aims to assess oesophageal motility patterns in relation to acid and bile reflux to the oesophagus. METHODS: Forty-nine subjects with and without reflux disease underwent 24-hour ambulatory recordings of oesophageal pH, bile and 3-channel manometry. Gastroscopy was performed to assess severity of oesophagitis. The percentage of effective peristaltic contractions (oesophageal contractions with a peristaltic pattern and a pressure >30 mm Hg) were correlated to the degree of acid and bile reflux. Ten subjects were re-evaluated within 2 years post-fundoplication. RESULTS: Acid and bile reflux were associated with fewer effective contractions (R(2) = 0.07, p = 0.06 and R(2) = 0.21, p = 0.008, respectively). However, in a multivariate model including acid, bile, age and gender dependency, only bile could show a systematic effect on the variation in percentage of effective peristaltic contractions (R(2) = 0.22, p = 0.001). One year after laparoscopic fundoplication, 24-hour oesophageal motility was unchanged. CONCLUSION: Reflux of duodenal juice to the oesophagus is associated with less effective oesophageal motility, which in turn can perpetuate the disease by less effective oesophageal clearance of bile and acid. The reduced oesophageal motility is not reversed by fundoplication.     

Effects of cisapride on parameters of oesophageal motility and on the prolonged intraoesophageal pH test in infants with gastro-oesophageal reflux disease.

The effect of cisapride, a new gastrointestinal prokinetic drug, on oesophageal motility and acid reflux was studied in 14 children with gastro-oesophageal reflux disease, receiving either placebo or cisapride 0.15 mg/kg intravenously. Cisapride significantly (p less than 0.01) increased the lower oesophageal sphincter pressure (+124%), the amplitude (+84%) and duration (+24%) of oesophageal peristaltic waves, whereas the placebo treatment did not produce any changes. Subsequently, all 14 children underwent 24 hour oesophageal pH-monitoring before and after four weeks of treatment with oral cisapride 0.2 mg/kg tid given in addition to postural therapy and thickened feedings. The 24 hour intraoesophageal pH recordings and symptomatic scores were compared with those of 10 control patients treated only by postural therapy and thickened feedings. When compared with baseline pH data, cisapride significantly reduced the oesophageal acid exposure time, the mean duration of each reflux episode, the duration of the longest reflux episode and the number of long lasting reflux episodes; the number of reflux episodes was not influenced. The effect of cisapride was marked and consistent during fasting and sleep periods. Oesophageal acid exposure was reduced more significantly in patients given cisapride (-61%) than in controls (-24%; p less than 0.001). Symptom improvement was greater after four weeks of cisapride treatment (score reduction: 61%) than after postural and dietary therapy alone (score reduction: 42%; p less than 0.01). No adverse effects occurred. These findings suggest that cisapride is a valuable drug in the management of gastro-oesophageal reflux disease in children.