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.     

Combined multichannel intraluminal impedance and pH monitoring is helpful in managing children with suspected gastro-oesophageal reflux disease

BackgroundGastro-oesophageal reflux is very common in the paediatric age group. There is no single and reliable test to distinguish between physiologic and pathological gastro-oesophageal reflux, and this lack of clear distinction between disease and normal can have a negative impact on the management of children.AimsTo evaluate the usefulness of 24-h oesophageal pH-impedance study in infants and children with suspected gastro-oesophageal reflux disease.MethodsPatients were classified by age groups (A–C) and reflux-related symptoms (typical and atypical). All underwent pH-impedance study. If the latter suggested an abnormal reflux, patients received therapy in accordance with NASPGHAN/ESPGHAN recommendations, while those with normal study had an additional diagnostic work-up. The efficacy of therapy was evaluated with a specific standardized questionnaire for different ages.ResultsThe study was abnormal in 203/428 patients (47%) while normal in 225/428 (53%). Of those with abnormal study, 109 exhibited typical symptoms (54%), and 94 atypical (46%). The great majority of the patients with abnormal study were responsive to medical anti-reflux therapy.ConclusionsWe confirm the utility of prolonged oesophageal pH-impedance study in detecting gastro-oesophageal reflux disease in children and in guiding therapy. Performing oesophageal pH-impedance monitoring in children with suspected gastro-oesophageal reflux disease is helpful to establish the diagnosis and avoid unnecessary therapy.     

Oesophageal motility and gastro-oesophageal reflux: Effect of variceal eradication by endoscopic sclerotherapy*

Endoscopic injection sclerotherapy (EIS) is known to produce oesophageal structural and motility changes; however, alterations in frequency and severity of gastro-oesophageal reflux (GER) following EIS have not been investigated in detail. We studied 22 patients with cirrhosis and oesophageal varices before EIS and 26 after variceal eradication with intravariceal EIS using manometry and 24 h pH monitoring. The post-EIS group had reduced oesophageal sphincter pressure (19.2 ± 11.4 vs 26.1 ± 16.4 mmHg, P < 0.05) and slower velocity of oesophageal peristalsis (2.47 ± 0.71 vs 3.06 ± 0.77 cm/s, P < 0.01) than the pre-EIS patients. There was no difference in the amplitude or duration of the contraction. Abnormal contraction wave-forms were observed more frequently in post-EIS than in the pre-EIS patients (3/22 vs 12/26, P < 0.05). Various quantitative parameters for GER were not increased in post-EIS compared with pre-EIS patients. Abnormal GER was present in nine of 21 pre-EIS and eight of 17 post-EIS patients (no significant difference). These results suggest that although persistent oesophageal motility changes are frequent after intravariceal EIS, these do not lead to a significant increase in GER.     

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.     

Ambulatory 24 hour intraoesophageal pH and pressure recordings v provocation tests in the diagnosis of chest pain of oesophageal origin.

Fifty patients with non-cardiac chest pain underwent 24 hour intraoesophageal pH and pressure recording and provocation tests to determine the relative value of both techniques in establishing the oesophageal origin of the chest pain. Twenty six patients (52%) had at least one positive provocation test: the acid perfusion test was positive related in 18 patients (36%), the edrophonium test in 16 patients (32%), the vasopressin test in five patients (10%), and the balloon distension test (performed in only 20 patients) in one (5%). The 24 hour pH and pressure recording correlated spontaneous chest pain attacks with abnormal motility or gastro-oesophageal reflux in 19 patients (38%). Fourteen of these patients also had at least one positive provocation test. Therefore, 24 hour pH and pressure recordings are only slightly better than a set of provocation tests in identifying the oesophagus as the cause of chest pain (10% diagnostic gain). In the case of oesophageal chest pain, however, 24 hour recording appeared to be the only way to identify the nature of the underlying oesophageal abnormality that caused the spontaneous pain attacks--for example, gastro-oesophageal reflux, motility disorders, or irritability of the oesophagus.     

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.     

Non-cardiac, non-oesophageal chest pain: the relevance of psychological factors

Background—No cause has been determined for chest pain that is neither cardiac nor oesophageal in origin.
Aims—To compare the prevalence of lifetime psychiatric disorders and current psychological distress in three consecutive series of patients with chronic chest or abdominal pain.
Patients—Thirty nine patients with non-cardiac chest pain and no abnormality on oesophagogastroduodenoscopy, oesophageal manometry, and 24 hour pH monitoring; 22 patients with non-cardiac chest pain having endoscopic abnormality, oesophageal dysmotility, and/or pathological reflux; and 36 patients with biliary colic.
Methods—The Diagnostic Interview Schedule and the 28 item General Health Questionnaire were administered to all patients.
Results—Patients with non-cardiac chest pain and no upper gastrointestinal disease had a higher proportion of panic disorder (15%), obsessive-compulsive disorder (21%), and major depressive episodes (28%) than patients with gallstone disease (0%, p<0.02; 3%, p<0.02; and 8%, p<0.05, respectively). In contrast, there were no differences between patients with non-cardiac chest pain and upper gastrointestinal disease and patients with gallstone disease in any of the DSM-111 defined lifetime psychiatric diagnoses. Using the General Health Questionnaire, 49% of patients with non-cardiac chest pain without upper gastrointestinal disease scored above the cut off point (that is, more than 4), which was considered indicative of non-psychotic psychiatric disturbance, whereas only 14% of patients with gallstones did so (p<0.005). The proportions of such cases were however similar between patients with non-cardiac chest pain and upper gastrointestinal disease (27%) and patients with gallstones.
Conclusions—Psychological factors may play a role in the pathogenesis of chest pain that is neither cardiac nor oesophagogastric in origin.

Keywords: chest pain;  oesophageal manometry;  gastro-oesophageal reflux disease;  oesophageal pH monitoring;  psychiatric illness

     

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.     

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.     

Role of oesophageal manometry in clinical practice

The present study evaluates the role of oesophageal manometry in clinical practice. Over 5 years, 347 consecutive patients were evaluated in our oesophageal laboratory. The reasons for referral were: dysphagia (11.5%), gastro-oesophageal reflux disease (GORD) (46.7%), non-cardiac chest pain (28.5%), connective tissue disease (6.9%) and other symptomatology (6.3%). Patients were classified into the following five groups according to the referral diagnosis: dysphagia (40 patients), gastro-oesophageal reflux disease (GORD) (162 patients), non-cardiac chest pain (99 patients), connective tissue disease (24 patients) and other symptomatology (22 patients). Abnormalities in oesophageal motility were detected in 90% of patients with dysphagia, in 40.1% of patients with GORD, in 47.5% of subjects with non-cardiac chest pain, in 45.8% of patients with connective tissue disease and in 18.2% of subjects with other symptomatology. The high prevalence of abnormalities in the dysphagia group was statistically significant (p < 0.001), and the range of 95% confidence intervals (0.81-0.99) suggests that the value found may be a reasonably good estimate of percentage of anomalies detectable in the dysphagia patient population. In the dysphagia group, the initial diagnosis was confirmed in 40% of patients and changed in 52.5%; in only 7.5% of cases were the manometry results not relevant for determining an appropriate diagnosis. Manometry substantially contributed to patients receiving the correct treatment in 82.5% of cases (p < 0.001 among all groups). In the GORD group and in the non-cardiac chest pain group, the results of manometry were not relevant for confirming or changing a diagnosis in 59.8% and 53.5% of cases respectively; nevertheless, in both groups, on the basis of manometry results, the treatment was changed in 42.5% of patients (p < 0.01 vs. other symptomatology group). In conclusion, on the basis of the present data, we can emphasize the usefulness of oesophageal manometry assessment in patients with dysphagia or non-cardiac chest pain, with negative routine examinations, and also in patients with refractory GORD who have been considered for antireflux surgery.     

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.     

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).     

Gastric dysrhythmias occur in gastro-oesophageal reflux disease complicated by food regurgitation but not in uncomplicated reflux

AIM: To investigate gastric pacemaker activity in gastro-oesophageal reflux disease using the electrogastrogram. PATIENTS: Forty patients with gastro-oesophageal reflux disease (20 with acid reflux, 20 with the additional symptom of food regurgitation) and 30 asymptomatic controls. METHODS: Patients were studied using an electrogastrogram, oesophageal manometry, and 24 hour ambulatory oesophageal pH analysis. RESULTS: An abnormal electrogastrogram was recorded in two (7%) controls, two (10%) patients with acid reflux, and 10 (50%) patients with food regurgitation. Food regurgitators had significantly more gastric dysrhythmias (tachygastrias) both before (p<0.02) and after (p<0.01) a test meal. Gastric pacemaker activity was also significantly less stable following the test meal in food regurgitators (p<0.003). Patients with food regurgitation and an abnormal electrogastrogram had higher oesophageal acid exposure than those with a normal electrogastrogram (p<0.05). CONCLUSIONS: The electrogastrogram is usually normal in gastro-oesophageal reflux disease but an abnormal rhythm occurred in half of our patients with the additional symptom of food regurgitation. Furthermore, an abnormal electrogastrogram is associated with increased oesophageal acid exposure.     

A prospective study of oesophageal function in patients with normal coronary angiograms and controls with angina

Aims—To compare the incidence of oesophagealabnormalities and their correlation with chest pain in patients withnormal coronary angiograms, and in controls with angina.
Patients—Sixty one patients with normal coronaryangiograms (NCA group) referred to a single cardiac centre betweenMarch 1990 and April 1991; 25 matched controls with confirmed coronary artery disease (CAD group).
Setting—Cardiac referral centre and oesophagealfunction testing laboratory.
Main outcome measures—Oesophageal manometry,provocation tests, and 24 hour ambulatory pH monitoring.
Results—Simultaneous contractions were morecommon (6.7% versus 0.8%, p<0.01), and the duration of peristalticcontractions was longer (2.9 versus 2.4 seconds, p<0.01) in the NCAgroup than in the CAD group. There were no group differences in theamplitude of peristaltic contractions, and none had nutcrackeroesophagus. Ten (16%) patients with NCA and no patients with CAD haddiffuse spasm (p=0.03). Twenty one (34%) patients with NCA, and five(20%) patients with CAD had abnormal gastro-oesophageal reflux(p>0.05). There was no significant difference between the groups inthe number of patients whose pain was temporally related to pH events. Particular chest pain characteristics, or the presence of additional oesophageal symptoms, were not predictive of an oesophageal abnormality.
Conclusion—Oesophageal function testscommonly implicate the oesophagus as a source of pain in patients withnormal coronary angiograms. With the exception of simultaneouscontractions during manometry however, the incidence of abnormalitiesand in particular the correlation of pH events with chest pain are ascommon in patients with normal coronary angiograms as in controlswith angina. The oesophagus may often be an unrecognised source of painin both groups of patients.

Keywords:oesophageal function; coronary artery disease; chest pain

     

Autonomic nervous function in Helicobacter pylori-infected patients with atypical chest pain studied by analysis of heart rate variability

OBJECTIVES: Cardiovascular autonomic nervous system (ANS) activity estimated by analysis of heart rate variability (HRV) was compared in Helicobacter pylori-positive and H. pylori-negative male patients suffering from atypical chest pain to verify the hypothesis that autonomic neural system might be the way linking chronic H. pylori infection with gastrointestinal tract disorders. METHODS: We have analysed data obtained from 101 male patients examined in our clinic due to atypical chest pain, without evidence of serious cardiovascular, respiratory and digestive tract or metabolic diseases. In each patient, besides interview and physical examination, were performed: gastroscopy with mucosa biopsy (for urease test and histology), oesophageal pH-metry and manometry, ultrasound abdomen examination, chest X-ray, exercise test on running track, 24-h ECG Holter monitoring with time-domain and frequency-domain HRV analysis, and echocardiography. RESULTS: In comparison with H. pylori-negative, in all H. pylori-infected patients (n = 63) a significantly greater low frequency power, an index of sympathetic activity, and higher values of vagal tone parameters [pNN50, percentage of differences between RR intervals that are greater than 50 ms; high-frequency power in HRV analysis (HF)] were observed. The relationship between H. pylori infection and the HF value was confirmed in multi-factorial analysis. The aforementioned ANS activity differences were accompanied by: significantly fewer gastro-oesophageal acid reflux episodes, lower gastric acidity and more effective and complete oesophageal peristalsis in H. pylori-positive patients. CONCLUSIONS: H. pylori infection may affect ANS activity and via this way also contribute to gastro-oesophageal and cardiovascular pathology.     

Laparoscopic fundoplication versus lansoprazole for gastro-oesophageal reflux disease. A pH-metric comparison

BACKGROUND: Treatment strategies that abolish abnormal reflux could prevent long-term complications of gastro-oesophageal reflux disease. AIMS: To compare the efficacy of laparoscopic fundoplication and lansoprazole in abolishing abnormal reflux in patients with gastro-oesophageal reflux disease. PATIENTS: Study population comprised 130 patients referred for possible antireflux surgery and with heartburn as the dominant symptom. METHODS: After oesophageal manometric and pH-metric evaluation and detailed information 55 patients asked to undergo laparoscopic antireflux surgery while 75 chose a medical treatment regimen based on lansoprazole. Treatment efficacy was assessed by ambulatory oesophageal pH-monitoring. RESULTS: All 55 patients who underwent fundoplication became free of heartburn: oesophageal pH-monitoring gave normal results in 85%. In patients treated with lansoprazole, at individualized daily dosages titrated to abolish both heartburn and abnormal acid reflux, normal pH-metric results were obtained in 96% of cases (p<0.05 vs surgically treated patients). CONCLUSIONS: Lansoprazole at individualized dosages was significantly more effective than laparoscopic fundoplication, in the short-term, in abolishing abnormal reflux in gastro-oesophageal reflux disease patients.     

Alkaline Oesophageal Reflux-An Artefact Due to Oxygen Corrosion of Antimony pH Electrodes

Antimony electrodes are widely used for gastro-oesophageal pH monitoring. They are also sensitive to oxygen, however, especially at low Po₂ levels, which are known to shift recorded values in the alkaline direction. This study, which compares antimony and glass electrodes for oesophageal pH monitoring in six adults, shows that values recorded by antimony electrodes are 2.1 ± 0.8 pH units (mean ± SD) higher than by glass electrodes (p < 0.001; n = 7642). A further 52 patients with suspected gastro-oesophageal reflux were investigated by 24-h pH monitoring by means of antimony electrodes. In these patients the oesophageal pH was higher than 8.0 for 7% of the time (range, 0–60%). The alkaline periods recorded with antimony electrodes were all protracted in time, smoothly increasing from a neutral pH, and did not correspond to a sudden increase in pH, which would be expected if alkaline reflux had occurred. It is concluded that high pH values obtained by antimony electrodes are due to the oxygen sensitivity of the electrodes. The diagnosis of alkaline reflux seems to be valid only when pH monitoring is performed with glass electrodes or when values obtained with antimony electrodes are adjusted for the influence of the oxygen tension in the oesophagus.     

Gastroesophageal reflux in patients with angiographically normal coronary arteries: an uncommon cause of exertional chest pain.

OBJECTIVES--To investigate the association between exertional chest pain and gastroesophageal reflux in patients with normal coronary angiograms and in controls by measuring oesophageal pH during treadmill exercise tests and to compare the results with routine ambulatory monitoring. DESIGN--Case control study. SETTING--Tertiary referral cardiac unit. PATIENTS--50 consecutive patients with chest pain and completely normal coronary angiograms and 16 controls with coronary artery stenoses. MAIN OUTCOME MEASURES--Episodes of acid reflux and chest pain during treadmill exercise; a symptom index expressing the percentage of episodes of pain related to acid reflux during ambulatory monitoring. RESULTS--Four (8%) patients and two (12%) controls had reflux during treadmill exercise (NS). 32 (64%) and 16 (100%) reported chest pain, but only three (6%) and two (12%) had coincident reflux (NS). Reflux was as frequent before, during, and after treadmill exercise (five (8%) v six (9%) v two (3%)) in the 66 subjects; (NS). 19 (38%) patients and three (19%) controls had abnormal reflux on ambulatory monitoring (NS). Eight (16%) and three (19%) had a symptom index > 50%, but six and two of these reported pain without coincident reflux during treadmill exercise. CONCLUSION--There are many potential causes of chest pain in patients with angiographically normal coronary arteries. Although gastroesophageal reflux is commonly implicated and many patients have a high incidence of spontaneous reflux during ambulatory monitoring, it rarely occurs during exertion and the association with chest pain is poor.     

Phenylephrine-induced atypical chest pain in patients with prolapsing mitral valve leaflets

The syndrome of midsystolic click and late systolic murmur is usually associated with mild mitral regurgitation. Since patients with the click-murmur syndrome often have atypical chest pain we considered the possibility that alterations in afterload, which affect myocardial oxygen demand, may be partially responsible for this precordial discomfort. Systolic arterial pressure and electrocardiographic and phonocardiographic recordings were monitored before and during intravenous infusion of phenylephrine in 21 patients with the click-murmur syndrome, 9 of whom gave a history of atypical precordial pain. An identical protocol was carried out in nine control patients, three of whom had a history of atypical chest discomfort. In each patient with the click-murmur syndrome the diagnosis was confirmed by two or more of these findings: (1) a typical phonocardiographic response to the Valsalva maneuver, inhalation of amyl nitrite or a postural change, (2) a characteristic echocardiogram, or (3) a diagnostic left ventriculogram. During phenylephrine infusion 8 of the 9 patients with the clickmurmur syndrome and a previous history of chest pain had precordial discomfort, whereas none of the other 12 patients with the syndrome had pain (P < 0.004); none of these patients exhibited pain during infusion of 0.9 percent sodium chloride. The mean increase in systemic systolic arterial blood pressure did not differ between the two groups ($\text{33 ± 4.3 [}\text{standard error}\text{]}\text{vs}\text{. 38 ± 1.5}\text{mm Hg}\text{, P}\text{\$}\text{?}\text{0.1}$). Both the appearance and disappearance of pain occurred at similar systolic arterial pressures ($\text{146 ± 8.8}\text{vs}\text{. 143 ± 7.7}\text{mm Hg}\text{, P}\text{\$}\text{?}\text{0.8}$). No significant alterations in heart rate were present at these times. None of the patients with the click-murmur syndrome who experienced precordial pain had evidence of coronary artery disease. Only one control patient had pain during infusion of phenylephrine, but this patient also had chest discomfort during infusion of the saline solution. These data indicate that atypical chest pain can be induced in patients with billowing mitral leaflets by increasing systolic arterial pressure, and suggest the possibility that a discrepancy between myocardial oxygen supply and demand may be at least partially responsible for this symptom in patients with the click-murmur syndrome.     

Utility of ambulatory 24-hour esophageal pH and motility monitoring in noncardiac chest pain: report of 90 patients and review of the literature

It is unclear whether prolonged motility monitoring improves the diagnostic yield of standard esophageal tests in patients with noncardiac chest pain. Our aim was to assess the diagnostic value of ambulatory 24-hr pH and pressure monitoring in patients with noncardiac chest pain. Stationary manometry, edrophonium testing, and ambulatory pH and motility studies were performed in 90 consecutive patients with recurrent chest pain and normal coronary angiograms. Normality limits of ambulatory 24-hr motility were established in 30 healthy controls. The diagnoses of specific esophageal motility disorders (nutcracker esophagus and diffuse esophageal spasm) by stationary and ambulatory manometry were discordant in 48% of the patients. Edrophonium testing was positive in 9 patients, but correlated poorly with esophageal diagnoses. During ambulatory studies, 144 chest pain events occurred in 42 patients, and 72 (50%) were related to esophageal dysfunction. Strict temporal associations of events with esophageal dysfunction in relation to ambulatory 24-hr pH'motility scores permitted four patient categorizations: true positives (event-related and abnormal tests), N = 15; true negatives (event-unrelated and abnormal tests), N = 10; reduced esophageal pain threshold (event-related and normal tests), N = 4; and indeterminate origin (event-unrelated and normal tests), N = 13. Overall, 19 patients (21%) had a probable esophageal cause for chest pain (14 esophageal motility disorder, 4 acid reflux, 1 both). In conclusion, ambulatory manometry increases the diagnostic yield of standard esophageal testing in noncardiac chest pain, but the gain is small. Causes of chest pain other than high esophageal pressures and acid reflux must still be sought in most patients with chest pain of unknown origin after a negative cardiac work-up.