Esophageal Motility of Patients with Chagas' Disease and Idiopathic Achalasia

Chagas' disease and idiopathic achalasia have the same neuropathic lesion—the loss of ganglion cells within the esophageal myenteric plexus—with similar clinical, radiologic, and manometric features. However, it is suggested that there are some differences between them. We studied the esophageal motility of 45 patients with Chagas' disease (seven with esophageal dilation), 27 patients with idiopathic achalasia (13 with esophageal dilation), and 40 asymptomatic volunteers. We used the manometric method with continuous perfusion. The lower esophageal sphincter (LES) pressure was measured by the rapid pull-through method. Esophageal contractions was evaluated at 5, 10, and 15 cm above the LES, after 10 swallows of a 5-ml bolus of water alternated with 10 dry swallows. LES pressure was higher in achalasia than in Chagas' disease patients and controls (P < 0.05). Amplitude of contraction was lower in all patient groups compared with controls (P < 0.01) and lower in patients with dilation compared with patients without dilation (P < 0.05). The contraction duration was longer in patients with achalasia than in patients with Chagas' disease and controls (P < 0.05). The percentage of failed contractions was higher in Chagas' disease than in achalasia and controls (P < 0.05), and the percentage of simultaneous contractions was higher in patients with idiopathic achalasia than in patients with Chagas' disease and controls (P < 0.05). The results suggest the possibility that the extent of impairment of esophageal innervation differs between Chagas' disease and idiopathic achalasia.     

Effect of an oral beta2-adrenergic agonist on lower esophageal sphincter pressure in normals and in patients with achalasia

The effect of the beta₂-adrenergic agonist, carbuterol, was studied on the lower esophageal sphincter (LES) pressure in normals and in patients with achalasia. In normals, the mean LES pressure decreased from 23.1±6.2 mm Hg (mean±sem) to 16.0±5.0 mm Hg at a 4.0-mg dose of carbuterol (P<0.05). In patients with achalasia, the mean LES pressure decreased from 50.1±5.1 mm Hg to 22.7±2.4 mm Hg after a 4.0-mg dose of carbuterol (P<0.01). The duration of action following oral administration exceeded 90 min. These studies indicate that the LES in man has beta₂-adrenergic receptors that mediate a reduction in pressure. The magnitude of LES pressure reduction in patients with achalasia suggests that this drug may be of therapeutic benefit.     

Achalasia in the elderly

Clinical and manometric data from 13 elderly subjects with idiopathic achalasia (mean age 79±2 years) were compared with findings from younger subjects with the same disease (n=79) to see if aging altered the presentation and outcome of this motor disorder. Fewer elderly subjects complained of chest pain (27% vs 53%), and the pain was significantly less severe (P<0.01). Other presenting features (including sex, duration of symptoms, and presence and severity of dysphagia) did not differ between the groups. Across all patients, age weakly and inversely correlated with residual postdeglutitive lower esophageal sphincter (LES) pressure (R=–0.34), and residual pressure was significantly lower in the older subjects (8.0±1.3 mm Hg vs 11.9±0.8 mm Hg;P=0.02). No differences in basal LES pressure or esophageal-body contraction amplitudes were present between the groups. Initial success with pneumatic dilation was similar in the two subject groups, but the number of older subjects available for analysis was too small to draw strong conclusions. These results indicate that aging decreases the elevation of LES residual pressure that occurs with achalasia. As elderly achalasia patients also present with less chest pain, the findings may be interrelated.Supported in part by grant AMO7130 from the United States Public Health Service. Dr. Todorczuk is supported by an educational grant from Smith, Kline, and French.     

Esophageal contractions in Chagas' disease and in idiopathic achalasia

GOALS: The aim of this study was to compare the esophageal contractions in Chagas' disease and in idiopathic achalasia. BACKGROUND: It is suggested that the esophageal involvement caused by Chagas' disease and by idiopathic achalasia, although similar, shows some differences. STUDY: We studied the contractions at 2, 7, 12, and 17 cm below the upper esophageal sphincter in 25 patients with idiopathic achalasia (15 with dilatation), 52 with Chagas' disease (22 with dilatation), and 18 controls. Each subject performed 5 swallows of a 5-mL bolus of water alternated with 5 dry swallows. RESULTS: In the distal esophageal body, the amplitude was lower in patients than in controls. Among patients with esophageal dilatation, the proximal amplitude was lower in patients with idiopathic achalasia, and the time interval between the contractions at 2 and 7 cm was longer in patients with Chagas' disease, the number of failed contractions was higher in Chagas' disease, and simultaneous contractions were more frequent in idiopathic achalasia. The simultaneous isobaric pressure in the distal esophagus was associated with an increase in proximal pressure that was higher than distal but lower than proximal swallowing pressure. CONCLUSION: The results suggested that idiopathic achalasia and Chagas' disease cause similar impairment of distal esophageal motility, but in patients with esophageal dilatation the impairment of proximal motility may be not the same.     

Differences in response of the proximal esophagus to wet swallows in patients of Chagas'' disease and idiopathic achalasia

Chagas' disease and idiopathic achalasia have similar esophageal manifestations such as absent or incomplete lower esophageal sphincter relaxation and aperistalsis in the esophageal body (alterations seen mainly in the distal esophageal body). Our aim in this paper was to study the response of the proximal esophageal body to wet swallows in patients with Chagas' disease and patients with idiopathic achalasia. We retrospectively analyzed the time interval between the onset of the pharyngeal contractions 1 cm proximal to the upper esophageal sphincter, as well as 5 cm distal to the pharyngeal measurement. Amplitude, duration and area under the curve of contractions in the proximal esophagus were also determined in 42 patients with Chagas' disease (15 with associated esophageal dilatation), 21 patients with idiopathic achalasia (14 with concomitant esophageal dilatation) and 31 control subjects. The time between the onset of pharyngeal and proximal esophageal contractions was longer in patients with Chagas' disease and in those with esophageal dilatation (1.39 +/- 0.16 s) than in control subjects (0.86 +/- 0.04 s, P < 0.01). The amplitude of proximal esophageal contractions was lower in patients with idiopathic achalasia and esophageal dilatation (60.9 +/- 16.3 mmHg) than in control subjects (89.7 +/- 6.9 mmHg, P = 0.06). The authors conclude that in patients with advanced esophageal disease, the proximal esophageal contractions in Chagas' disease have a delayed response to wet swallows when compared with controls, and that the amplitude of proximal esophageal contractions was lower than expected in patients with idiopathic achalasia.     

Comparison of idiopathic achalasia and Chagas' disease esophagopathy at the light of high‐resolution manometry

The comparison between idiopathic achalasia (IA) and Chagas' disease esophagopathy (CDE) may evaluate if treatment options and their outcomes can be accepted universally. This study aims to compare IA and CDE at the light of high‐resolution manometry. We studied 86 patients with achalasia: 45 patients with CDE (54% females, mean age 55 years) and 41 patients with IA (58% females, mean age 49 years). All patients underwent high‐resolution manometry. Upper esophageal sphincter parameters were similar (basal pressure CDE = 72 ± 45 mmHg, IA = 82 ± 57 mmHg; residual pressure CDE = 9.9 ± 9.9 mmHg, IA = 9.8 ± 7.5 mmHg). In the body of the esophagus, the amplitude was higher in the IA group than the CDE group at 3 cm (CDE = 15 ± 14 mm Hg, IA = 42 ± 52 mmHg, P = 0.003) and 7 cm (CDE = 16 ± 15 mmHg, IA = 36 ± 57 mmHg, P = 0.04) above the lower esophageal sphincter (LES). The LES basal pressure (CDE = 17 ± 16 mmHg, IA = 40 ± 22 mmHg, P < 0.001) and residual pressure (CDE = 12 ± 11 mmHg, IA = 27 ± 13 mmHg, P < 0.001) were also higher in the IA group. Our results show that: (i) there is no difference in regards to the upper esophageal sphincter; (ii) higher pressures of the esophageal body are noticed in patients with IA; and (iii) basal and residual pressures of the LES are lower in patients with CDE. Our results did not show expressive manometric differences between IA and CDE. Some differences may be attributed to a more pronounced esophageal dilatation in patients with CDE.     

Hypocontraction of the esophagus in patients with Chagas' disease and with primary achalasia

The esophageal contraction amplitude is low in patients with Chagas' disease and patients with primary achalasia but not every swallow is followed by low contraction amplitude. We evaluated the number of low contraction amplitude in 40 normal volunteers, 99 Chagas' disease patients and 14 patients with primary achalasia. Each subject performed 10 swallows of a 5 mL bolus of water and the esophageal motility was measured at 5, 10 and 15 cm above the lower esophageal sphincter by the manometric method with continuous perfusion. The amplitude of contraction was considered to be low when its value was below 30 mm Hg. There was a hypotensive contraction when the amplitude was low or when the contraction failed. The number of hypotensive contractions was higher in patients with Chagas' disease and patients with achalasia than in healthy volunteers (P < 0.05). Patients with Chagas' disease and abnormal esophageal radiological examination but without dilation had more frequent hypotensive contraction than patients with normal esophageal radiologic examination (P < 0.01). The same results were obtained for subjects with three or more hypotensive contractions (P < 0.01). The patients with Chagas' disease and dysphagia had more hypotensive contractions than patients without dysphagia (P < 0.05). We conclude that patients with Chagas' disease and patients with primary achalasia have a higher number of hypotensive contractions following wet swallows than normal volunteers, a fact that should influence the symptomatology of the patients.     

Pathological esophageal acidification and pneumatic dilatation in achalasic patients too much or not enough?

Endoscopy, esophageal manometry and pH monitoring, gastric emptying test, and heartburn quantification on a visual analog scale were performed in 22 achalasic patients in order to clarify which events are associated with pathological esophageal acidification after successful LES dilatation. Five patients presented pathological acidification. Dilatation reduced LES tone from 38.3 ± 4.2 to 14.6 ± 1.1 mm Hg (mean ±sem); there was, however, no difference between nonrefluxers and refluxers (14.8 ± 1.2 vs 13.8 ± 2.5 mm Hg). The emptying time in achalasic patients was delayed compared to controls (315.9 ± 20.9 min vs 209 ± 10.4) due to prolonged lag-phase and reduced slope of the antral section-time curve, but, again, there was no difference between refluxers and nonrefluxers. The acid clearance was delayed in refluxers compared to nonrefluxers (15.9 ± 4.5 vs 2.5 ± 1.8 min,P<0.05). Two refluxers presented grade 1 esophagitis; one of them developed an esophageal ulcer. The heartburn score was the same in refluxers and nonrefluxers. Pathological acidification after pneumatic dilatation is associated with persistent problems in esophageal emptying rather than with excessive sphincter divulsion.     

Proximal and distal esophageal contractions in patients with vigorous or classic esophageal Chagas' disease

BACKGROUND: Some patients with achalasia have distal esophageal contraction amplitude in the normal range, a condition called vigorous achalasia, and others have low contraction amplitude, a condition named classic achalasia. The difference in distal contraction amplitude may also be associated with a difference in proximal contraction amplitude. AIM: To study the proximal and distal esophageal contractions in patients with Chagas' disease. MATERIAL AND METHODS: We studied 28 patients with Chagas' disease, all with dysphagia and an esophageal radiologic examination with retention without dilation, and 18 controls. The patients with Chagas' disease had vigorous achalasia (distal amplitude over 34 mm Hg, n = 13) or classic achalasia (distal amplitude below 34 mm Hg, n = 15). We measured the contractions by the manometric method with continuous perfusion at 2, 7, 12 and 17 cm below the upper esophageal sphincter after five swallows of a 5 mL bolus of water. RESULTS: There was no difference in proximal amplitude of contractions between classic or vigorous achalasia, and controls. In the proximal esophagus there was also no difference in duration or area under curve of contractions. In the distal esophagus, duration and area under curve were lower in classic than vigorous disease. Failed and simultaneous contractions were more frequent in patients than controls. Simultaneous contractions were seen more frequently in classic disease, and peristaltic contractions were seen more frequently in vigorous disease. CONCLUSION: We did not find differences in proximal esophageal contractions of patients with classical or vigorous esophageal Chagas' disease, except for the higher number of simultaneous contractions seen in classic disease.     

Manometry and impedance characteristics of achalasia. Facts and myths

BACKGROUND: Achalasia is defined manometrically by an aperistaltic esophagus. Variations in the manometric findings occur in achalasia suggesting that all manometric features should not be required to diagnose achalasia. Combined multichannel intraluminal impedance and esophageal manometry (MII-EM) allows both a functional and a manometric evaluation of esophageal motility and identifies chronic fluid retention. AIM: To compare manometric and MII characteristics in patients with achalasia. METHODS: Retrospective review of 73 MII-EM tracings from patients with achalasia done in our laboratory between October 2001 and December 2004 (38 females; mean age=53.5 y). Patients with previous esophageal interventions were excluded. Manometric and MII characteristics were identified and compared during 10 liquid and 10 viscous swallows. Patients were also divided into 2 groups: vigorous achalasia (VA) and achalasia. RESULTS: Twenty-two of the seventy-one (31%) achalasia patients had a hypertensive lower esophageal sphincter (LES). The mean lower esophageal sphincter pressure (LESP) for the 71 patients with achalasia was 37.9+/-21.2 mm Hg compared with 27.3+/-9.3 mm Hg (P<0.05) in the 73 patients with normal motility. The mean LESP in patients with achalasia was 36+/-20.3 mm Hg compared with 47+/-23.2 mm Hg (P<0.05) in patients with VA. Elevated intraesophageal pressure (IEP) was noted in 45/73 (61.6%). The mean LESP in this group was 41.1+/-22.9 mm Hg compared with 32.5+/-17 mm Hg (P<0.05) with normal IEP. The mean baseline impedance for achalasia was 801+/-732 compared with 1265.2+/-829.5 Omega (P<0.05) for the VA patients. CONCLUSIONS: Most patients with achalasia have elevated IEP, elevated LES residual pressure, normal LES pressure, and low baseline impedance. All manometric features should not be required to diagnose achalasia. Patients with an elevated IEP are likely to have an elevated LES pressure and LES residual pressure. Low MII values identify chronic fluid retention and helps confirm the diagnosis.     

Mean pressure obtained by modified rapid pull-through technique used to assess lower esophageal sphincter function

Lower esophageal sphincter pressure, length of sphincter, and contraction of the crural diaphragm are determinants of esophageal function. Mean pressure manometrics in modified rapid pull-through reflects these three factors. Reproducibility and interobserver variability were studied to assess this method's efficacy and were compared with the maximum expiratory pressure in station pull-through in 44 individuals divided into three groups: achalasia, gastroesophageal reflux, and healthy volunteers. Mean pressure in rapid pull-through showed high reproducibility, no significant differences (14.4 ± 8.4 vs 12.6 ± 8.2 mm Hg) between two measurements, and a high correlation coefficient (r = 0.9). Interobserver variability was lower than that seen for maximum expiratory pressure (P < 0.001). Mean pressure was lower than maximum expiratory pressure in patients with achalasia (21.1 ± 7 vs 30.7 ± 8.6 mm Hg). Both methods showed identical sensitivity to establish a hypotensive sphincter in patients with reflux (73%). We think that mean pressure obtained by rapid pull-through is a good methodology to assess lower esophageal sphincter competence. It is rapid, simple, shows good reproducibility and low interobserver variability, and is clinically valid.     

Intraesophageal Balloon Distension Test in Chagas' Disease Patients with Noncardiac Chest Pain

Patients with Chagas' disease often have chestpain as a prominent symptom. The objective of this studywas to compare the results of intraesophageal balloondistension in chagasic and nonchagasic patients with chest pain not caused by coronaryobstruction. We studied 40 patients with chest pain andangiographically normal coronary arteries, 25 with apositive serologic test for Chagas' disease (Chagasgroup, 16 women, mean age 53 ± 10 years), and15 with a negative serologic test (control group, 11women, mean age 46 ± 10 years). All patients hadradiologic and endoscopic examinations of esophagus,stomach, and duodenum, esophageal manometry with theacid infusion test in the distal esophagus, andintraesophageal balloon distension. None of them hadesophageal dilation or any signs of cardiovasculardisease. A 25-mm-long latex balloon located 10 cm abovethe lower esophageal sphincter was inflated and deflatedover a period of 10 sec at 1-ml increments of air untilthe subjects reported chest pain or to a maximum volume of 20 ml. The test caused chest pain in14 subjects in the control group (93%) and in 12 in theChagas' disease group (48% , P < 0.05). The meanvolume of air that caused chest pain was 10 ± 3ml in the control group and 15 ± 4 ml in theChagas' disease group (mean ± SD, P < 0.05).The maximum intraesophageal pressure during theexamination was higher in Chagas' disease patients withchest pain during balloon distension (60 ± 21mm Hg) than in patients who did not have chest pain (37± 18 mm Hg, P < 0.05) and did not differ fromthe control group (48 ± 16 mm Hg, P > 0.05).With the other examinations there was no differencebetween groups or between patients with or without chestpain during the balloon distension test. Althoughesophagitis was observed in 47% of patients in the control group and in 40% of the Chagas' diseasegroup, the acid infusion test was positive in 27% ofpatients in the control group and in 4% of patients inthe Chagas' disease group. We conclude that, as compared to a group of patients with similarchest pain, chagasic patients are less sensitive toesophageal distension. Thus, it is unlikely that theirchest pain is related to esophagealmechanisms.     

Comparison between idiopathic achalasia and achalasia caused by Chagas' disease: a review on the publications about the subject

BACKGROUND: Although idiopathic achalasia and achalasia caused by Chagas' disease have the same clinical manifestations and treatment, both with destruction of the esophageal myenteric plexus, it is possible that there are differences in the alterations of esophageal motility between the two diseases, caused by different grades of impairment of the excitatory and inhibitory esophageal neurons. AIMS: We performed a review of papers with results about the pathophysiology and esophageal motility alterations in idiopathic achalasia and Chagas' disease. DATE SOURCES: We reviewed papers which included data about the characteristics of idiopathic achalasia and Chagas' disease. DATA SYNTHESIS: Impairment of inhibitory esophageal neurons was shown in the two diseases. The results of the studies of the effects of atropine, edrophonium and botulin toxin suggested that the excitatory innervation is more intensely impaired in Chagas' disease than in idiopathic achalasia, explaining the increase in the lower esophageal sphincter pressure found in achalasia. The patients with Chagas' disease have more circulating muscarinic cholinergic receptor M2 autoantibodies than patient with idiopathic achalasia. The duration of the contractions in the esophageal body is longer in idiophatic achalasia than in Chagas' disease. CONCLUSIONS: The papers that studied Chagas' disease and idiopathic achalasia, mainly those which studied both diseases with the same methods, suggested that there are different grades of esophageal involvement by the two diseases, mainly the most important involvement of excitatory innervation in Chagas' disease than in idiopathic achalasia.     

Vigorous achalasia in Chagas'' disease

The study investigated the esophageal motility of 98 patients with Chagas' disease and 40 asymptomatic volunteers, with the objective of comparing patients with vigorous achalasia (distal amplitude contractions >/= 37 mmHg) and patients with classical achalasia (amplitude < 37 mmHg). The Chagas' disease patients had normal esophageal radiologic transit (n=60) or esophageal slow transit and retention without dilation (n=38). The manometric method with continuous perfusion was used to study esophageal motility. Comparison of classical and vigorous achalasia showed no difference in duration of contractions, lower and upper esophageal sphincter pressure, proportion of patients with dysphagia, or the number of multipeaked contractions. The number of failed contractions was higher in patients with classic achalasia than in patients with vigorous achalasia. We conclude that the distinction between classical and vigorous achalasia does not seem to be important for the classification of Chagas' disease.     

A clinical trial with pre- and post-treatment manometry comparing pneumatic dilation with bouginage for treatment of Chagas' megaesophagus

The physiologic similarities between the megaesophagus of Chagas' disease and idiopathic achalasia are well documented. Therefore, it would seem reasonable that comparisons of controlled trials of therapy for the more common Chagas' megaesophagus could be applied to idiopathic achalasia, where the paucity of cases makes such a controlled comparison difficult. We had the opportunity to study 18 patients with achalasia secondary to Chagas' disease. All of the patients were from the mid central states of Brazil, all had symptoms of dysphagia and radiographic documentation of dilated esophagus and abnormal peristalsis (Rezende Groups II and III), as well as positive serologic evidence of Chagas' disease. Perfused intraluminal manometric studies were performed on all patients. Resting sphincter pressures ranged from 20-35 mm./Hg., mean of 25 (normal 5-12 mm./Hg.) with aperistalsis. Patients were randomly dilated with either bouginage (44-55 ff catheter) or pneumatic dilator (4-4.5 kg./6.5 cm.2 x 2 min.). Although all patients reported symptomatic improvement several days after either procedure, repeat manometric tracings demonstrated no change in the sphincter pressure in the bouginage group. The pneumatically dilated group, however, demonstrated a decrease in sphincter pressure to normal levels (mean 12 mm./Hg.). Follow-up studies one year after the procedure confirmed the persistence of normal sphincter pressure in the pneumatically dilated group but no change, as well as return of initial symptoms, in the bouginage group.     

Reevaluation of manometric criteria for vigorous achalasia

Clinical and manometric data from 97 consecutive patients with idiopathic achalasia were analyzed to see if a distinct subset with vigorous achalasia could be identified. Statistical analyses failed to detect a unique group of subjects based on the distribution of contraction wave amplitudes alone. Because of this, patients falling above the 95th percentile (N=4, mean wave amplitude>100 mm Hg for each) were compared with those having mean amplitudes above the conventional threshold for the diagnosis of vigorous achalasia (mean amplitude 60–100 mm Hg,N=4), and with the remainder (N=89, mean amplitude <60 mm Hg). Subjects with mean amplitudes <60 mm Hg and with mean amplitudes 60–100 mm Hg closely resembled each other in all measured clinical features, whereas subjects with mean amplitudes >100 mm Hg were all male, were older (67±4 years vs 47±2 years; P<0.01), and appeared to have somewhat longer duration of symptoms when compared with the remainder (82±41 vs 44±10 months;P=0.4). Chest pain and other esophageal symptoms, basal and residual lower sphincter pressures, and response to first treatment did not differ among the three groups. These data indicate that high-fidelity manometry techniques identify a rare subset of achalasia patients with mean contraction amplitudes exceeding 100 mm Hg that, although older and possibly with greater duration of symptoms, presents similarly to others with idiopathic achalasia. Outcome from conventional treatment is also similar for the vigorous and nonvigorous patients, making the distinction of questionable value.Supported in part by a grant (AM07130) from the United States Public Health Service. Dr. Todorczuk is supported by a grant from Smith Kline and French.     

Manometric and Radiologic Correlations in Achalasia

Achalasia is an esophageal motor disorder distinguished by clinical, radiologic, and manometric features. To evaluate the correlation among these features, we studied 109 achalasia patients. The four most common clinical complaints, the four most commonly encountered radiologic findings, and two manometric parameters were analyzed with a correlation matrix test and a multiple regression analysis. Significant correlation existed among symptoms of dysphagia, regurgitation, and weight loss. In contrast, chest pain inversely correlated with these symptoms. Dysphagia and weight loss significantly correlated with a bird-beak deformity but not with esophageal dilatation or a sigmoid esophagus. Moreover, no significant relationship between lower esophageal sphincter pressure and esophageal dilatation or sphincter pressure and sigmoid esophagus was found. However, in those patients with a resting lower esophageal sphincter pressure greater than 45 mm Hg, a reasonable correlation among clinical, radiologic, and manometric parameters did exist. In conclusion, although in a subset of patients with markedly increased lower esophageal sphincter pressure, a good correlation between clinical, radiologic, and manometric findings exists, such a correlation cannot be established in all of the achalasia patients; esophageal dilatation or a sigmoid esophagus may not be due to a hypertensive sphincter, and their presence must not necessarily be interpreted as an indication of severity of the disease; there is an inverse correlation between chest pain and symptoms of dysphagia, regurgitation, and weight loss; and finally, achalasia and hiatal hernia may coexist in 6% of the patients.     

Dysphagia in Patients with Chagas' Disease

Some patients with Chagas' disease and apparent normal esophageal function complain of dysphagia. With the objective of investigating the esophageal motility of these patients we studied the esophageal contraction amplitude, duration, velocity, and lower esophageal sphincter (LES) pressure of 34 patients with a positive serologic test for Chagas' disease, normal radiologic esophageal examination, peristaltic contractions in the esophageal body, and complete LES relaxation. Fourteen patients complained of dysphagia and 20 had no symptoms. The results were compared with those of 22 healthy controls. We used the manometric method with continuous perfusion. In patients without dysphagia, the LES pressure (17.8 ± 1.2 mmHg, mean ± SEM) and distal esophageal amplitude (71.8 ± 7.9 mmHg) were lower than those of control subjects (24.3 ± 1.8 mmHg and 100.4 ± 10.6 mmHg, respectively). The velocity of peristaltic contractions was higher in patients than in controls, but there was no difference between patients with or without dysphagia. The duration of contraction in the distal esophagus was longer in patients with dysphagia (3.9 ± 0.2 sec) than in patients without dysphagia (3.1 ± 0.2 sec) and controls (3.2 ± 0.2 sec). We conclude that dysphagia in patients with Chagas' disease and a nondilated esophagus with peristaltic contractions and complete LES relaxation is related to a longer duration of contractions in the middle and distal esophageal body.     

Lower esophageal sphincter pressure as an index of gastroesophageal acid reflux

The purpose of this study was to determine the relationship of lower esophageal sphincter (LES) pressure and the volume of acid placed into the stomach required to induce gastroesophageal reflux in man. LES pressure was recorded continuously and by station pull-through by three radially oriented catheters in both symptomatic and asymptomatic subjects during the graded infusions of 0.1 N HCl acid into the stomach. Sumptomatic subjects had a mean LES pressure of 7.5±0.7 mm Hg and refluxed at a volume of 140.0±21.0 ml. Fifty-five percent of asymptomatic subjects refluxed at a mean volume of 380.0±24.7 ml, and had a mean LES pressure of 13.8±0.4 mm Hg. Asymptomatic nonrefluxers at a volume of 500 ml of 0.1 HCL acid had a mean LES pressure of 18.9±1.1 mm Hg. The mean LES pressure and acid volumes showed statistical significance between the three groups (P<0.01). There was an excellent overall correlation between LES pressure and acid volume required to produce reflux in all subjects (r=0.91,P<0.001). Following reflux, asymptomatic but not symptomatic subjects showed a significant increase in LES pressure. These studies suggest that: (1) LES pressure does provide an accurate index of the gastroesophageal antireflux mechanism, provided that acid volume is considered; and (2) asymptomatic subjects showing acid reflux have higher LES pressures, reflux at higher volumes, and develop an LES contractile response after the reflux episode.This work was supported by a grant from the Smith Kline & French Laboratories, Philadelphia, Pennsylvania.