Refining the criterion for an abnormal Integrated Relaxation Pressure in esophageal pressure topography based on the pattern of esophageal contractility using a classification and regression tree model

Background The Integrated Relaxation Pressure (IRP) is the esophageal pressure topography (EPT) metric used for assessing the adequacy of esophagogastric junction (EGJ) relaxation in the Chicago Classification of motility disorders. However, because the IRP value is also influenced by distal esophageal contractility, we hypothesized that its normal limits should vary with different patterns of contractility. Methods Five hundred and twenty two selected EPT studies were used to compare the accuracy of alternative analysis paradigms to that of a motility expert (the ‘gold standard’). Chicago Classification metrics were scored manually and used as inputs for MATLAB? programs that utilized either strict algorithm‐based interpretation (fixed abnormal IRP threshold of 15 mmHg) or a classification and regression tree (CART) model that selected variable IRP thresholds depending on the associated esophageal contractility. Key Results The sensitivity of the CART model for achalasia (93%) was better than that of the algorithm‐based approach (85%) on account of using variable IRP thresholds that ranged from a low value of >10 mmHg to distinguish type I achalasia from absent peristalsis to a high value of >17 mmHg to distinguish type III achalasia from distal esophageal spasm. Additionally, type II achalasia was diagnosed solely by panesophageal pressurization without the IRP entering the algorithm. Conclusions & Inferences Automated interpretation of EPT studies more closely mimics that of a motility expert when IRP thresholds for impaired EGJ relaxation are adjusted depending on the pattern of associated esophageal contractility. The range of IRP cutoffs suggested by the CART model ranged from 10 to 17 mmHg.     

What is new in Chicago Classification version 4.0?

Since publication of Chicago Classification version 3.0 in 2015, the clinical and research applications of high‐resolution manometry (HRM) have expanded. In order to update the Chicago Classification, an International HRM Working Group consisting of 52 diverse experts worked for two years and utilized formally validated methodologies. Compared with the prior iteration, there are four key modifications in Chicago Classification version 4.0 (CCv4.0). First, further manometric and non‐manometric evaluation is required to arrive at a conclusive, actionable diagnosis of esophagogastric junction (EGJ) outflow obstruction (EGJOO). Second, EGJOO, distal esophageal spasm, and hypercontractile esophagus are three manometric patterns that must be accompanied by obstructive esophageal symptoms of dysphagia and/or non‐cardiac chest pain to be considered clinically relevant. Third, the standardized manometric protocol should ideally include supine and upright positions as well as additional manometric maneuvers such as the multiple rapid swallows and rapid drink challenge. Solid test swallows, postprandial testing, and pharmacologic provocation can also be considered for particular conditions. Finally, the definition of ineffective esophageal motility is more stringent and now encompasses fragmented peristalsis. Hence, CCv4.0 no longer distinguishes between major versus minor motility disorders but simply separates disorders of EGJ outflow from disorders of peristalsis.     

3D‐high resolution manometry of the esophagogastric junction

Background The esophagogastric junction (EGJ) is a complex structure that challenges accurate manometric recording. This study aimed to define EGJ pressure morphology relative to the squamocolumnar junction (SCJ) during respiration with 3D‐high resolution manometry (3D‐HRM). Methods A 7.5‐cm long 3D‐HRM array with 96 independent solid‐state pressure sensors (axial spacing 0.75 cm, radial spacing 45°) was used to record EGJ pressure in 15 normal subjects. Concurrent videofluoroscopy was used to localize the SCJ marked with an endoclip. Ex vivo experiments were done on the effect of bending the probe to match that seen fluoroscopically. Key Results 3D‐high resolution manometry EGJ pressure recordings were dominated by an asymmetric pressure peak superimposed on the lower esophageal sphincter (LES) attributable to the crural diaphragm (CD). Median peak CD pressure at expiration and inspiration (51 and 119 mmHg, respectively) was much greater in 3D‐HRM than evident in HRM with circumferential pressure averaging. Esophagogastric junction length, defined as the zone of circumferential pressure exceeding that of adjacent esophagus or stomach was also substantially shorter (2.4 cm) than evident in conventional HRM. No consistent circumferential EGJ pressure was evident distal to the SCJ in 3D‐HRM recordings and ex vivo experiments suggested that the intra‐gastric pressure peak seen contralateral to the CD related to bending the assembly rather than the sphincter per se. Conclusions & Inferences 3D‐high resolution manometry demonstrated a profoundly asymmetric and vigorous CD component to EGJ pressure superimposed on the LES. Esophagogastric junction length was shorter than evident with conventional HRM and the distal margin of the EGJ sphincteric zone closely correlated with the SCJ.     

Manometric features of eosinophilic esophagitis in esophageal pressure topography

Background Although most of the patients with eosinophilic esophagitis (EoE) have mucosal and structural changes that could potentially explain their symptoms, it is unclear whether EoE is associated with abnormal esophageal motor function. The aims of this study were to evaluate the esophageal pressure topography (EPT) findings in EoE and to compare them with controls and patients with gastro‐esophageal disease (GERD). Methods Esophageal pressure topography studies in 48 EoE patients, 48 GERD patients, and 50 controls were compared. The esophageal contractile pattern was described for ten 5‐mL swallows for each subject and each swallow was secondarily characterized based on the bolus pressurization pattern: absent, pan‐esophageal pressurization, or compartmentalized distal pressurization. Key Results Thirty‐seven percent of EoE patients were classified as having abnormal esophageal motility. The most frequent diagnoses were of weak peristalsis and frequent failed peristalsis. Although motility disorders were more frequent in EoE patients than in controls, the prevalence and type were similar to those observed in GERD patients (P = 0.61, chi‐square test). Pan‐esophageal pressurization was present in 17% of EoE and 2% of GERD patients while compartmentalized pressurization was present in 19% of EoE and 10% of GERD patients. These patterns were not seen in control subjects. Conclusions & Inferences The prevalence of abnormal esophageal motility in EoE was approximately 37% and was similar in frequency and type to motor patterns observed in GERD. Eosinophilic esophagitis patients were more likely to have abnormal bolus pressurization patterns during swallowing and we hypothesize that this may be a manifestation of reduced esophageal compliance.     

Effects of lidocaine on esophageal secondary peristalsis in humans

Background Secondary peristalsis is important for the clearance of retained food bolus or refluxate from the esophagus. Lidocaine has been used to evaluate the role of mucosa‐mediating pathways of esophageal reflexes in animal model, but its effects on esophageal secondary peristalsis are yet unclear in humans. We aimed to investigate whether esophageal secondary peristalsis can be affected by intraluminal infusion of lidocaine into the esophagus. Methods After a baseline recording esophageal motility, secondary peristalsis was generated by slow and rapid mid‐esophageal injections of air in 13 healthy subjects. Two separate sessions with saline and lidocaine were randomly performed to test their effects on esophageal secondary peristalsis by mid‐esophageal air distension. Key Results Secondary peristalsis can be induced by slow or rapid air infusion. Secondary peristalsis was triggered less frequently in response to rapid air distension after lidocaine infusion (P = 0.001). After lidocaine infusion, the threshold volume to generate secondary peristalsis was significantly increased during rapid (P = 0.001), but not slow air infusions (P = NS). Infusion of lidocaine or saline did not affect pressure wave amplitude or duration during rapid and slow air infusions (P = NS). Conclusions & Inferences We have demonstrated selectively inhibitory effect of lidocaine on the triggering of esophageal secondary peristalsis during acute gaseous esophageal distension. The data suggest that part of the activation of secondary peristalsis is probably mediated by lidocaine‐sensitive mechanoreceptors; however, the infusion of lidocaine does not lead to any motility change in secondary peristalsis induced by either slow or rapid air infusions.     

The impact of primary peristalsis,contractile reserve,and secondary peristalsis on esophageal clearance measured by timed barium esophagogram

Background

Primary and secondary peristalsis facilitate esophageal bolus transport; however, their relative impact for bolus clearance remains unclear. We aimed to compare primary peristalsis and contractile reserve on high-resolution manometry (HRM) and secondary peristalsis on functional lumen imaging probe (FLIP) Panometry with emptying on timed barium esophagogram (TBE) and incorporate findings into a comprehensive model of esophageal function.

Methods

Adult patients who completed HRM with multiple rapid swallows (MRS), FLIP, and TBE for esophageal motility evaluation and without abnormal esophagogastric junction outflow/opening or spasm were included. An abnormal TBE was defined as a 1-min column height >5 cm. Primary peristalsis and contractile reserve after MRS were combined into an HRM–MRS model. Secondary peristalsis was combined with primary peristalsis assessment to describe a complementary neuromyogenic model.

Key Results

Of 89 included patients, differences in rates of abnormal TBEs were observed with primary peristalsis classification (normal: 14.3%; ineffective esophageal motility: 20.0%; absent peristalsis: 54.5%; p = 0.009), contractile reserve (present: 12.5%; absent: 29.3%; p = 0.05), and secondary peristalsis (normal: 9.7%; borderline: 17.6%; impaired/disordered: 28.6%; absent contractile response: 50%; p = 0.039). Logistic regression analysis (akaike information criteria, area under the receiver operating curve) demonstrated that the neuromyogenic model (80.8, 0.83) had a stronger relationship predicting abnormal TBE compared to primary peristalsis (81.5, 0.82), contractile reserve (86.8, 0.75), or secondary peristalsis (89.0, 0.78).

Conclusions and Inferences

Primary peristalsis, contractile reserve, and secondary peristalsis were associated with abnormal esophageal retention as measured by TBE. Added benefit was observed when applying comprehensive models to incorporate primary and secondary peristalsis supporting their complementary application.     

Effects of mosapride on esophageal secondary peristalsis in humans

Background Secondary peristalsis is important for the clearance of refluxate or retained food bolus from the esophagus. Mosapride is a prokinetic agent that enhances GI motility by stimulating 5‐hydroxytrypatamine₄ (5‐HT₄) receptors, but its effects on secondary peristalsis are yet unclear in humans. We aimed to investigate the effect of a 5‐HT₄ agonist mosapride on esophageal distension‐induced secondary peristalsis in normal subjects. Methods After a baseline recording esophageal motility, secondary peristalsis was generated by slow and rapid mid‐esophageal injections of air in 15 healthy subjects. Two separate sessions with 40 mg oral mosapride or placebo were randomly performed to test their effects on esophageal secondary peristalsis. Key Results Mosapride decreased the threshold volume for triggering secondary peristalsis during rapid air distension (4.5 ± 0.3 vs 5.3 ± 0.4 mL; P = 0.04) but not slow air distension (14.3 ± 1.2 vs 13.3 ± 1.3 mL; P = 0.41). Secondary peristalsis was triggered more frequently in response to rapid air distension after application of mosapride [100% (90–100%) vs 90% (80–100%); P = 0.02]. Mosapride significantly increased pressure wave amplitudes of secondary peristalsis during slow (135.4 ± 13.8 vs 105.0 ± 12.9 mmHg; P = 0.001) and rapid air distensions (124.0 ± 11.6 vs 95.9 ± 14.0 mmHg; P = 0.002). Conclusions & Inferences Mosapride enhances sensitivity to distension‐induced secondary peristalsis and facilitates secondary peristaltic contractility. These data provide an evidence for modulation of esophageal secondary peristalsis by the 5‐HT₄ agonist mosapride, as well support for its clinical utility.     

Effects of capsaicin‐containing red pepper sauce suspension on esophageal secondary peristalsis in humans

Background Capsaicin‐sensitive afferents have been implicated in the modulation of gastrointestinal sensorimotor functions. Secondary peristalsis is important for the clearance of retained refluxate or material from the esophagus. The aim of this study was to evaluate the effects of capsaicin‐containing red pepper sauce suspension on esophageal secondary peristalsis in healthy adults. Methods After a baseline recording of esophageal motility, secondary peristalsis was generated by slow and rapid mid‐esophageal injections of air in 10 healthy subjects. Two separate sessions with saline and capsaicin‐containing red pepper sauce were randomly performed to test their effects on esophageal secondary peristalsis. Key Results Infusion of capsaicin significantly increased pressure wave amplitude during rapid (P = 0.002) and slow air infusions (P = 0.01). After capsaicin, the threshold volume to generate secondary peristalsis was significantly decreased during rapid (P < 0.05) and slow air infusions (P = 0.02). Infusion of saline did not affect any parameters of secondary peristalsis during rapid or slow air infusion. The administration of capsaicin was accompanied by the occurrence of heartburn in all subjects. Conclusions & Inferences The acute administration of capsaicin‐containing red pepper sauce suspension enhances sensitivity to distension‐induced secondary peristalsis and facilitates secondary peristaltic contractility. These data suggest the involvement of capsaicin‐sensitive afferents in the modulation of esophageal distension‐induced secondary peristalsis in humans.     

Control of esophageal distension‐induced secondary peristalsis by the GABAB agonist baclofen in humans

Background Secondary peristalsis is important for the clearance of retained food bolus or refluxate from the esophagus. The effects of the gamma aminobutyric acid receptor type B (GABA_B) agonist on secondary peristalsis remain unclear in humans. We aimed to investigate the effect of a GABA_B agonist baclofen on esophageal secondary peristalsis. Methods After a baseline recording of esophageal motility, secondary peristalsis was generated by slow and rapid mid‐esophageal injections of air in 15 healthy subjects. Two separate sessions with 40 mg oral baclofen or placebo were randomly performed to test their effects on secondary peristalsis. Key Results Baclofen increased the threshold volume for triggering secondary peristalsis during slow air distension (P = 0.003) and rapid air distension (P = 0.002). Baclofen reduced the rate of secondary peristalsis by rapid air distension from 90% to 30% (P = 0.0002). Baclofen increased basal lower esophageal sphincter pressure (P = 0.03). Baclofen did not affect any of peristaltic parameters during primary or secondary peristalsis. Conclusions & Inferences This study provides an evidence for inhibitory modulation of esophageal secondary peristalsis by the GABA_B agonist baclofen. Activation of secondary peristalsis is probably modulated by GABA_B receptors; however, baclofen does not lead to any motility change in secondary peristalsis.     

Failure to respond to physiologic challenge characterizes esophageal motility in erosive gastro‐esophageal reflux disease

Background Non‐specific esophageal dysmotility with impaired clearance is often present in patients with gastro‐esophageal reflux disease (GERD), especially those with erosive disease; however the physio‐mechanic basis of esophageal dysfunction is not well defined. Methods Retrospective assessment of patients with erosive reflux disease (ERD; n = 20) and endoscopy negative reflux disease (ENRD; n = 20) with pathologic acid exposure on pH studies (>4.2% time/24 h) and also healthy controls (n = 20) studied by high resolution manometry. Esophageal motility in response to liquid and solid bolus swallows and multiple water swallows (MWS) was analyzed. Peristaltic dysfunction was defined as failed peristalsis, spasm, weak or poorly coordinated esophageal contraction (>3 cm break in 30 mmHg isocontour). Key Results Peristaltic dysfunction was present in 33% of water swallows in controls, 56% ENRD and 76% ERD respectively (P < 0.023 vs controls, P = 0.185 vs ENRD). The proportion of effective peristaltic contractions improved with solid compared to liquid bolus in controls (18%vs 33%, P = 0.082) and ENRD (22%vs 54%, P = 0.046) but not ERD (62%vs 76%, P = 0.438). Similarly, MWS was followed by effective peristalsis in 83% of controls and 70% ENRD but only 30% ERD patients (P < 0.017 vs controls and P < 0.031 vs ENRD). The association between acid exposure and dysmotility was closer for solid than liquid swallows (r = 0.52 vs 0.27). Conclusions & Inferences Peristaltic dysfunction is common in GERD. ERD patients are characterized by a failure to respond to the physiologic challenge of solid bolus and MWS that is likely also to impair clearance following reflux events and increase exposure to gastric refluxate.     

Chicago classification criteria of esophageal motility disorders defined in high resolution esophageal pressure topography

BACKGROUND: The Chicago Classification of esophageal motility was developed to facilitate the interpretation of clinical high resolution esophageal pressure topography (EPT) studies, concurrent with the widespread adoption of this technology into clinical practice. The Chicago Classification has been an evolutionary process, molded first by published evidence pertinent to the clinical interpretation of high resolution manometry (HRM) studies and secondarily by group experience when suitable evidence is lacking. PURPOSE: This publication summarizes the state of our knowledge as of the most recent meeting of the International High Resolution Manometry Working Group in Ascona, Switzerland in April 2011. The prior iteration of the Chicago Classification was updated through a process of literature analysis and discussion. The major changes in this document from the prior iteration are largely attributable to research studies published since the prior iteration, in many cases research conducted in response to prior deliberations of the International High Resolution Manometry Working Group. The classification now includes criteria for subtyping achalasia, EGJ outflow obstruction, motility disorders not observed in normal subjects (Distal esophageal spasm, Hypercontractile esophagus, and Absent peristalsis), and statistically defined peristaltic abnormalities (Weak peristalsis, Frequent failed peristalsis, Rapid contractions with normal latency, and Hypertensive peristalsis). The Chicago Classification is an algorithmic scheme for diagnosis of esophageal motility disorders from clinical EPT studies. Moving forward, we anticipate continuing this process with increased emphasis placed on natural history studies and outcome data based on the classification.     

Esophageal provocation tests: Are they useful to improve diagnostic yield of high resolution manometry?

High resolution manometry (HRM) is the gold standard to diagnose esophageal motility disorders but has some limitations. The inclusion of provocative tests might enhance the diagnostic yield of HRM. These tests are easy to perform and to add to the regular manometry protocol. Multiple rapid swallows (MRS; 5 2‐mL swallows) is useful to assess the contractile reserve and deglutitive inhibition. The optimal number of MRS to perform might be 3 as suggested by Mauro et al. in this issue of Neurogastroenterology & Motility. The absence of contractile reserve might be associated with gastro‐esophageal reflux disease and with an increased risk of post fundoplication dysphagia. Single viscous and solid swallows might enhance the detection of esophageal motility disorders but are not significantly associated with symptom occurrence. Test meal has the advantage to represent a real‐life scenario and is promising to depict significant motility findings responsible for esophageal symptoms. Post‐prandial recording might also be of interest to diagnose rumination and belching disorders. The best indication of rapid drink challenge test (free drinking of 200 mL) is currently the diagnosis of esophago‐gastric junction obstruction. Finally, abdominal compression might be an option to evaluate response of esophageal peristalsis in a context of outflow resistance as proposed by Brink et al. in this issue. These provocative maneuvers appear to provide a complementary role in the evaluation of esophageal motility but require prospective studies to determine the validity of the findings and whether they will lead to changes in clinical practice.     

Achalasia: new perspectives on an old disease

Achalasia is defined by esophageal outflow obstruction from abnormal relaxation of the lower esophageal sphincter (LES) due to deranged inhibitory control. In genetically predisposed individuals, an autoimmune response to an unknown inciting agent, perhaps a viral infection, results in inflammation and sometimes loss of myenteric plexus ganglia and neurons. The net result is varying degrees of inhibitory dysfunction, at times associated with imbalanced and exaggerated excitatory function, with manometrically distinct achalasia phenotypes on high resolution manometry. There is new evidence in the current issue of this Journal suggesting that type 1 achalasia, with esophageal outflow obstruction and absent esophageal body contractility, is an end‐stage phenotype from progression of type 2 achalasia, which is characterized by panesophageal compartmentalization of pressure in the untreated patient, and partial recovery of peristalsis after treatment. Esophageal outflow obstruction with premature peristalsis (type 3 achalasia) or intact peristalsis may result from plexitis in the myenteric plexus but can also be encountered in other settings including chronic opioid medication usage and structural processes at the esophagogastric junction and distally. In most instances when idiopathic esophageal outflow obstruction is confirmed, some form of pharmacologic manipulation or disruption of the LES provides durable symptom relief. This review will focus on current understanding of pathophysiology, diagnosis, and principles of management of achalasia in light of emerging literature on the topic.     

High‐resolution manometry changes our views of gastrointestinal motility

High‐resolution manometry using catheters with 36 solid‐state sensors spaced 1 cm apart has already become an established technique for esophageal manometry where it has replaced water‐perfused and station pull‐through manometry. Spatiotemporal plots with color coding of pressure have greatly facilitated the analysis of esophageal peristalsis. Although suitable for the length of the esophagus, the solid‐state catheter is insufficient for the study of longer segments of the gastrointestinal tract. A new technique with fiber‐optic sensors has made it possible to construct catheters with 72–144 sensors. Studies of colonic motility have revealed that the most common motor pattern of the colon is a peristaltic contraction that travels 7–10 cm in the retrograde direction. Earlier studies using low‐resolution manometry with 7–45 cm between sensors led us to erroneous conclusions regarding direction and frequency of contractions and they largely missed both antegrade and retrograde contractions traveling short distances. Fiber‐optic high‐resolution manometry holds promise for greatly improving our understanding of gut motor physiology and hopefully also our understanding of patients with symptoms of disordered gut motility.     

Swallow induces a peristaltic wave of distension that marches in front of the peristaltic wave of contraction

Background Current understanding is that swallow induces simultaneous inhibition of the entire esophagus followed by a sequential wave of contraction (peristalsis). We observed a pattern of luminal distension preceding contraction which suggested that inhibition may also traverses in a peristaltic fashion. Our aim is to determine the relationship between contraction and luminal distension during bolus transport. Methods Eight subjects using two solid‐state pressure and two ultrasound (US) transducers were studied. Synchronous pressure and US images were obtained with wet swallows and after edrophonium and atropine. Luminal cross‐sectional area (CSA) at 2 cm and 12 cm above the lower esophageal sphincter (LES) were recorded. Relationship between pressure and CSA at each site, propagation velocity of peak pressure and peak distension waves were determined. Fluoroscopy coupled with manometry was also performed in five normal subjects. Key Results Esophageal distension precedes contraction wave at both‐recorded sites. During distension, esophageal pressure remains constant while luminal CSA increases significantly. The onset and the peak of distension wave traverses in a peristaltic fashion between both sites. A tight coupling exists between the peak distension and peak contraction waves with similar velocities (3.7 cm s^?1 and 3.6 cm s^?1) of propagation. The degree of distension is greater at 2 cm compared to 12 cm. Atropine and edrophonium reduced and increased the contraction pressure respectively, without affecting the distension wave. Fluoroscopic study confirmed that the wave of distension traverses the esophagus in a peristaltic fashion. Conclusions & Inferences Distension and contraction waves are tightly coupled to each other and both traverse in a peristaltic fashion.     

Automated calculation of the distal contractile integral in esophageal pressure topography with a region-growing algorithm

Background The distal contractile integral (DCI) is an index of contractile vigor in high‐resolution esophageal pressure topography (EPT) calculated as the product of amplitude, duration, and span of the distal esophageal contraction. The aim of this study was to develop an automated algorithm calculating DCI. Methods The DCI was calculated conventionally using ManoView? (Given Imaging, Los Angeles, CA, USA) software in EPT studies from 72 controls and 20 patients and compared to the calculation using a MATLAB? (Version 7.9.0, R2009b; The MathWorks Inc., Natick, MA, USA) ‘region‐growing’ algorithm. This algorithm first established the spatial limits of the distal contraction (the proximal pressure trough to either the distal pressure trough or to the superior margin of the lower esophageal sphincter at rest). Pixel‐by‐pixel horizontal line segments were then analyzed within this span starting at the pressure maximum and extending outward from that point. The limits of ‘region‐growing’ were defined either by the spatial DCI limits or by encountering a pressure <20 mmHg. The DCI was then calculated as the total units of mmHg s cm greater than 20 mmHg within this domain. Key Results Excellent correlation existed between the two methods (r = 0.98, P < 0.001). The DCI values obtained with the conventional calculation were slightly but significantly greater than with the region‐growing algorithm. Differences were attributed to the inclusion of vascular pressures in the conventional calculation or to differences in localization of the distal limit of the DCI. Conclusions & Inferences The proposed region‐growing algorithm provides an automated method to calculate DCI that limits inclusion of vascular pressure artifacts and minimizes the need for user input in data analysis.     

Multiple rapid swallow responses segregate achalasia subtypes on high‐resolution manometry

Background Multiple rapid swallows (MRS) inhibit esophageal peristalsis and lower esophageal sphincter (LES) tone; a rebound excitatory response then results in an exaggerated peristaltic sequence. Multiple rapid swallows responses are dependent on intact inhibitory and excitatory neural function and could vary by subtype in achalasia spectrum disorders. Methods Consecutive subjects with incomplete LES relaxation on high‐resolution manometry (HRM) (Sierra Scientific, Los Angeles, CA, USA) in the absence of mechanical obstruction were prospectively identified. Achalasia spectrum disorders were classified and HRM plots reviewed according to Chicago criteria. Esophageal peristaltic performance and LES function were assessed after 10 wet swallows and MRS (five 2 mL water swallows 2–3 s apart). Findings were compared with 18 healthy controls (28.5 ± 0.6 years, 44% women). Key Results A total of 46 subjects (57.1 ± 2.1 years, 52.2% women) met inclusion criteria. There was complete failure of peristalsis with MRS in all subjects with achalasia subtypes 1 and 2. In contrast, 80% of achalasia subtype 3 and incomplete LES relaxation (EGJ outflow obstruction) with preserved esophageal body peristalsis had a contractile response to MRS (P < 0.001 compared with subtypes 1 and 2); controls demonstrated 94.4% peristalsis. Percent decrease in LES residual pressure during MRS (compared to wet swallows) segregated achalasia subtypes; those with aperistalsis (subtypes 1 and 2) had a lesser decline (22.6%) compared to those with retained esophageal body peristalsis (40.5%) and controls (51.3%, P < 0.001 across groups). Conclusions & Inferences Multiple rapid swallow responses segregate achalasia spectrum disorders into two patterns differentiated by presence or absence of esophageal body contraction response to wet swallows. These findings support subtyping of achalasia, with pathophysiologic implications.     

Postprandial proximal gastric acid pocket and gastric pressure in patients after gastric surgery

Background An unbuffered postprandial proximal gastric acid pocket (PPGAP) has been demonstrated in normal individuals (NI) and patients with gastro‐esophageal reflux disease (GERD). The role of gastric anatomy and gastric motility in the physiology of the PPGAP remains elusive. This study aims to analyze the correlation of PPGAP with proximal gastric pressure after gastric surgery. Methods A total of 26 individuals were studied: eight patients after open Roux‐en‐Y gastric bypass (RYGB) for morbid obesity, six patients after laparoscopic Nissen fundoplication for GERD, seven patients after open subtotal gastrectomy for gastric cancer and five NI. Patients underwent high resolution manometry to identify the location of the lower border of the lower esophageal sphincter (LBLES) and measure gastric pressure 1, 2, 3, 4 and 5 cm below the LBLES, immediately before swallow and after the end of the LES relaxation. A station pull‐through pH monitoring was performed in all but NI, from 5 cm below the LBLES to the LBLES in increments of 1 cm in a fasting state and 10 min after a standardized fatty meal. Key Results Our results show that: (i) proximal gastric pressures are lower after swallow compared with before swallow in NI; (ii) patients after gastric surgery tend to have higher gastric pressure before and lower after swallow compared with NI and (iii) patients after RYGB with PPGAP have an increased gastric pressure after swallows in the segment where the PPGAP is noticed. Conclusions & Inferences Gastric motility may play a role in the genesis of PPGAP in patients after RYGB. The contribution of gastric motility for the genesis of PPGAP is still elusive in other patients.     

Measurement of acid exposure of proximal esophagus: a better tool for diagnosing non‐erosive reflux disease

Background The sensitivity of 24‐h pH monitoring is poor in non‐erosive reflux disease (NERD). In NERD patients, the proximal extent of acid reflux is one of the main determinants of reflux perception. The present study was aimed to compare the diagnostic accuracy of acid exposure time (AET), at 5 cm above the lower esophageal sphincter, with those at 10 cm and at 3 cm below the upper esophageal sphincter as well as the reproducibility of these parameters. Methods A total of 93 consecutive NERD patients, with typical symptoms responsive to proton pump inhibitor treatment, and 40 controls underwent esophageal manometry and multi‐channel 24‐h pH‐test; 13 patients underwent the same study on two occasions. Symptom association probability (SAP) values were evaluated at each esophageal level. Key Results The ROC curve indicates that the area under the curve was 0.79 at distal (SE = 0.039), 0.87 (SE = 0.032) at proximal (P = 0.029 vs distal), and 0.85 (SE = 0.033) at very proximal esophagus (P = 0.148). AET showed a reproducibility of 61% (Kappa 0.22) at distal esophagus, 77% (Kappa 0.45) at proximal and 53% (Kappa 0.05) at very proximal esophagus. The percentage of patients with a positive SAP was not significantly different when assessed at the distal compared with the proximal esophagus. Conclusions & Inferences In NERD patients, the diagnostic yield of the pH test is significantly improved by the assessment of AET at the proximal esophagus. As this variable seems to be less affected by the day to day variability, it could be considered a reliable and useful diagnostic tool in NERD patients.