According to the World Obesity Atlas 2023 report [35], “38% of the global population is currently either overweight or obese, based on the WHO criteria. By 2035, the global prevalence of overweight and obesity is projected to reach 51%”. Furthermore, by 2030, 78% of US adults are projected to be overweight/obese [36]. The cost of this global obesity pandemic is estimated to be more than four trillion US dollars of potential income in 2035 [35]. With the rapidly increasing global prevalence of obesity, bariatric surgery is routinely implemented to prevent the development of several chronic conditions and their associated complications. According to the International Federation for Surgery of Obesity and Metabolic Disorders (IFSO) 8TH Global Registry Report published in 2023 [37], 480,970 bariatric procedures were performed in 2021 and 2022. Of these, 60.4% were LVSG, 29.5% were laparoscopic Roux-en-Y gastric bypass (LRYGB), 4.3% were laparoscopic one-anastomosis gastric bypass (LOAGB), and 5.8% were others [37]. The revision rate for LVSG was 23.8%, the reasons for which were not specified. However, one can speculate that weight regain and GERD are the two most common reasons for revision surgery. Two recent meta-analyses comparing 5-year GER outcomes following LVSG and LRYGB have shown significantly worsened GERD, including the development of de novo GERD at 5-year following LVSG vs LRYGB (19.1% vs 3.4%) requiring either pharmacological or surgical intervention [5, 6]. Other recent publications reporting 5- to 10-year outcomes for LVSG vs LRYGB demonstrated ongoing worsened GERD outcomes for patients in the former compared to the latter group [38,39,40]. A number of possible explanations have been put forward to explain this phenomenon, which include (a) the presence of hiatal hernia (HH), which reduces LESP compared to those without HH (13 vs 8 mm Hg) [41] (b) the impact of sleeve shape on the degree of intraluminal (or intragastric) pressure, which is inversely proportional to the diameter of the gastric lumen post LVSG [42]; (c) the effect of resection of the fundus, which leads to decreased vasovagal reflex and complete elimination of physiological postprandial gastric relaxation, further increasing the intragastric pressure (IIGP) [5]; (d) poor surgical techniques resulting in sleeve stenosis, kinking, angulation, and/or cicatrization of the sleeve leading to IIGP [5, 6]; and (e) a more obtuse esophagogastric angle in the majority (78%) of patients following LVSG, which is associated with decreased intra-abdominal length and resting pressure of the LES [31]. However, assessing the effect of GERD after LVSG is challenging due to the lack of standardized reporting, varying definitions, and often lack of objective assessment with the EFTs [5, 6].

Fyke et al. [43] were the first to describe an HPZ at the human EGJ in 1956. Two further studies [44, 45] provided undeniable evidence for the presence of LES and its importance in preventing GER. However, what constitutes LES remains a source of contention. Liebermann-Meffert et al. [46] described the sling muscle fibers on the greater curvature of the stomach and the clasp muscle fibers on the lesser curvature, both within the gastric cardia, and considered them to be the major anatomic component within the HPZ [47]. Stein et al. [47] compared three-dimensional manometric pressure images with muscular thickness and architecture in the human LES and concluded that the LES is not a muscular ring, and the arrangement of muscular structures at the EGJ indicates that the gastric sling fibers at the greater curvature and the semicircular clasps at the lesser curvature are the anatomic correlates of the manometric LES in human beings and are important in maintaining EGJ integrity. Zifran et al. [48] recently studied the myoarchitecture of the LES and esophageal hiatus using optical sectioning microscopy. According to them, the circular muscle fibers at the lower end of the esophagus cross its dorsal surface, close to the angle of His, and continue as oblique muscle fibers on the anterior and posterior surfaces of the stomach (from the greater curvature to the lesser curvature). According to the authors, the spiral muscle fibers of the distal esophagus, crossing at the angle of His, will provide a circumferential squeeze at the lower end of the esophagus and act like a “noose” around the esophagus, providing a barrier against GER.

As mentioned above, LES therefore plays an important role in the pathophysiology of GERD, both pre- and post-LVSG. Several studies have investigated the relevance of manometry and 24-h pH study to gauge the impact of LVSG on LESP and LESL in patients with morbid obesity, an area that seems to have been under-researched in the pathophysiology of GERD post-bariatric surgery. To date, all cohort studies comparing pre- and post-LVSG esophageal function data have been underpowered because of the small sample size, which may reduce the chance of detecting a true effect of surgery on LES, leading to unreliable conclusions. Therefore, our aim was to pool data from several independent studies to provide a more precise estimate of the outcome of LVSG for LESP, LESL, and GERD. Thus, we analyzed the objective data on the anatomical changes at the EGJ/LES, which may result in a reduction in the total and/or abdominal LESL and lead to dynamic failure by affecting the LESP profile [49]. These changes can be attributed to iatrogenic injury of the sling fibers at the cardia while dissecting around the angle of His during the LVSG procedure [50, 51].

Zaninotto et al. [2] were the first to illustrate the importance of not only TL and intraluminal LESP but also of AL in maintaining the competence of the LES. The overall LESL in healthy individuals varies between 2.5 and 5.5 cm. Several studies have analyzed LESL and its association with GER [4, 52] and have shown that LESL is reduced in GERD. Therefore, we evaluated the impact of LVSG on LESP, LESL (TL), LESAL, and DMS.

Except for one study [31], none of the other 19 studies in our meta-analysis provided manometry data on LESAL. Our efforts to contact corresponding authors of several of these studies repeatedly via email were unsuccessful and therefore, we excluded this variable from our analysis.

Although 12 studies provided data on LESL both pre- and post-LVSG, only nine studies [17, 19,20,21, 25, 26, 28, 31, 33], three performed HRM [19, 31, 33], and six CM [17, 20, 21, 25, 26, 28] were analyzable. All HRM studies have consistently shown a significant decrease in LESL, and in one case, significantly [31]. In contrast, all CM studies have shown no profound changes in the LESL after LVSG. Meta-analysis of pooled data from these studies failed to show any significant anatomical changes in the LESL pre- and post-LVSG (Fig. 3). However, when we performed leave out sensitivity analysis with the removal of Keldi’s et al. study [17] it showed significant decrease of 0.16 cm in LESL (WMD 0.16, 95% CI 0.00 to 0.32, Z = 2.00, p = 0.045) suggesting disproportionate influence of this study on the overall analysis (Fig. 3). Moreover, we feel that the analytical disparity between HRM and CM is due to the fact that the former is far more accurate than the latter in recognizing LESL changes pre- and post-LVSG due to the distribution of closely placed pressure sensors (every 1 cm), which prevents loss of relevant information, leading to a more accurate measurement of LESL along with high resolution, which leads to greater reproducibility. The present analysis, based on a combination of CM and HRM data, failed to show any substantial anatomical reduction in LESL post-LVSG (if one does not exclude any studies) and therefore cannot be considered a contributing factor to GERD. We hope that future large-scale multicenter trials will provide more accurate information on the impact of LVSG on LESL using HRM data alone.

Next, we analyzed pre- and post-LVSG LESP manometry data from 16 studies [16, 18,19,20,21, 23,24,25,26,27,28, 30,31,32,33,34] (HRM = 8 [18, 19, 24, 27, 31,32,33,34] CM = 8 [16, 20, 21, 23, 25, 26, 28, 30]), as the data from the remaining three studies [17, 22, 29] were not analyzable. It was evident that post-LVSG, there was a dynamic failure of LES due to a decrease in LESP in all studies except for two [19, 32]. The pooled data from these studies showed a significant reduction in post-LVSG LESP of 3.82 mm Hg (Fig. 2). Subgroup analysis for both HRM and CM showed a similar significant reduction in LESP in post-LVSG patients (Fig. 2). Furthermore, when we applied sensitivity analysis, our results across multiple iterations did not significantly change the outcome and the pooled WMD and heterogeneity (>80%) remained relatively unchanged, indicating that the overall conclusions are robust.

LESP at rest is maintained between 10 and 30 mmHg in healthy individuals. Even if the LES is relaxed, the pressure remains slightly higher than that of the IGP to prevent reflux. Following LVSG, reduced LESP and increase in intragastric pressure (IIGP) due to removal of 80–90% of the stomach augments the condition for GERD, leading to worsening of GER symptoms or even producing de novo GERD. Yehoshua et al. [53] undertook volume and pressure assessments pre- and post-LVSG using an electronic barostat. According to these authors, the primary motor function of the stomach is to receive, store, and prepare food for digestion. This task is made possible by the accommodation reflex, which, through active relaxation of the gastric fundus, allows for a volume increase without an IIGP, thus enabling the stomach to accommodate large volumes during food intake. According to them, the distensibility of the total stomach and excised fundus was 10-fold higher than that of the gastric sleeve, providing for the first time conclusive evidence that the distensible region of the stomach is removed during LVSG, leading to IIGP. Mion et al. [42] undertook high-resolution impedance manometry postoperatively to evaluate the impact of LVSG on esophagogastric motility, particularly in patients with upper gastrointestinal symptoms. They concluded that IIGP occurred in 77% of patients after water swallow, and impedance reflux episodes were observed in 53% of patients with LVSG, especially those with GER symptoms and ineffective esophageal motility, and were more pronounced in sleeves with smaller volumes and diameters. In another prospective study, IIGP after water swallows was observed in 50% of LVSG patients with de novo GERD (49 mmHg) than in those without this complication (25 mmHg). Five studies [18, 24, 28, 31,