Division of Gastroenterology, Department of Translational Research and New Technology in Medicine and Surgery, University of Pisa, Pisa, Italy.
Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri, USA.
Am J Gastroenterol. 2021 Feb 1;116(2):263-273. doi: 10.14309/ajg.0000000000001061.
Hypercontractile esophagus (HE) is a heterogeneous major motility disorder diagnosed when ≥20% hypercontractile peristaltic sequences (distal contractile integral >8,000 mm Hgscm) are present within the context of normal lower esophageal sphincter (LES) relaxation (integrated relaxation pressure < upper limit of normal) on esophageal high-resolution manometry (HRM). HE can manifest with dysphagia and chest pain, with unclear mechanisms of symptom generation. The pathophysiology of HE may entail an excessive cholinergic drive with temporal asynchrony of circular and longitudinal muscle contractions; provocative testing during HRM has also demonstrated abnormal inhibition. Hypercontractility can be limited to the esophageal body or can include the LES; rarely, the process is limited to the LES. Hypercontractility can sometimes be associated with esophagogastric junction (EGJ) outflow obstruction and increased muscle thickness. Provocative tests during HRM can increase detection of HE, reproduce symptoms, and predict delayed esophageal emptying. Regarding therapy, an empiric trial of a proton pump inhibitor, should be first considered, given the overlap with gastroesophageal reflux disease. Calcium channel blockers, nitrates, and phosphodiesterase inhibitors have been used to reduce contraction vigor but with suboptimal symptomatic response. Endoscopic treatment with botulinum toxin injection or pneumatic dilation is associated with variable response. Per-oral endoscopic myotomy may be superior to laparoscopic Heller myotomy in relieving dysphagia, but available data are scant. The presence of EGJ outflow obstruction in HE discriminates a subset of patients who may benefit from endoscopic treatment targeting the EGJ.
高收缩性食管（HE）是一种异质性的主要运动障碍，当正常食管下括约肌（LES）松弛（整合松弛压力<正常上限）时，存在≥20%的高收缩蠕动序列（远端收缩积分>8000mmHgscm）时即可诊断为 HE[1,2]。HE 可表现为吞咽困难和胸痛，但症状发生的机制尚不清楚。HE 的病理生理学可能涉及胆碱能驱动过度，环形和纵向肌肉收缩的时间不同步；食管高分辨率测压（HRM）期间的激发试验也显示出异常抑制[3,4]。高收缩性可局限于食管体，也可包括 LES；很少情况下，这个过程仅限于 LES[5]。高收缩性有时可伴有食管胃结合部（EGJ）流出道梗阻和肌肉厚度增加[6]。HRM 期间的激发试验可增加 HE 的检出率，再现症状，并预测食管排空延迟[7,8]。关于治疗，鉴于与胃食管反流病的重叠，应首先考虑质子泵抑制剂的经验性试验[9]。钙通道阻滞剂、硝酸盐和磷酸二酯酶抑制剂已被用于降低收缩力，但症状缓解效果不理想[10,11]。内镜下注射肉毒杆菌毒素或气动扩张治疗与可变反应相关[12,13]。经口内镜肌切开术可能优于腹腔镜 Heller 肌切开术缓解吞咽困难，但现有数据有限[14,15]。HE 中 EGJ 流出道梗阻的存在可区分出一组可能受益于针对 EGJ 的内镜治疗的患者[16,17]。
