Cappell M S
Department of Medicine/Gastroenterology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903-0019.
Dig Dis Sci. 1995 Jan;40(1):166-76. doi: 10.1007/BF02063961.
The roentgenographic, echocardiographic, endoscopic, and manometric findings were studied in five consecutive patients with cardiovascular dysphagia, including four with a dilated left atrium and one with an anomalous left subclavian artery. Common and different manometric findings were found in the two types of cardiovascular dysphagia. The major manometric abnormality in all cases was an elevated baseline pressure, with superimposed large rhythmic pressure waves occurring at the same frequency as the electrocardiogram in the mid-esophagus. This manometric abnormality, produced by pulsatile cardiovascular compression, provides direct evidence that cardiovascular dysphagia is caused by esophageal luminal obstruction from cardiovascular compression. Indirect evidence supporting this mechanism includes smooth extrinsic compression and hang-up of ingested barium in the mid-esophagus on esophagogram and transmitted mural pulsations and a compressed lumen in the mid-esophagus at panendoscopy. Two of the five patients had deranged esophageal peristalsis within the high-pressure zone, which also contributed to the dysphagia. Autopsy in one patient with deranged peristalsis revealed a band of ischemic esophageal mucosa in the zone compressed by the dilated left atrium. A novel manometric maneuver might distinguish dysphagia due to an anomalous left subclavian artery from dysphagia due to a dilated left atrium. Left arm elevation during manometry in the single patient with the anomalous artery significantly increased the mean mid-esophageal baseline pressure by 92% (N = 10 trials), and mean pressure wave amplitude by 93% (N = 10 trials, P < 0.002 for each, nonparametric signed rank test). Left arm elevation in this patient also increased the observed luminal obstruction during endoscopy. These manometric and endoscopic findings may be explained by increased arterial compression of the esophagus produced by arterial stretch and anterior displacement with arm elevation.
对连续5例患有心血管性吞咽困难的患者进行了X线、超声心动图、内镜及测压检查,其中4例左心房扩大,1例左锁骨下动脉异常。在两种类型的心血管性吞咽困难中发现了共同和不同的测压结果。所有病例的主要测压异常是基线压力升高,在食管中段出现与心电图频率相同的叠加大的节律性压力波。这种由搏动性心血管压迫产生的测压异常提供了直接证据,表明心血管性吞咽困难是由心血管压迫导致的食管腔梗阻引起的。支持这一机制的间接证据包括食管造影显示食管中段有光滑的外部压迫和摄入的钡剂滞留,以及在内镜检查时食管中段有传递性的壁层搏动和受压的管腔。5例患者中有2例在高压区内食管蠕动紊乱,这也导致了吞咽困难。对1例蠕动紊乱患者的尸检显示,在被扩大的左心房压迫的区域有一条缺血性食管黏膜带。一种新的测压手法可能有助于区分左锁骨下动脉异常导致的吞咽困难和左心房扩大导致的吞咽困难。在患有异常动脉的单一患者测压过程中抬高左臂,可使食管中段平均基线压力显著增加92%(N = 10次试验),平均压力波幅度增加93%(N = 10次试验,每次P < 0.002,非参数符号秩检验)。该患者抬高左臂还增加了内镜检查时观察到的管腔梗阻。这些测压和内镜检查结果可能是由于手臂抬高时动脉伸展和向前移位导致食管动脉压迫增加所致。