, Volume 40, Issue 1, pp 166-176

Endoscopic, radiographic, and manometric findings associated with cardiovascular dysphagia

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Abstract

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.