Iatrogenic esophageal dysmotility as a barrier to transplantation in pulmonary arterial hypertension

TL;DR

PDE5i medications used for PAH can cause esophageal issues that prevent lung transplants, but stopping the drugs can reverse this problem.

Contribution

Identifies PDE5i-induced esophageal dysmotility as a reversible barrier to lung transplantation in PAH patients.

Findings

Two PAH patients were denied transplant listing due to PDE5i-induced esophageal dysmotility.

Discontinuation of PDE5i led to improved esophageal motility and eligibility for transplant within 14 days.

PDE5i off-target effects can be mitigated to improve transplant access for PAH patients.

Abstract

Esophageal dysmotility is identified as a contraindication to lung transplantation at some centers due to increased risks of acute rejection, pulmonary infection, and chronic lung allograft dysfunction. Phosphodiesterase-type 5 inhibitors (PDE5i) are a cornerstone pharmacotherapy for pulmonary arterial hypertension (PAH) and are known to exert off-target effects that may impact lung transplant candidacy, including impaired esophageal contractility and decreased lower esophageal sphincter tone. We report 2 patients with PAH who were initially declined listing for lung transplantation due to iatrogenic esophageal dysmotility induced by PDE5is. Upon discontinuation of PDE5i therapy, these patients experienced significant improvement in esophageal motility within 14 days and met the criteria for transplant listing at their centers. Recognizing and mitigating the off-target effects of PDE5i medications is critical for maximizing access to transplant for patients with PAH.

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