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Increased pulmonary serotonin transporter in patients with chronic obstructive pulmonary disease who developed pulmonary hypertension.

Authors
  • Frille, Armin1, 2
  • Rullmann, Michael2, 3
  • Becker, Georg-Alexander3
  • Patt, Marianne3
  • Luthardt, Julia3
  • Tiepolt, Solveig3
  • Wirtz, Hubert1
  • Sabri, Osama3
  • Hesse, Swen2, 3
  • Seyfarth, Hans-Juergen4
  • 1 Department of Respiratory Medicine, University Hospital Leipzig, Liebigstrasse 20, 04103, Leipzig, Germany. , (Germany)
  • 2 Integrated Research and Treatment Center (IFB) Adiposity Diseases, University Medical Center Leipzig, 04013, Leipzig, Germany. , (Germany)
  • 3 Department of Nuclear Medicine, University Hospital Leipzig, 04103, Leipzig, Germany. , (Germany)
  • 4 Department of Respiratory Medicine, University Hospital Leipzig, Liebigstrasse 20, 04103, Leipzig, Germany. [email protected] , (Germany)
Type
Published Article
Journal
European Journal of Nuclear Medicine
Publisher
Springer-Verlag
Publication Date
Apr 01, 2021
Volume
48
Issue
4
Pages
1081–1092
Identifiers
DOI: 10.1007/s00259-020-05056-7
PMID: 33009594
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Pulmonary hypertension (PH) is characterized by a progressive remodelling of the pulmonary vasculature resulting in right heart failure and eventually death. The serotonin transporter (SERT) may be involved in the pathogenesis of PH in patients with chronic-obstructive pulmonary disease (COPD). This study investigated for the first time the SERT in vivo availability in the lungs of patients with COPD and PH (COPD+PH). SERT availability was assessed using SERT-selective [11C]DASB and positron emission tomography/computed tomography (PET/CT) with dynamic acquisition over 30 min in 4 groups of 5 participants each: COPD, COPD+PH, pulmonary arterial hypertension, and a healthy control (HC). Time activity curves were generated based on a volume of interest within the middle lobe. Tissue-to-blood concentration ratios after 25 to 30 min (TTBR25-30) served as receptor parameter for group comparison and were corrected for lung tissue attenuation. Participants underwent comprehensive pulmonary workup. Statistical analysis included group comparisons and correlation analysis. [11C]DASB uptake peak values did not differ among the cohorts after adjusting for lung tissue attenuation, suggesting equal radiotracer delivery. Both the COPD and COPD+PH cohort showed significantly lower TTBR25-30 values after correction for lung attenuation than HC. Attenuation corrected TTBR25-30 values were significantly higher in the COPD+PH cohort than those in the COPD cohort and higher in non-smokers than in smokers. They positively correlated with invasively measured severity of PH and inversely with airflow limitation and emphysema. Considering all COPD patients ± PH, they positively correlated with right heart strain (NT-proBNP). By applying [11C]DASB and PET/CT, semiquantitative measures of SERT availability are demonstrated in the lung vasculature of patients with COPD and/or PH. COPD patients who developed PH show increased pulmonary [11C]DASB uptake compared to COPD patients without PH indicating an implication of pulmonary SERT in the development of PH in COPD patients.

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