Trial reportRespiratory research2009
Endothelin receptor antagonist and airway dysfunction in pulmonary arterial hypertension.
Trial report in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 8 citations in OpenAlex.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn idiopathic pulmonary arterial hypertension (IPAH), peripheral airway obstruction is frequent. This is partially attributed to the mediator dysbalance, particularly an excess of endothelin-1 (ET-1), to increased pulmonary vascular and airway tonus and to local inflammation. Bosentan (ET-1 receptor antagonist) improves pulmonary hemodynamics, exercise limitation, and disease severity in IPAH. We hypothesized that bosentan might affect airway obstruction.
methodsIn 32 IPAH-patients (19 female, WHO functional class II (n = 10), III (n = 22); (data presented as mean +/- standard deviation) pulmonary vascular resistance (11 +/- 5 Wood units), lung function, 6 minute walk test (6-MWT; 364 +/- 363.7 (range 179.0-627.0) m), systolic pulmonary artery pressure, sPAP, 79 +/- 19 mmHg), and NT-proBNP serum levels (1427 +/- 2162.7 (range 59.3-10342.0) ng/L) were measured at baseline, after 3 and 12 months of oral bosentan (125 mg twice per day). RESULTS AND DISCUSSION: At baseline, maximal expiratory flow at 50 and 25% vital capacity were reduced to 65 +/- 25 and 45 +/- 24% predicted. Total lung capacity was 95.6 +/- 12.5% predicted and residual volume was 109 +/- 21.4% predicted. During 3 and 12 months of treatment, 6-MWT increased by 32 +/- 19 and 53 +/- 69 m, respectively; p < 0.01; whereas sPAP decreased by 7 +/- 14 and 10 +/- 19 mmHg, respectively; p < 0.05. NT-proBNP serum levels tended to be reduced by 123 +/- 327 and by 529 +/- 1942 ng/L; p = 0.11). There was no difference in expiratory flows or lung volumes during 3 and 12 months.
conclusionThis study gives first evidence in IPAH, that during long-term bosentan, improvement of hemodynamics, functional parameters or serum biomarker occur independently from persisting peripheral airway obstruction.
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