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No changes in N‐terminal pro‐brain natriuretic peptide in a longitudinal cohort of patients with systemic sclerosis‐associated pulmonary arterial hypertension on therapy with bosentan
Author(s) -
Rotondo Cinzia,
Praino Emanuela,
Nivuori Mariangela,
Serio Francesca,
Lapadula Giovanni,
Ian Florenzo
Publication year - 2017
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.12721
Subject(s) - bosentan , medicine , pulmonary hypertension , cardiology , brain natriuretic peptide , cohort , natriuretic peptide , n terminal pro brain natriuretic peptide , heart failure , endothelin receptor , receptor
Aim The aim of this study was to evaluate N ‐terminal pro‐brain natriuretic peptide ( NT ‐pro BNP ) in patients with systemic sclerosis ( SS c)‐associated pulmonary arterial hypertension ( PAH ) and changes after therapy with bosentan. Method Twenty‐one patients with SS c‐ PAH on bosentan therapy were enrolled. PAH was diagnosed by right heart catheterization. NT ‐pro BNP levels, 6‐min walking test (6 MWT ), Doppler echocardiography to estimated systolic pulmonary arterial pressure ( sPAP ), New York Heart Association ( NYHA ) functional class for dyspnea and carbon monoxide lung diffusion capacity ( DL co) were recorded at baseline, and after 1 and 2 years. Fifty‐two SS c patients without PAH were also evaluated as controls. Results NT ‐pro BNP plasma levels were significantly higher in SS c‐ PAH at 385 pg/mL ( SD ± 427) than in SS c without PAH and 72 pg/mL ( SD ± 52, P < 0.001) at baseline, but did not significantly change following bosentan therapy at 1 year (330 pg/mL [ SD ± 291] and 2 years (374 pg/mL [ SD ± 291]). However, NYHA class significantly improved at 2 years ( P = 0.01) as well as 6 MWT ( P = 0.04). NT ‐pro BNP levels were positively correlated only with sPAP but not with DL co, NYHA class or 6MWT. Conclusions NT ‐pro BNP levels were found to be significantly higher in SS c‐ PAH at baseline. Serial assessment of NT ‐pro BNP in SS c‐ PAH patients on bosentan therapy showed no relation to the clinical improvement. This suggests that NT ‐pro BNP may lack ‘sensitivity to change’, but further studies are warranted to assess the role of NT ‐pro BNP as a biomarker of the therapeutic response in larger cohorts of SS c patients.