Pulmonary Vascular Disease: Pulmonary Vascular Disease I |

Prostacyclin Therapy Suppresses Plasma BNP Levels Independent of Pulmonary Hemodynamic Effects in Patients With PAH FREE TO VIEW

Samuel Belok, MD; Sabnam Shakya; Corey Ventetuolo, MD; James Klinger, MD
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Alpert Medical School of Brown University, Providence, RI

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(4_S):1171A. doi:10.1016/j.chest.2016.08.1280
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SESSION TITLE: Pulmonary Vascular Disease I

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 26, 2016 at 01:30 PM - 02:30 PM

PURPOSE: Plasma BNP level is a widely used biomarker to assess disease severity in patients with pulmonary arterial hypertension (PAH). However, the effect of PAH medications on plasma BNP levels is not known. We have observed that many PAH patients on prostacyclin therapy have remarkably low plasma BNP levels despite severely elevated pulmonary arterial (PA) pressure. The purpose of this study, was to determine if prostacyclin treatment lowers plasma BNP levels in PAH patients independent of its effect on pulmonary hemodynamics.

METHODS: A retrospective study was conducted on all patients who underwent right heart catheterization (RHC) for evaluation of pulmonary hypertension between January 2012 through December, 2014. Patients were included in the study if they had WHO group 1 PAH and were on PAH specific medication at the time of RHC. Plasma BNP levels recorded closest to the time of RHC were compared in patients taking prostacyclin therapy with or without a phosphodiesterase inhibitor or endothelin receptor antagonist to plasma BNP levels in patients taking PAH specific medications that did not include a prostacyclin derivative. Plasma BNP levels in patients with and without prostacyclin therapy were correlated with mean pulmonary artery pressure (mPAP) and cardiac output (CO).

RESULTS: Patients on prostacyclin therapy were younger than those without (49.5 (22 - 75) years vs. 65.5 (31 - 81) years, P < 0.0001. Despite no differences in right heart filling pressures, mPAP or CO between treatment groups, plasma BNP levels were significantly lower in patients on prostacyclin therapy than in those not on prostacyclin therapy(27.4 pg/mL [2.7 - 181] vs. 92.2 pg/mL [4.1 - 1117.2]). Use of prostacyclin was associated with a -204.5 pg/ml decrease in BNP (95 % CI -367.9 - -41.2, p = 0.015) without multivariate adjustment. After adjustment for age and sex, there was a trend towards a decrease in plasma BNP levels with use of prostacyclin (-138 pg/mL 95% CI -341.1 - 65.1, p = 0.178). In patients not on prostacyclin therapy, plasma BNP levels correlated directly with mPAP (r = 0.39, P=0.05) and tended to correlate inversely with CO (r = -0.41, p=0.07), whereas no correlation between plasma BNP and mPAP or CO was seen in patients on prostacyclin therapy (r = 0.11, p = 0.65 for mPAP, r = -0.04, p = 0.89 for CO).

CONCLUSIONS: Prostacyclin therapy is associated with a decrease in plasma BNP levels that is independent of its pulmonary hemodynamic effect. Plasma BNP does not correlate with mPAPor CO in patients on prostacyclin therapy.

CLINICAL IMPLICATIONS: Plasma BNP levels are suppressed in PAH patients on prostacyclin therapy and should not be used as a biomarker of disease progression in this patient population.

DISCLOSURE: The following authors have nothing to disclose: Samuel Belok, Sabnam Shakya, Corey Ventetuolo, James Klinger

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