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Pulmonary Vascular Disease |

Endothelin-1 Levels in Pulmonary Hypertension: A Comparison Between Pulmonary Arterial Hypertension and COPD-Induced Pulmonary Hypertension

Jeremy Mazurek*, MD; Thiago Jabuonski, MD; Ronald Zolty, MD
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Jacobi Medical Center, Bronx, NY


Chest. 2012;142(4_MeetingAbstracts):851A. doi:10.1378/chest.1390581
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Abstract

SESSION TYPE: DVT/PE/Pulmonary Hypertension Posters II

PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Endothelin-1 (ET-1), a potent vasoconstrictor, is elevated in pulmonary arterial hypertension (PAH), and ET-1 receptor antagonists (ERAs) have become a mainstay of PAH treatment. In contrast to PAH, which is a rare disease, chronic obstructive pulmonary disease (COPD)-induced pulmonary hypertension (COPD-PH) is a relatively common condition, affecting ~50% of all patients with COPD. To date, however, no PAH-specific therapies including ERAs have been approved for COPD-induced PH. Additionally, there has never been a comparison of ET-1 levels in patients with COPD-PH as compared to patients with PAH. We therefore decided to evaluate ET-1 levels in these two patient populations as a first step to evaluating the possible role of ERAs in the treatment of COPD-PH.

METHODS: We measured serum ET-1 levels via ELISA method, in patients referred to our pulmonary hypertension clinic with PAH (mean PA pressure ≥25 mmHg, PCWP <15 mmHg, without evidence of obstructive lung disease on pulmonary function testing [PFTs]), and compared them with patients with COPD-PH (mean PA pressure ≥25 mmHg, PCWP <15 mmHg, and FEV1/FVC ratio <70% on PFTs).

RESULTS: Ten and 21 patients comprised the COPD-PH and PAH groups, respectively. Median ET-1 levels did not differ between COPD-PH and PAH groups (1.85 fmol/ml, range 0.59-10.0 vs. 1.30 fmol/ml, range 0.02-101.1; p=0.568). Additionally, there was no statistical difference in age ([years]; 63.9±6.54 vs. 56.4±13.8; p=0.197), mean PA pressure ([mm Hg]; 45.70±12.4 vs. 47.6±9.83; p=0.512), PCWP ([mm Hg]; 9.89±4.57 vs. 8.95±4.93; p=0.540), pulmonary vascular resistance ([dyn.s/cm5]; 604±348 vs. 857±392; p=0.113) or cardiac output ([l/min]; 3.57±1.01 vs. 4.09±1.43; p=0.375) between the two groups.

CONCLUSIONS: This study is the first to evaluate ET-1 levels in patients with COPD-PH as compared to patients with PAH. We show that patients with moderate to severe COPD-PH have similar levels of ET-1 as their PAH counterparts.

CLINICAL IMPLICATIONS: This finding suggests ET-1 has a role in the pathogenesis of COPD-PH, and perhaps serves as a treatment target in this condition.

DISCLOSURE: Ronald Zolty: Consultant fee, speaker bureau, advisory committee, etc.: Actellion, Consultant fee, speaker bureau, advisory committee, etc.: Gilead

The following authors have nothing to disclose: Jeremy Mazurek, Thiago Jabuonski

No Product/Research Disclosure Information

Jacobi Medical Center, Bronx, NY

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