Acute Effects of Benzbromaron on the Pulmonary Circulation
Status:
Completed
Trial end date:
2016-08-01
Target enrollment:
Participant gender:
Summary
Actual studies suggest that a calcium activated chlorid channel (TMEM16A) may play a relevant
role in the pathogenesis of pulmonary arterial hypertension (PAH). The inhibition of this
channel led to pulmonary vasorelaxation in preclinical studies. Benzbromarone is a well known
inhibitor of the TMEM16A channel and is used in patients with gout.
In this pilot study the investigators plan to investigate if Benzbromarone has an acute
effect on the pulmonary arteries in humans. This will be investigated within the frame of a
right heart catheterization performed in patients with known PAH due to clinical reasons. The
investigators hypothesize that the application of Benzbromarone leads to pulmonary
vasodilation, which can be recognized by the decrease in pulmonary vascular resistance. In
addition, the change in pulmonary and systemic arterial pressure, pulmonary arterial wedge
pressure, heart rate and arterial oxygen saturation will be assessed. Due to clinical reasons
patients will receive NO (15 ppm) during right heart catheterization. Hemodynamic changes
upon NO and Benzbromarone may be compared.
Phase:
Phase 2
Details
Lead Sponsor:
Medical University of Graz
Collaborator:
Ludwig Boltzmann Institute for Lung Vascular Research