To study the acute effect of acetazolamide (AZA) on pulmonary hemodynamics in patients with pulmonary hypertension (PH) undergoing clinically indicated right heart catheterisation (RHC).
Pulmonary hypertension (PH) of various etiologies causes dyspnea, impairs exercise performance and is associated with reduced quality of life (QoL) and survival. Treatment options include therapy for any underlying causes, pulmonary vasodilator drugs, oxygen and, in selected cases, pulmonary endarterectomy or lung transplantation. Unfortunately, PH specific drugs are expensive, associated with side effects and even combined pharmacological treatment is often not sufficient to achieve clinical benefits. Therefore, novel therapeutic drugs are needed. The investigators have recently demonstrated that sleep related breathing disorders, which are common in PH patients, can be improved by both nocturnal oxygen therapy and acetazolamide (AZA). AZA is a carbonic anhydrase (CA) inhibitor that acts as a respiratory stimulant thereby improving oxygenation and possibly PH. There are even data suggesting that CA-inhibitors have a direct pulmonary vasodilator effect. However, the potential role of AZA in the treatment of PH has not been conclusively studied. Therefore, the purpose of the current project is to investigate, the acute hemodynamic clinical effects of AZA in PH patients.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
33
University Hospital Zurich
Zurich, Switzerland
Pulmonary vascular resistance (PVR) AZA vs. Placebo (rest)
At the end of phase at rest
Time frame: 60 minutes
PVR AZA vs. Placebo (exercise)
At the end of phase at exercise
Time frame: 60 minutes
PVR AZA vs. Placebo (hypoxia)
At the end of phase under hypoxia
Time frame: 60 minutes
partial pressure of the oxygen
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
Oxygen uptake
Time frame: 15 minutes
minute ventilation
Time frame: 15 minutes
arterial oxygenation
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
tissue oxygenation
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
mean pulmonary arterial pressure
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
cardiac output
At the end of each phase (rest, exercise and hypoxia)
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.
Time frame: 60 minutes
cardiac index
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
pulmonary wedge pressure
At the end of each phase (rest, exercise and hypoxia)
Time frame: 60 minutes
Borg scale dyspnea and leg effort
Time frame: 15 minutes