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. 2024 Oct 28;10(5):00040-2024.
doi: 10.1183/23120541.00040-2024. eCollection 2024 Sep.

Effects of acetazolamide on sleep disordered breathing in pulmonary vascular disease: a randomised controlled trial

Affiliations

Effects of acetazolamide on sleep disordered breathing in pulmonary vascular disease: a randomised controlled trial

Esther I Schwarz et al. ERJ Open Res. .

Abstract

Background: Patients with pulmonary vascular disease (PVD) often suffer from nocturnal hypoxaemia, but also from sleep apnoea. Short-term use of acetazolamide increases ventilation due to metabolic acidosis and also reduces loop gain. We investigated whether prolonged use of acetazolamide improves sleep disordered breathing in PVD.

Methods: In a randomised controlled crossover trial, patients with PVD were randomly assigned to acetazolamide 250 mg and placebo twice daily for 5 weeks. Patients underwent respiratory polygraphy at baseline and at the end of each intervention phase. Outcomes of interest were the effect of acetazolamide on mean nocturnal oxygen saturation (S pO2 ), time with oxygen saturation <90% (t <90), apnoea-hypopnoea index (AHI) and sleep apnoea severity.

Results: In 20 patients with PVD (55% women, nine with pulmonary arterial hypertension, 11 with distal chronic thromboembolic pulmonary hypertension; mean±sd nocturnal S pO2 88.8±3.5%, obstructive AHI 12.6±12.3 events·h-1), 5 weeks of acetazolamide resulted in a significant improvement in nocturnal oxygenation compared to placebo (mean nocturnal S pO2 +2.3% (95% CI 1.3-3.3%); p<0.001 and t <90 -18.8% (95% CI -29.6- -8.0%); p=0.001). Acetazolamide increased the proportion of patients with mean nocturnal S pO2 ≥90% from 45% to 85%. The percentage of patients with AHI >5 events·h-1 was reduced from 75% to 60% and with AHI >15 events·h-1 from 30% to 15%. Two patients discontinued the study because of mild side-effects.

Conclusions: Acetazolamide given for 5 weeks reduces nocturnal hypoxaemia in PVD to a clinically relevant level and reduces the proportion of patients with obstructive sleep apnoea.

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Conflict of interest statement

Conflicts of interest: M. Lichtblau reports being early career member of European Respiratory Society (ERS) Assembly 13 (Pulmonary Vascular Disease), outside the submitted work. K.E. Bloch reports support for the present manuscript from the Swiss National Science Foundation. S. Ulrich reports support for the present manuscript from the Swiss National Science Foundation and is Chair of ERS Group 13.01 (Pulmonary Hypertension), outside the submitted work. The remaining authors have nothing to disclose.

Figures

FIGURE 1
FIGURE 1
Patient flow and availability of sleep studies.
FIGURE 2
FIGURE 2
Box-and-whisker plots showing median (interquartile range) of a) mean nocturnal oxygen saturation (measured by pulse oximetry (SpO2)) and b) time during the sleep study with oxygen saturation <90% (t<90) at baseline prior to randomisation, on placebo and on acetazolamide.
FIGURE 3
FIGURE 3
Pie charts of the distribution of apnoea–hypopnoea index (AHI) groups on a) placebo and b) acetazolamide. On placebo, 25% had AHI <5 events·h−1 and 70% had AHI <15 events·h−1; on acetazolamide, 40% had AHI <5 events·h−1 and 85% had AHI <15 events·h−1.

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