Citation:
Sharma S, Oldenburg O, Fox H. Sleep apnea and pulmonary hypertension: connecting the dots. J Clin Sleep Med. 2021;17(2):347–348.
With great interest we read the recent article by Samhouri et al,1 published in a recent issue of the Journal of Clinical Sleep Medicine, and we congratulate the authors on their effort to further shed light into the relationship between sleep apnea and pulmonary hypertension (PH). This is an important field, and the connection of both diseases has been incompletely investigated so far. We, however, disagree with the contention of the authors that PH hemodynamics are associated with the duration of nocturnal desaturation and not apnea-hypopnea index (AHI).
In our eyes, the authors have failed to address 2 important available randomized controlled trials particularly addressing sleep apnea and PH.2,3 In a study by Arias et al,2 patients with obstructive sleep apnea (OSA) with PH had a significantly higher AHI of 68.7 ± 24.9 events/h vs patients with OSA without PH of 25.1 ± 14.5 events/h (P = .0001), but the difference in hypoxemic burden (SaO2 <90%) was not significant in the OSA and PH group, showing 30.6 ± 24.6 minutes of desaturation vs 9.8 ± 10.6 minutes in patients with OSA without PH (P = .8). Multiple logistic regression analysis revealed the AHI to be an independent factor related to the development of PH. Subsequent continuous positive airway pressure use significantly reduced the pulmonary artery systolic pressures in this study. Similarly, a recent international randomized controlled trial by Sharma et al3 conducted in hospitalized patients with PH due to heart failure showed that use of automatic positive airway pressure therapy significantly reduces pulmonary artery systolic pressure as compared with standard-of-care therapy, which included oxygen. The mean paired difference in reduction of pulmonary artery systolic pressure was −15.8 + 3.2 mmHG in the intervention group vs −5.2 + 2.6 mmHG in the standard-of-care group (P = .025). Both groups were noted to have similar baseline nocturnal desaturation (with time below 90% saturations) during sleep of 231.2 ± 223.2 minutes in the intervention arm vs 233.3 ± 125.4 minutes in the standard-of-care group.3
Apnea events have been shown to have hemodynamic consequences with elevation of transmural pressures, preload, and afterload due to negative intrathoracic pressures resulting from repetitive glottis closure.4,5 These physiological and hemodynamic changes have further been shown to be reversible through application of positive airway pressure therapy.6,7 Use of continuous positive airway pressure therapy has also been shown to reduce pulmonary artery wedge pressure more than just oxygen and diuretics.6,7 Similarly, Solin et al8 showed a direct relationship of AHI in patients with central sleep apnea and pulmonary vascular pressures using right heart catheterization in patients with advanced heart failure.
While the duration of nocturnal hypoxemia may place an additional burden exacerbating pulmonary pressures, we believe the present assertion may be misleading especially in light of the randomized controlled trials showing a direct relationship of AHI to pulmonary pressures.
DISCLOSURE STATEMENT
All authors have seen and approved the manuscript. The authors report no conflicts of interest.
REFERENCES
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