In the present study of 36 clinically stable patients with precapillary PH, 75.0% were found to suffer from a degree of SDB, with the vast majority of SDB fulfilling the criteria of OSA. Furthermore, 50% of the subjects had evidence of nocturnal hypoxemia. Despite the high prevalence of OSA in the cohort, most patients were classified as having mild OSA, but the prevalence of nocturnal hypoxemia was elevated, regardless of the presence of SDB. Moreover, mPAP values were the only significant and independent predictor of the average SpO2 values, suggesting that the severity of PH (estimated by mPAP) can infer the presence of sleep hypoxemia. Our findings concur with those of previous studies and show that PH severity is associated with the degree of hypoxemia during sleep [15, 29].
The frequency of SDB in patients with precapillary PH is generally high, with some studies reporting a high prevalence of both OSA and CSA [17, 20, 30], and another suggesting a marked predominance of OSA over CSA . In one cross-sectional study that evaluated 52 subjects with Group 1 PAH, SDB was present in 71% (56% had OSA and 44% CSA) . Similarly, among 38 outpatients with idiopathic PAH (n = 23) or CTEPH (n = 15), a high SDB prevalence was found, with CSA being clearly predominant . However, in another recent study that evaluated 71 patients with precapillary PH (41% males) and 35 matched controls, OSA was detected in 68% of the precapillary PH patients as compared to 5% among controls . Moreover, only 1 PAH patient had CSA (AHI: 12 events/h) without Cheyne-Stokes respiration . Similar to our findings, nocturnal hypoxemia was present in 48% of patients with PAH, and the presence of nocturnal hypoxemia was unrelated to the presence of OSA .
We should emphasize that sleep-related hypoxemia is a prevalent disturbance among precapillary PH patients with a widely variable percentage of subjects displaying sleep-related hypoxemia depending on the oximetry-derived criterion used to assess nocturnal desaturation [32, 33]. All such studies, albeit only a few in number, suggest that the presence of nocturnal hypoxemia occurs regardless of the presence of SDB, and when present is frequently associated with a worse prognosis in patients suffering from PAH [20, 32, 33]. In a small cohort of 13 PAH individuals, nocturnal hypoxemia was reported in 10/13 patients . Another study found that 30 of 43 PAH patients exhibited nocturnal desaturation, with those patients with desaturations during sleep also suffering from higher mPAP values and lower cardiac index . In a cohort of 63 individuals with PAH or CTEPH, 63% had nocturnal hypoxemia , while in another previous study that included 15 PAH patients, only 2 had sleep apnea, but 8 patients had sleep-related hypoxemia without the presence of sleep apnea .
Although hypoxemia during sleep is frequent in precapillary PH, the underlying mechanism still remains unclear. It is usually advanced that ventilation-perfusion mismatch and narrowing of the distal airways, increasing the pulmonary physiologic dead space underlie the higher frequency of hypoxemic events in PAH [36–38]. Of note, the presence of continuous nocturnal hypoxemia, rather than the presence of SDB-related intermittent hypoxemia has been implicated in a poor prognosis among PAH patients , possibly because chronic hypoxemia promotes hypoxic pulmonary vasoconstriction and pulmonary vascular remodeling . Notwithstanding, pulse oximetry has been proposed as part of the routine assessment of patients with PAH to detect the presence of nocturnal hypoxemia . However, oximetry alone may not be a sufficiently accurate diagnostic test for identifying SDB in precapillary PH patients  because of inadequate discriminatory power when compared to PSG .
Our study is not without limitations. First, it was conducted in a single institution, which may limit its generalizability and therefore requires external validation. Second, the sample size was relatively small, which could lead to type 2 beta errors, such that our findings must be considered with caution. Third, all study participants were evaluated with a sleep test on a single night and the possibility of night-to-night variability must be considered. Fourth, the diagnosis of OSA was based on the RDI obtained from an HSAT, which may underestimate the actual prevalence and severity of SDB. Finally, as the hemodynamic parameters were not evaluated in close temporal proximity or concurrently with the HSAT, inferences from the associations between these two sets of measures require caution.