Study Objectives: Sleep-disordered breathing and nocturnal hypoxia are prevalent among patients with precapillary pulmonary hypertension (PAH). The rationale for these associations remains unclear and these relationships have not been well studied in other forms of pulmonary hypertension (PH). We hypothesized that severity of sleep-disordered breathing and nocturnal hypoxia are associated with worsening pulmonary hemodynamics, regardless of hemodynamic profile. Methods: Four hundred ninety-three patients were divided into 4 groups: 1) no PH, 2) postcapillary pulmonary hypertension, 3) PAH, and 4) mixed PAH/postcapillary pulmonary hypertension. The relationship between right heart catheterization measurements and apnea-hypopnea index or the percentage of sleep time spent with oxygen saturation < 90% (T90) was calculated using multiple linear regression. Analysis of variance was used for betweengroup comparisons. Statistical models were adjusted for known confounders. Results: Apnea-hypopnea index did not differ between hemodynamic subgroups (P =.27) and was not associated with right atrial pressure (.11 ± .19, P =.55), cardiac index (.25 ± 1.64, P = .88), mean pulmonary artery pressure (−.004 ± .09, P = .97), or pulmonary artery occlusion pressure (.16 ± .14, P = .26). While patients with PH had a higher T90 than those without (mean 24.2% vs 11.7%, P < .001), there was no difference in T90 between individual PH subgroups (P =.70). T90 was associated with mean pulmonary artery pressure (.

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The high prevalence of pulmonary arterial hypertension (PAH) in patients with obstructive sleep apnea (OSA) and the putative pathophysiologic connections have been extensively documented. Conversely, patients with established PAH are at risk for sleep-related ventilatory instability, including OSA, central sleep apnea, and nocturnal desaturations. This chapter reviews the prevalence and pathophysiologic interactions of these conditions, the interplay with associated disorders, and the effects of continuous positive airway pressure therapy on pulmonary hemodynamics. In patients with OSA, chronic effects of repetitive hypoxia as well as comorbidities, including chronic obstructive pulmonary disease and left-sided heart dysfunction, play a role in promoting pulmonary hypertension. Sleep disordered breathing, representing a spectrum of sleep-related breathing disorders inclusive of OSA, is highly prevalent among patients with established pulmonary hypertension. Obstructive events, central sleep apnea, and nocturnal hypoxia are within the spectrum of sleep-related breathing disorders in pulmonary hypertension. The mechanisms for these associations remain speculative.