PULMONARY-HYPERTENSION AND HYPOXEMIA IN OBSTRUCTIVE SLEEP-APNEA SYNDROME

To determine whether pulmonary hypertension (PH) can occur in obstruct ive sleep apnea syndrome (OSAS) in the absence of lung or primary card iac disease, we studied 27 patients (26 males, mean age 49 +/- 10 yr) with OSAS (respiratory disturbance index [RDI] > 10 events/h) in whom clinically significant lung or cardiac diseases were excluded. Pulsed Doppler measurements of pulmonary hemodynamics, pulmonary function tes ts, arterial blood gas analysis, and polysomnography were performed. A total of 11 OSAS patients (41%) were found to have pulmonary hyperten sion. The levels of PH were relatively mild ((Ppa) over bar less than or equal to 26 mm Hg). There were no differences between PH and non-PH patients in body mass index (BMI), smoking history, or lung function. PH patients were more hypoxemic when awake than non-PH patients (Pa-O 2 = 72.2 +/- 7.6 versus 77.6 +/- 7.3 mm Hg, respectively; p < 0.05) bu t did not differ in severity of sleep apnea (RDI = 51.9 +/- 25.1 versu s 56.8 +/- 26.2 events/h, respectively; p = NS) or indices of sleep de saturation. The hypoxemia in PH patients could not be explained by imp airment of lung function, greater body mass, or a higher prevalence of smoking, and Pa-O2 in the study population was significantly correlat ed with (Ppa) over bar (r = -0.46, p < 0.02) but not with FEV(1) or BM I. We conclude that lung disease is not a prerequisite for PH in OSAS. We speculate that the development of PH in OSAS patients depends more on individual differences in the response of the pulmonary circulatio n to the episodic alveolar hypoxia and respiratory acidosis associated with sleep apneas than on differences in the frequency or severity of the apneas. Repetitive elevation of Ppa during sleep into the PH rang e may lead to pulmonary vascular remodeling in ''responders'' and ther eby daytime PH and hypoxemia.