Daytime pulmonary hypertension (PH) is relatively common in obstructive sleep apnea (OSA) and is thought to be associated with pulmonary vascular remodeling (PRm). The extent to which PH is reversible with treatment is uncertain. To study this, we measured pulmonary hemodynamics (Doppler echocardiography) in 20 patients with OSA (apnea-hypopnea index [AHI] 48.6 +/- 5.2/h, mean +/- SEM) before and after 1 and 4 mo of CPAP treatment (compliance 4.7 +/- 0.5 h/night). Patients had normal lung function, and no cardiac disease or systemic hypertension. Doppler studies were performed at three levels of inspired oxygen concentration (11%, 21%, and 50%) and during incremental increases in pulmonary blood flow (10, 20, and 30 microg/kg/min dobutamine infusions). Treatment resulted in a decrease in pulmonary artery pressure (Ppa, 16.8 +/- 1.2 mm Hg before CPAP versus 13.9 +/- 0.6 mm Hg after 4 mo CPAP, p < 0.05) and total pulmonary vascular resistance (231.1 +/- 19.6 versus 186.4 +/- 12.3 dyn. s. cm(-)(5), p < 0.05). The greatest treatment effects occurred in the five patients who were pulmonary hypertensive at baseline. The pulmonary vascular response to hypoxia decreased after CPAP (DeltaPpa/DeltaSa(O(2)) 10.0 +/- 1.6 mm Hg before versus 6.3 +/- 0.8 mm Hg after 4 mo CPAP, p < 0.05). The curve of Ppa versus cardiac output (Q), derived from the incremental dobutamine infusion, shifted downward in a parallel fashion during treatment. Systemic diastolic blood pressure also fell significantly. Improvements in pulmonary hemodynamics were not attributable to changes in left ventricular diastolic function or Pa (O(2)). We conclude that CPAP treatment reduces Ppa and hypoxic pulmonary vascular reactivity in OSA and speculate that this may be due to improved pulmonary endothelial function.
To determine whether pulmonary hypertension (PH) can occur in obstructive sleep apnea syndrome (OSAS) in the absence of lung or primary cardiac 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 tests, arterial blood gas analysis, and polysomnography were performed. A total of 11 OSAS patients (41%) were found to have pulmonary hypertension. The levels of PH were relatively mild (Ppa < or = 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 (PaO2 = 72.2 +/- 7.6 versus 77.6 +/- 7.3 mm Hg, respectively; p < 0.05) but did not differ in severity of sleep apnea (RDI = 51.9 +/- 25.1 versus 56.8 +/- 26.2 events/h, respectively; p = NS) or indices of sleep desaturation. The hypoxemia in PH patients could not be explained by impairment of lung function, greater body mass, or a higher prevalence of smoking, and PaO2 in the study population was significantly correlated with Ppa (r = -0.46, p < 0.02) but not with FEV1 or BMI. We conclude that lung disease is not a prerequisite for PH in OSAS.(ABSTRACT TRUNCATED AT 250 WORDS)
It is controversial whether obstructive sleep apnea (OSA) causes pulmonary hypertension (PH) in the absence of hypoxemic lung disease. To investigate this further we measured awake pulmonary hemodynamics, pulmonary gas exchange, and small airways function in 32 patients with OSA (apnea- hypopnea index, mean +/- SE, 46.2 +/- 3. 9/h) who had normal screening lung function. Pulmonary artery pressure (Ppa) and cardiac output were measured by Doppler echocardiography at three levels of inspired oxygen (FIO2 0.50, 0.21, and 0.11) and during incremental increases in pulmonary blood flow (10, 20, and 30 microgram/kg/min dobutamine infusions) while breathing 50% oxygen. Eleven patients had PH (mean Ppa >/= 20 mm Hg, Group I). They did not differ from patients without PH (Group II) in lung function, severity of sleep-disordered breathing, age, or body mass. Compared with Group II, Group I patients had increased small airways closure during tidal breathing (FRC-closing capacity: Group I, -0.16 +/- 0.11; Group II, 0.27 +/- 0.09 L; p < 0.05), more ventilation-perfusion inequality (AaPO2: 23.8 +/- 2.8; 19.8 +/- 1.4 mm Hg; p = 0.08), a greater pulmonary artery pressor response to hypoxia (DeltaPpa FIO2, 0.50 to 0.11: 16.4 +/- 1.93; 6.4 +/- 0.77 mm Hg; p < 0.05) and a marked rise in Ppa during increased pulmonary blood flow. We conclude that PH may develop in some patients with OSA without lung disease and that it is associated with small airways closure during tidal breathing and heightened pulmonary pressor responses to hypoxia and during increased pulmonary blood flow. Such changes are consistent with remodeling of the pulmonary vascular bed in affected patients with OSA, seemingly unrelated to severity of sleep-disordered breathing.
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