Pulmonary arterial hypertension in patients with sleep apnoea syndrome

Background-Pulmonary arterial hypertension (PAH) in patients with sleep apn oea syndrome (SAS) is classically ascribed to associated chronic obstructiv e pulmonary disease (COPD). The aim of this retrospective study was to eval uate the possible occurrence of PAH as a complication of SAS in patients wi thout COPD. Methods-Right heart catheterisation was performed in 44 patients with SAS a nd without COPD confirmed by polysomnography (apnoea index >5/h) admitted f or the administration of nasal continuous positive airway pressure (CPAP). Results-Precapillary PAH, defined as mean pulmonary arterial pressure of >2 0 mm Hg with pulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44 (27%) patients with SAS. There were no significant differences in apn oea index between patients with (PAH+) and those without PAH (PAH-) (42.6 ( 26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differed significantly from the PAH- group in the following respects: lower daytime arterial oxyge n tension (Pao(2)) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher dayt ime arterial carbon dioxide tension (Paco(2)) (5.8 (0.5) versus 5.3 (0.5) k Pa, p=0.002); more severe nocturnal hypoxaemia with a higher percentage of total sleep time spent at Pao(2) <80% (32.2 (28.5)% versus 10.7 (18.8)%, p= 0.005); and higher body mass index (BMI) (37.4 (6) versus 30.3 (6.7)kg/m(2) , p=0.002). The PAH+ patients had significantly lower values of vital capac ity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced e xpiratory volume in one second (FEV,) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory reserve volume (40 (16)% predicted versus 7 7 (41)% predicted, p=0.003), and total lung capacity (87 (13)% predicted ve rsus 98 (18)% predicted, p=0.04). Stepwise multiple regression analysis sho wed that mean pulmonary artery pressure (PAPm) was positively correlated wi th BMI and negatively with Pao(2). Conclusion-Pulmonary arterial hypertension is frequently observed in patien ts with SAS, even when COPD is absent, and appears to be related to the sev erity of obesity and its respiratory mechanical consequences.