Bady E, Achkar A, Pascal S, Orvoen-Frija E, Laaban J P
Department of Pneumology, Hotel-Dieu, 75181 Paris Cedex 04, France.
Thorax. 2000 Nov;55(11):934-9. doi: 10.1136/thorax.55.11.934.
Pulmonary arterial hypertension (PAH) in patients with sleep apnoea syndrome (SAS) is classically ascribed to associated chronic obstructive pulmonary disease (COPD). The aim of this retrospective study was to evaluate the possible occurrence of PAH as a complication of SAS in patients without COPD.
Right heart catheterisation was performed in 44 patients with SAS and without COPD confirmed by polysomnography (apnoea index >5/h) admitted for the administration of nasal continuous positive airway pressure (CPAP).
Precapillary PAH, defined as mean pulmonary arterial pressure of >20 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 apnoea 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 oxygen tension (PaO(2)) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbon dioxide tension (PaCO(2)) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higher percentage of total sleep time spent at SaO(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 capacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV(1)) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory reserve volume (40 (16)% predicted versus 77 (41)% predicted, p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)% predicted, p=0.04). Stepwise multiple regression analysis showed that mean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with PaO(2).
Pulmonary arterial hypertension is frequently observed in patients with SAS, even when COPD is absent, and appears to be related to the severity of obesity and its respiratory mechanical consequences.
睡眠呼吸暂停综合征（SAS）患者的肺动脉高压（PAH）传统上归因于相关的慢性阻塞性肺疾病（COPD）。这项回顾性研究的目的是评估在无COPD的患者中，PAH作为SAS并发症的可能发生率。
对44例经多导睡眠图证实（呼吸暂停指数>5次/小时）且无COPD的SAS患者进行右心导管检查，这些患者因接受鼻持续气道正压通气（CPAP）治疗而入院。
在44例SAS患者中，12例（27%）观察到毛细血管前性PAH，定义为平均肺动脉压>20 mmHg且肺毛细血管楔压<15 mmHg。PAH阳性（PAH+）患者和PAH阴性（PAH-）患者的呼吸暂停指数无显著差异（分别为42.6（26.3）次/小时和35.8（21.7）次/小时）。PAH+组与PAH-组在以下方面存在显著差异：白天动脉血氧分压（PaO₂）较低（9.6（1.1）kPa对11.3（1.5）kPa，p = 0.0006）；白天动脉血二氧化碳分压（PaCO₂）较高（5.8（0.5）kPa对5.3（0.5）kPa，p = 0.002）；夜间低氧血症更严重，SaO₂<80%的总睡眠时间百分比更高（32.2（28.5）%对10.7（18.8）%，p = 0.005）；体重指数（BMI）更高（37.4（6）kg/m²对30.3（6.7）kg/m²，p = 0.002）。PAH+患者的肺活量（VC）（预计值的87（14）%对105（20）%，p = 0.005）、一秒用力呼气容积（FEV₁）（预计值的82（14）%对101（17）%，p = 0.001）、呼气储备容积（预计值的40（16）%对77（41）%，p = 0.003）和肺总量（预计值的87（13）%对98（18）%，p = 0.04）显著更低。逐步多元回归分析显示，平均肺动脉压（PAPm）与BMI呈正相关，与PaO₂呈负相关。
即使没有COPD，SAS患者也经常观察到肺动脉高压，并且似乎与肥胖的严重程度及其呼吸力学后果有关。
