Faculté de Médecine, Université Paris-Sud, Le Kremlin-Bicêtre; Assistance Publique-Hôpitaux de Paris, Unité de Médecine du Sommeil, Hôpital Antoine-Béclère, Clamart; Faculté de Pharmacie, Université Paris-Sud, EA3544, Châtenay-Malabry, France.
Faculté de Médecine, Université Paris-Sud, Le Kremlin-Bicêtre; Assistance Publique-Hôpitaux de Paris, Unité de Médecine du Sommeil, Hôpital Antoine-Béclère, Clamart; Institut National de la Santé et de la Recherche Médicale U999 Hypertension Artérielle Pulmonaire: Physiopathologie et Innovation Thérapeutique, Le Plessis-Robinson.
Chest. 2013 Jan;143(1):47-55. doi: 10.1378/chest.11-3124.
The occurrence and mechanisms of nocturnal hypoxemia in precapillary pulmonary hypertension (PH) are not clearly defined.
In an observational, prospective, and transversal design, we studied 46 clinically stable patients with PH and a BMI < 35 kg/m(2), an FEV(1) > 60% predicted, and idiopathic pulmonary arterial hypertension (n = 29) or chronic thromboembolic pulmonary hypertension (n = 17). They underwent nocturnal polysomnography with transcutaneous capnography.
Most patients (69.6%) had New York Heart Association functional class II disease. Mean pulmonary artery pressure was 44 ± 13 mm Hg, and the cardiac index was 3.2 ± 0.6 L/min/m(2). Duration of sleep time spent with oxygen saturation as measured by pulse oximetry <90% was 48.9% ± 35.9%, and 38 of 46 patients (82.6%) had nocturnal hypoxemia. Mean apnea-hypopnea index was 24.9 ± 22.1/h, and 41 patients (89%) had sleep apnea. The major mechanism of nocturnal hypoxemia was a ventilation/perfusion mismatch alone or associated with obstructive apneic events. Multivariate logistic regression identified both FEV(25%-75%) (OR, 0.9519; 95% CI, 0.9089-0.9968; P = .036) and mean pulmonary artery pressure (OR, 1.1068; 95% CI, 1.0062-1.2175; P = .037) as significant predictors of nocturnal hypoxemia. Clinical symptoms were not predictive of nocturnal hypoxemia.
The occurrence of nocturnal hypoxemia is high in PH and should be screened for systematically. Further studies are needed to determine the impact of nocturnal hypoxemia on the outcome of patients with PH.
ClinicalTrials.gov; No.: NCT01371669; URL: www.clinicaltrials.gov
毛细血管前肺动脉高压(PH)患者夜间低氧血症的发生和机制尚不清楚。
采用观察性、前瞻性、横断设计,我们研究了 46 例临床稳定的 PH 患者,BMI<35kg/m2,FEV1>60%预计值,特发性肺动脉高压(n=29)或慢性血栓栓塞性肺动脉高压(n=17)。他们接受了经皮二氧化碳描记法的夜间多导睡眠图。
大多数患者(69.6%)患有纽约心脏协会心功能 II 级疾病。平均肺动脉压为 44±13mmHg,心指数为 3.2±0.6L/min/m2。脉搏血氧饱和度测定的睡眠时间中,氧饱和度<90%的时间为 48.9%±35.9%,46 例患者中有 38 例(82.6%)存在夜间低氧血症。平均呼吸暂停低通气指数为 24.9±22.1/h,41 例(89%)存在睡眠呼吸暂停。夜间低氧血症的主要机制是通气/灌注不匹配,或伴有阻塞性呼吸暂停事件。多变量逻辑回归确定了 FEV25%-75%(比值比,0.9519;95%可信区间,0.9089-0.9968;P=0.036)和平均肺动脉压(比值比,1.1068;95%可信区间,1.0062-1.2175;P=0.037)是夜间低氧血症的显著预测因素。临床症状不能预测夜间低氧血症。
PH 患者夜间低氧血症的发生率较高,应进行系统筛查。需要进一步研究来确定夜间低氧血症对 PH 患者预后的影响。
ClinicalTrials.gov;编号:NCT01371669;网址:www.clinicaltrials.gov