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Original Research: Sleep Disorders |

High Occurrence of Hypoxemic Sleep Respiratory Disorders in Precapillary Pulmonary Hypertension and MechanismsPulmonary Hypertension and Sleep Hypoxemia

Fadia Nicolas Jilwan, MD; Pierre Escourrou, MD, PhD; Gilles Garcia, MD, PhD; Xavier Jaïs, MD; Marc Humbert, MD, PhD; Gabriel Roisman, MD, PhD
Author and Funding Information

From the Faculté de Médecine (Drs Jilwan, Escourrou, Garcia, Jaïs, Humbert, and Roisman), Université Paris-Sud, Le Kremlin-Bicêtre; Assistance Publique-Hôpitaux de Paris, Unité de Médecine du Sommeil (Drs Jilwan, Escourrou, Garcia, and Roisman), Hôpital Antoine-Béclère, Clamart; Assistance Publique-Hôpitaux de Paris, Service de Pneumologie et Réanimation Respiratoire (Drs Jaïs and Humbert), Hôpital Antoine-Béclère, Clamart; Institut National de la Santé et de la Recherche Médicale U999 Hypertension Artérielle Pulmonaire: Physiopathologie et Innovation Thérapeutique (Drs Garcia, Jaïs, and Humbert), Le Plessis-Robinson; and Faculté de Pharmacie (Drs Jilwan and Escourrou), Université Paris-Sud, EA3544, Châtenay-Malabry, France.

Correspondence to: Gabriel Roisman, MD, PhD, Unité de Médecine du Sommeil, Hôpital Antoine-Béclère, 157 Rue de la Porte de Trivaux, 92140 Clamart, France; e-mail: gabriel.roisman@abc.aphp.fr


Funding/support: The sponsor was Assistance Publique-Hôpitaux de Paris (Département de la Recherche Clinique et du Développement).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(1):47-55. doi:10.1378/chest.11-3124
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Background:  The occurrence and mechanisms of nocturnal hypoxemia in precapillary pulmonary hypertension (PH) are not clearly defined.

Methods:  In an observational, prospective, and transversal design, we studied 46 clinically stable patients with PH and a BMI < 35 kg/m2, an FEV1 > 60% predicted, and idiopathic pulmonary arterial hypertension (n = 29) or chronic thromboembolic pulmonary hypertension (n = 17). They underwent nocturnal polysomnography with transcutaneous capnography.

Results:  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/m2. 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 FEV25%-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.

Conclusions:  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.

Trial registry:  ClinicalTrials.gov; No.: NCT01371669; URL: www.clinicaltrials.gov

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