Author: Boyer L1,2, Audureau E3, Margarit L4, Marcos E5, Bizard E6, Le Corvoisier P7, Macquin-Mavier I8, Derumeaux G9, Damy T10, Drouot X11, Covali-Noroc A12, Boczkowski J13, Bastuji-Garin S14,15, Adnot S16
Affiliation: <sup>1</sup>Inserm, U955 , faculté de médecine , 8 rue du Général Sarrail , Créteil, France , 94010.
<sup>2</sup>APHP, Groupe Henri-Mondor Albert-Chenevier, Physiologie Explorations Fonctionnelles , 51, av du Maréchal de Tassigny , Créteil, France , 94010 ; laurent.boyer@hmn.aphp.fr.
<sup>3</sup>APHP, Groupe Henri-Mondor Albert-Chenevier, Santé Publique, Créteil, France ; etienne.audureau@aphp.fr.
<sup>4</sup>APHP, Groupe Henri-Mondor Albert Chenevier, Physiologie-Explorations Fonctionnelles, Creteil, France ; laurent.margarit@hmn.aphp.fr.
<sup>5</sup>INSERM U955, Faculté de Médecine, DHU A-TVB, Creteil, France ; elisabeth.marcos@inserm.fr.
<sup>6</sup>INSERM U955, Faculté de Médecine, DHU A-TVB, Créteil, France ; emilie.bizard@hotmail.fr.
<sup>7</sup>APHP, Groupe Henri-Mondor Albert-Chenevier, Centre d'Investigation Clinique , Créteil, France ; philippe.lecorvoisier@aphp.fr.
<sup>8</sup>APHP Groupe Henri-Mondor Albert Chenevier, Pharmacologie Clinique, Créteil, France ; isabelle.macquin-mavier@aphp.fr.
<sup>9</sup>INSERM U955, Département de Physiologie, Hôpital Henri Mondor, AP-HP, DHU A-TVB, Creteil, France ; gderumeaux@gmail.com.
<sup>10</sup>APHP Groupe Henri-Mondor Albert Chenevier, Cardiologie, Créteil, France ; thibaud.damy@aphp.fr.
<sup>11</sup>Centre Hospitalo-Universitaire de Poitiers, Physiologie-Explorations Fonctionnelles, Créteil, France ; Xavier.DROUOT@chu-poitiers.fr.
<sup>12</sup>APHP, Groupe Henri-Mondor Albert-Chenevier, Physiologie-Explorations Fonctionnelles, Créteil, France ; alanoroc@hotmail.fr.
<sup>13</sup>INSERM, U955 , 8 rue du General Sarrail , Creteil, France , 94010 ; jorge.boczkowski@inserm.fr.
<sup>14</sup>Henri-Mondor hospital, Public Health and Clinical research , 51 avenue du Maréchal de Lattre de Tassigny , Créteil, France , 94010.
<sup>15</sup>Université Paris 12, LIC , service de santé publique 51 avenue du Maréchal de Lattre de Tassigny , Créteil, France , 94010 ; sylvie.bastuji-garin@hmn.aphp.fr.
<sup>16</sup>Hôpital Henri Mondor, Service de Physiologie et des Explorations Fonctionnelles , Avenue du marechal de Lattre de Tassigny , Créteil, France , 94010 ; serge.adnot@inserm.fr.
Conference/Journal: Ann Am Thorac Soc.
Date published: 2016 May 10
Other:
Word Count: 200
RATIONALE: Sleep disorders may lead to stress-induced premature aging and telomere shortening.
OBJECTIVES: To determine whether obstructive sleep apnea syndrome causing intermittent hypoxemia episodes was associated with telomere shortening independently from the comorbidities associated with this syndrome.
METHODS: Cross-sectional study in 161prospectivelly enrolled untreated middle-aged men free of known comorbidities related or unrelated to sleep apnea. Each participant underwent full standard overnight polysomnography. Patients with apnea sleep syndrome were naïve of treatment.
MEASUREMENTS AND MAIN RESULTS: By univariate analysis, telomere shortening was associated with older age, apnea-hypopnea index, oxygen desaturation index, apnea-hypopnea index, waist circumference, and fat mass. After adjustment for age, only apnea-hypopnea index and oxygen desaturation index were significantly related to telomere shortening. Mean telomere length ratio was 0.70±0.37 in the participants without sleep apnea, compared to 0.61±0.22 and 0.53±0.16 in those with mild-to-moderate and severe sleep apnea, respectively (P=0.01). By multivariate analysis, oxygen desaturation index was the only factor independently associated with telomere length. Arterial stiffness assessed by carotid-femoral pulse wave velocity correlated negatively with telomere length.
CONCLUSIONS: Intermittent hypoxemia due to obstructive sleep apnea syndrome is a major contributor to telomere shortening in middle-aged males. Oxidative stress may explain this finding.
PMID: 27163410 [PubMed - as supplied by publisher]