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Vol. 45. Issue S1.
Pages 3-10 (February 2009)
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Vol. 45. Issue S1.
Pages 3-10 (February 2009)
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Novedades en la epidemiología, la historia natural, el diagnóstico y el tratamiento del síndrome de apneas-hipopneas durante el sueño
Innovations in the Epidemiology, Natural History, Diagnosis and Treatment of Sleep Apnea-Hypopnea Syndrome
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Concepción Hernándeza,
Corresponding author
CONCEPCION.HERN@telefonica.net

Autor para correspondencia.
, Joaquín Durán-Cantollab, Patricia Lloberesc, Mónica Gonzálezd
a Servicio de Neumología, Hospital Universitario de Canarias, La Laguna, Tenerife, España
b Unidad Respiratoria de Trastornos del Sueño, Hospital Txagorritxu, Vitoria, Álava, España
c Servicio de Neumología, Hospital Vall d’Hebron, Barcelona, España
d Unidad de Sueño y Ventilación, Servicio de Neumología, Hospital Universitario Marqués de Valdecilla, Santander, Cantabria, España
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Resumen

En la siguiente revisión se sintetizan los artículos más relevantes publicados en relación con el síndrome de apneas-hipopneas durante el sueño (SAHS) durante el presente año. El análisis de los múltiples factores que participan en el riesgo de enfermedad cardiovascular asociada al SAHS ocupa en la actualidad gran parte del interés de la comunidad científica. En este sentido, son numerosos los estudios que ponen de manifiesto el papel de los mediadores inflamatorios e inmunológicos, su relación con el daño endotelial y su influencia en la génesis de enfermedad cardiovascular en pacientes con SAHS. El papel de la CPAP en evitar este riesgo cardiovascular ha tenido resultados diversos. Si bien en la insuficiencia cardíaca no existen evidencias sobre el beneficio o perjuicio de su uso, en el accidente cerebrovascular se ha confirmado el SAHS como factor predisponente y el aumento de mortalidad constatado justificaría el intento de tratar el SAHS en estos pacientes. De igual modo, la reducción de las cifras de presión arterial encontradas en sujetos en tratamiento con CPAP reduciría el riesgo de enfermedad cardiocerebrovascular. Los conocimientos recientes que demuestran la expresión plurifenotípica del SAHS permiten vislumbrar un futuro de enfermedad basado en diferentes fenotipos específicos, donde la tradicional sintomatología que definía el síndrome no limite su tratamiento. Conseguir un método diagnóstico fiable y coste-efectivo, que responda a las demandas del problema de salud pública que representa el SAHS, especialmente en sectores de la población que permanecen más infradiagnosticados y menos conocidos, como los niños, las mujeres y la pobla ción anciana, es otro de los retos que se refleja en los estudios publicados. En resumen, los crecientes conocimientos sobre la biología del SAHS, sus implicaciones cardiovasculares y su repercusión en la morbimortalidad de la población nos permitirán en los próximos años comprender la verdadera dimensión de esta enfermedad.

Palabras clave:
Síndrome de apneas-hiponeas durante el
sueño (SAHS)
CPAP
Riesgo cardiovascular
Métodos diagnósticos
Mediadores inflamatorios
Abstract

The following review summarises the most important articles published on sleep apnea-hypopnea syndrome (SAHS) during the current year. The analysis of the many factors implicated in the risk of cardiovascular diseases associated with SAHS is currently of great interest to the scientific community. There are many studies on this subject that demonstrate the role of inflammatory and immunological mediators, their relationship with endothelial damage and their influence in the genesis of cardiovascular disease in patients with SAHS. The role of CPAP in preventing this cardiovascular risk has had varied results. Although there is no evidence of benefit or harm in its use in heart failure, in cerebrovascular accidents SAHS has been confirmed as a predisposing factor and the reported increase in mortality would justify the intention to treat SAHS in these patients. Likewise, the reduction in blood pressure found with CPAP treatment could reduce the risk of cardio-cerebrovascular disease. The recent knowledge that there is expression of multiple phenotypes of SAHS gives a glimpse in the future of a disease based on different specific phenotypes, where the traditional symptomatology that defined the syndrome does not limit its treatment. To obtain a reliable and cost-effective diagnostic method that responds to the demands of the public health problem that is SAHS, particularly in sectors of the population that remain under-diagnosed and less well known, such as children, women and the elderly population is another one of the challenges reflected in published studies. In short, the growing knowledge on the biology of SAHS, its cardiovascular implications and its effect on the morbidity and mortality of the population will enable us to understand the true dimension of this disease in the next few years.

Keywords:
Sleep apnea-hypopnea syndrome (SAHS)
CPAP
Cardiovascular risk
Diagnostic methods
Inflammatory mediators
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Bibliografía
[1.]
M. Dematteis, C. Julián, C.H. Guillermet, N. Sturm, S. Lantuejoul, M. Mallaret, et al.
Intermittent hypoxia induces early functional cardiovascular remodelling in mice.
Am J Respir Crit Care Med, 177 (2008), pp. 227-235
[2.]
M.D. Cross, N.L. Mills, M. Al-Abri, R. Riha, M. Vennelle, T.W. Mackay, et al.
Continuous positive airway pressure improves vascular function in obstructive sleep apnoea/hypopnoea syndrome: a randomised controlled trial.
Thorax, 63 (2008), pp. 578-583
[3.]
S. Jelic, M. Padeletti, S.M. Kawut, C. Higgins, S.M. Canfield, D. Onat, et al.
Inflammation, oxidative stress, and repair capacity of the vascular endothelium in obstructive sleep apnea.
Circulation, 117 (2008), pp. 2270-2278
[4.]
B. Lefebvre, J.L. Pépin, J.P. Baguet, R. Tamisier, M. Roustit, K. Riedweg, et al.
Leukotriene B4: early mediator of atherosclerosis in obstructive sleep apnoea?.
Eur Respir J, 32 (2008), pp. 113-120
[5.]
M.A. Arias, F. García-Río, A. Alonso-Fernández, A. Herranz, R. Hidalgo, V. Martínez-Mateo, et al.
Continuous positive airway pressure decreases elevated plasma levels of soluble tumor necrosis factor-α receptor 1 in obstructive sleep apnea.
Eur Respir J, 32 (2008), pp. 1009-1015
[6.]
CAFE Investigators, for the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Investigators, CAFE Steering Committee and Writing Committee, et al. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) Study. Circulation. 2006;13:1213-25.
[7.]
C.L. Phillips, B. Yee, Q. Yang, A.T. Villaneuva, J. Hedner, N. Berend, R. Grunstein.
Effects of continuous positive airway pressure treatment and withdrawal in patients with obstructive sleep apnea on arterial stiffness and central BP.
Chest, 134 (2008), pp. 94-100
[8.]
M. Kohler, L. Ayers, J.C.T. Pepperell, K.L. Packwood, B. Ferry, N. Crosthwaite, et al.
Effects of continuous positive airway pressure on systemic inflammation in patients with moderate to severe obstructive sleep apnoea: a randomised controlled trial.
Thorax, (2008),
[9.]
A. Sánchez, A.R. Schwartz, P.L. Sánchez, J.L. Fenández, J. Ramos, F. Martín-Herrero, et al.
Marcadores hemodinámicos e inflamatorios del síndrome de apneas-hipopneas durante el sueño e hipoxemia nocturna. Efectos del tratamiento nasal con presión positiva continua de la vía aérea nasal.
Arch Bronconeumol, 44 (2008), pp. 531-539
[10.]
I. Almendros, A. Carreras, J. Ramírez, J.M. Montserrat, D. Navajas, R. Farré.
Upper airway collapse and reopening induce inflamation in a sleep apnoea model.
Eur Repir J, 32 (2008), pp. 399-404
[11.]
D. Gozal, O. Sans Capdevila, L. Kheirandish-Gozal.
Metabolic alterations and systemic inflammation in obstructive sleep apnea among nonobese ando bese prepubertad children.
Am J Respir Care Med, 177 (2008), pp. 1142-1149
[12.]
A. Tamura, Y. Kawano, T. Watanabe, J. Kadota.
Relationship between the severity of obstructive sep apnea and impaired glucosa metabolism in patients with obstructive sleep apnea.
Respir Med, 1012 (2008), pp. 1412-1416
[13.]
D. Gozal, L. Kheirandish-Gozal.
Cardiovascular morbidity in obstructive sleep apnea. Oxidative stress, inflammation and much more.
Am J Respir Crit Care Med, 177 (2008), pp. 369-375
[14.]
J.M. Golbin, V.K. Somers, S.M. Caples.
Obstructive sleep apnea, cardiovascular disease, and pulmonary hypertension.
Proc Am Thorac Soc, 5 (2008), pp. 200-206
[15.]
V.K. Somers, D.P. White, R. Amin, W.T. Abraham, F. Costa, A. Culebras, et al.
Sleep apnea and cardiovasculr disease. An american heart association/american college of cardiology foundation scientific statement from the american heart association council for high blood pressure research professional education committe, council on clinical cardiology, stroke council, and council on cardiovascular nursing council.
Circulation, 118 (2008), pp. 1-32
[16.]
R.N. Khayat, W.T. Abraham, B. Patt, M. Roy, K. Hua, D. Jarjoura.
Cardiac effects of continuous and bi-level positive airway pressure for patients with heart failure and obstructive sleep apnea: a pilot study.
Chest, (2008),
[17.]
J.A. Moro, L. Almenar, E. Fernández-Fabrellas, S. Ponce, R. Blanquer.
Disfunción miocárdica silente en pacientes con síndrome de apneas-hipopneas durante el sueño. Valor del índice de rendimiento miocárdico.
Arch Bronconeumol, 44 (2008), pp. 418-423
[18.]
A. Garcia-Touchard, V.K. Somers, L.J. Olson, S.M. Caples.
Central sleep apnea: implications for congestive heart failure.
Chest, 133 (2008), pp. 1495-1504
[19.]
S. Ulrich, M. Fischler, R. Speich, K.E. Bloch.
Sleep-breathing disorders in patients with pulmonary hypertension.
Chest, 133 (2008), pp. 1375-1380
[20.]
B. Jurado Gámez, A. Martín-Malo, M.C. Fernández Martín, A. Rodríguez-Benot, N. Pascual, L. Muñoz Cabrera, et al.
Trastornos del sueño en pacientes en lista de espera de trasplante renal.
Arch Bronconeumol, 44 (2008), pp. 371-375
[21.]
C. Sahlin, O. Sandberg, Y. Gustafson, G. Bucht, B. Carlberg, H. Stenlund, et al.
Obstructive sleep apnea is a risk factor for death in patients with stroke. A 10-year follow up.
Arch Intern Med, 168 (2008), pp. 297-301
[22.]
A.V. Chobanian, G.L. Bakris, H.R. Black, W.C. Cushman, L.A. Green, J.L. Izzo Jr, National heart, lung, and blood institute joint national committee on prevention, detection, evaluation, and treatment of high blood pressure; national high blood pressure education program coordinating committee, et al.
The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 reort.
JAMA, 289 (2003), pp. 2560-2572
[23.]
T. Young, L. Finn, P.E. Peppard, M. Szklo-Coxe, D. Austin, J. Nieto, et al.
Sleep disordered breathing and mortality: eighteen-year follow-up of the Wisconsin Sleep Cohort.
Sleep, 31 (2008), pp. 1071-1078
[24.]
V.K. Kapur, H.E. Resnick, D.J. Gottlieb, For the Sleep Heart Health Study Group.
Sleep disordered breathing and hypertension: does self-reported sleepiness modify the association?.
Sleep, 31 (2008), pp. 1127-1132
[25.]
G.V. Robinson, B.A. Langford, D.M. Smith, J. Stradling.
Predictors of blood pressure fal with continuous positive airway pressure (CPAP) treatment of obstructive sleep apnoea (OSA).
Thorax, 63 (2008), pp. 855-859
[26.]
M. Kohler, S. Craig, D. Nicoll, P. Leeson, R.J.O. Davies, J.R. Stradling.
Endothelial function and arterial stiffness in minimally symptomatic obstructive sleep apnea.
Am J Respir Crit Care Med, 178 (2008), pp. 984-988
[27.]
N.S. Marshall, K.K.H. Wong, P.Y. Liu, S.R.J. Cullen, M.W. Knuiman, R.R. Grunstein.
Sleep apnea as an independent risk factor for all-cause mortality: the Busselton Health Study.
Sleep, 31 (2008), pp. 1079-1085
[28.]
A.I. Pack, A.B. Platt, G.W. Pien.
Does untreated obstructive sleep apnea lead to death?.
Sleep, 31 (2008), pp. 1067-1068
[29.]
M.L. Alonso, J. Terán, J. Cordero, M. González, L. Rodríguez, J.L. Viejo, et al.
Fiabilidad de la poligrafía respiratoria domiciliaria para el diagnóstico del síndrome de apneas-hipopneas durante el sueño. Análisis de costes.
Arch Bronconeumol, 44 (2008), pp. 22-28
[30.]
B. Ciftci, T.U. Ciftci, S.F. Guven.
Polisomnografía de parte de la noche y polisomnografía de toda la noche: comparación entre la primera y la segunda parte de la noche.
Arch Bronconeumol, 44 (2008), pp. 3-7
[31.]
N. Roldan, G. Sampol, T. Sagalés, O. Romero, M.J. Jurado, J. Ríos, et al.
Análisis de coste-eficacia de la graduación automática de la presión positiva continua de la vía aérea en el domicilio: ¿una o 2 noches?.
Arch Bronconeumol, 44 (2008), pp. 664-670
[32.]
M.L. Alonso, J. Terán, J. Cordero, A.I. Navazo, E. Ordax, J.F. Masa, et al.
Fiabilidad de la poligrafía respiratoria para el diagnóstico del síndrome de apneas-hipopneas durante el sueño en niños.
Arch Bronconeumol, 44 (2008), pp. 318-323
[33.]
N.M. Punjabi, A.B. Newman, T.B. Young, H.E. Resnick, M.H. Sanders.
Sleep-disordered breathing and cardiovascular disease. An outcome-based definition of hypopneas.
Am J Respir Crit Care Med, 177 (2008), pp. 1150-1155
[34.]
M.A. Martínez-García, J.J. Soler-Cataluña, P. Román-Sánchez, C. Amorós, L. Quiles, E. Chiner-Vives, et al.
Eficacia de un plan de formación en atención primaria sobre el síndrome de apneas-hipopneas durante el sueño.
Arch Bronconeumol, 44 (2008), pp. 15-21
[35.]
N. Roure, O. Mediano, J. Duran-Cantolla.
Influencia del sexo en las variables clínicas y polisomnográficas del síndrome de apneas del sueño.
Arch Bronconeumol, 44 (2008), pp. 685-688
[36.]
Z. Xu, A. Jiaqing, L. Yuchuan, K. Shen.
A case-control study of obstructive sleep apnea-hypopnea síndrome in obese and nonobese chinese children.
Chest, 133 (2008), pp. 684-689
[37.]
A.M. Li, C.T. Au, R.Y.T. Sung, C. Ho, P.C. Ng, T.F. Fok, et al.
Ambulatory blood pressure in children with obstructive sleep apnoea: a community based study.
Thorax, 63 (2008), pp. 803-809
[38.]
R. Amin, L. Anthony, V. Somers, M. Fenchel, K. McConnell, J. Jefferies, et al.
Growth velocity predicts recurrente of sleep-disordered breathing 1 year after adenotonsillectomy.
Am J Respir Crit Care Med, 177 (2008), pp. 654-659
[39.]
E. Goff, D. O’Driscoll, A.K. Simonds, J. Trinder, M.J. Morell.
The cardiovascular response to arousal from sleep decreases with age in healthy adults.
Sleep, 31 (2008), pp. 1009-1017
[40.]
N.S. Marshall, B.J. Yee, A.V. Desai, P.R. Buchanan, K.K.H. Wong, R. Crompton, et al.
Two randomized placebo-controlled trials to evalulate the efficacy and tolerability of mirtazapine for the treatment of obstructive sleep apnea.
Sleep, 31 (2008), pp. 824-831
[41.]
O.M. Vanderveken, A. Devolver, M. Marklung, A.N. Boudewyns, M.J. Braem, W. Okkerse, et al.
Comparison of a custom-made and a thermoplastic oral appliance for the treatment of mild sleep apnea.
Am J Respir Crit Care Med, 178 (2008), pp. 197-202
[42.]
A.J. Piper, D. Wang, B.J. Yee, D.J. Barnes, R.R. Grunstein.
Randomised trial of CPAP vs bilevel support in the treatment of obesity hypoventilation síndrome without severe necturnal desaturation.
Eur Respir J, 63 (2008), pp. 395-401
[43.]
P.M. Macey, R. Kumar, M.A. Woo, E.M. Valladares, F.L. Yan-Go, R.M. Harper.
Brain structural changes in obstructive sleep apnea.
Sleep, 31 (2008), pp. 967-977
[44.]
G.K. Soukhova-O’Hare, Z.A. Shah, Z. Lei, A.D. Nozdrachev, C. Venkateswara Rao.
Erectile dysfunction in a murine model of sleep apnea.
Am J Respir Crit Care Med, 178 (2008), pp. 644-650
Copyright © 2009. Sociedad Española de Neumología y Cirugía Torácica
Archivos de Bronconeumología

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