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Vol. 44. Issue 10.
Pages 531-539 (January 2008)
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Vol. 44. Issue 10.
Pages 531-539 (January 2008)
Original Articles
DOI: 10.1016/S1579-2129(08)60099-3
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Hemodynamic and Inflammatory Markers of Sleep Apnea-Hypopnea Syndrome and Nocturnal Hypoxemia: Effects of Treatment With Nasal Continuous Positive Airway Pressure
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Amparo Sáncheza,
Corresponding author
arsanchez@nuevoiris.com

Correspondence: Dr A. Sánchez Servicio de Neumología, Hospital Universitario de Salamanca P.º de San Vicente, 58-182 37007 Salamanca, Spain
, Alan R. Schwartzb, Pedro L. Sánchezc, José L. Fernándeza, Jacinto Ramosa, Francisco Martín-Herrerod, Rafael González-Celador, Ricardo Ruano, Irene Bregóna, Cándido Martín-Luengod, Francisco P. Gómeza
a Servicio de Neumología, Hospital Universitario de Salamanca, Salamanca, Spain
b Johns Hopkins Sleep Disorders Center, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA
c Servicio de Cardiología, Hospital General Universitario Gregorio Marañón, Madrid, Spain
d Servicio de Cardiología, Hospital Universitario de Salamanca, Salamanca, Spain
Article information
Objective

In this study, we assessed factors associated with cardiovascular risk in patients with sleep apnea-hypopnea syndrome (SAHS) through analysis of plasma concentrations of N-terminal prohormone brain natriuretic peptide (NTproBNP) and high-sensitivity C-reactive protein (hsCRP). In addition, we analyzed the effect of nasal continuous positive airway pressure (nCPAP) on these markers.

Patients and Methods

Forty-two patients with SAHS (mild to moderate in 15 cases and severe in 27) were compared with 14 individuals without SAHS. The participants were not receiving drug treatment and they did not have diabetes, hypertension, marked dyslipidemia, or cardiovascular disease, which was ruled out both clinically and by echocardiography and 99mTc-tetrofosmin scintigraphy at rest and during exercise. The effects of nCPAP in patients with severe SAHS were analyzed after 6 months of treatment.

Results

Following adjustment for age, body mass index, and smoking habit, the mean concentrations of markers were not significantly higher in patients with severe SAHS than in those with mild-to-moderate SAHS or in control subjects. Nevertheless, in patients with SAHS the main factor influencing NTproBNP concentrations was the percentage of time with a nocturnal arterial oxygen saturation of less then 90% (r=0.37,P=.017). No variables predictive of hsCRP concentration were identified. The concentrations of the markers were reduced by nCPAP, but the differences were not statistically significant.

Conclusions

While nocturnal hypoxemia in SAHS is responsible for variations in the plasma concentration of NTproBNP (as a result of cardiovascular changes), SAHS appears not to be associated with the inflammatory marker hsCRP when patients with heart disease, cardiovascular risk factors, or those receiving pharmacologic treatment are excluded.

Key words:
Sleep apnea
Hypoxemia
ProBNP
Inflammation
Objetivo

Investigamos los factores del síndrome de apneas-hipopneas durante el sueño (SAHS) que activan los mecanismos de riesgo cardiovascular, a través del estudio de las concentraciones plasmáticas del fragmento N-terminal del precursor del péptido natriurético cerebral (NTproBNP) y de la proteína C reactiva de alta sensibilidad (PCRas), así como el efecto que sobre ellos tiene el tratamiento con presión positiva continua de la vía aérea nasal (CPAPn).

Pacientes Y Métodos

Se estudió a 42 pacientes con SAHS (leve-moderado en 15 casos y grave en 27), comparados con 14 personas sin SAHS. No tomaban fármacos ni presentaban diabetes, hipertensión, dislipemia importante o enfermedad cardiovascular, que se descartó tanto clínicamente como por ecocardiografía y tomografía computarizada por emisión de fotón cínico-esfuerzo con99mTc-tetrofosmina. En los pacientes con SAHS grave se estudiaron los efectos de 6 meses con CPAPn.

Resultados

Ajustando por edad, índice de masa corporal y tabaquismo, las medias de los biomarcadores no fueron significativamente más altas en los pacientes con SAHS grave que en aquéllos con SAHS leve-moderado o en los controles. Sin embargo, en los pacientes con SAHS el principal factor que influyó en las concentraciones de NTproBNP fue el porcentaje de tiempo con saturación arterial de oxígeno nocturna menor del 90% (r = 0,37; p = 0,017), sin que se encontrara ningún predictor de los valores séricos de la PCRas. La aplicación de CPAPn hizo descender, pero no significativamente, las concentraciones de los biomarcadores.

Conclusiones

Mientras que la hipoxemia nocturna en el SAHS es la responsable de las variaciones en los valores del NTproBNP, derivado de la afectación cardíaca, el SAHS no parece estar asociado con el biomarcador inflamatorio PCRas, cuando se excluye a los pacientes con alteraciones cardíacas, factores de riesgo cardiovascular o en tratamiento farmacológico.

Palabras clave:
Apnea del sueño
Hipoxemia
ProBNP
Inflamación
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