2008, Número 6
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Rev Invest Clin 2008; 60 (6)
Mecanismos de daño cardiovascular en apnea obstructiva del sueño
Torre-Bouscoulet L, Castorena-Maldonado A, Sada-Ovalle I, Meza-Vargas MS
Idioma: Español
Referencias bibliográficas: 175
Paginas: 502-516
Archivo PDF: 124.95 Kb.
RESUMEN
El síndrome de apnea obstructiva del sueño (SAOS) es un factor independiente y modificable de riesgo cardiovascular; sin embargo, los mecanismos fisiopatológicos subyacentes a esta asociación no se conocen por completo. La hipoxemia intermitente (HI), uno de los marcadores fisiológicos del SAOS, se caracteriza por periodos transitorios de desaturación de oxígeno seguidos por reoxigenación. Los ciclos de hipoxia-reoxigenación se asocian a estrés oxidativo a partir del cual se desencadenan vías de daño cardiovascular como el incremento en la sensibilidad de quimiorreceptores que induce sobreactivación del sistema nervioso simpático, disminución de sensibilidad de barorreceptores, activación de vías de inflamación sistémica mediadas principalmente por el factor de transcripción nuclear κB que favorecen el desarrollo de arterioesclerosis mediante la síntesis de citocinas y la expresión de moléculas de adhesión, disfunción endotelial con disminución en la disponibilidad de óxido nítrico, dislipidemia, resistencia a la insulina y activación del sistema renina angiotensina. Otros mecanismos propuestos son los alertamientos que aumentan la actividad del sistema nervioso simpático y los exagerados cambios de presión intratorácica que incrementan la presión transmural. La mayoría de estas vías son modificadas favorablemente por el uso de CPAP. El conocimiento de los mecanismos de daño cardiovascular abre la posibilidad de instituir nuevos tratamientos que contribuyan a limitar las consecuencias cardiovasculares asociadas al SAOS.
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