Mecanismos fisiopatológicos involucrados en la relación entre la apnea-hipopnea del sueño y el infarto cerebral
Resumen
OBJETIVO: Describir los mecanismos fisiopatológicos en la relación entre la apnea-hipopnea del sueño y el infarto cerebral.
ADQUISICIÓN DE LA EVIDENCIA: Se realizó una búsqueda bibliográfica en la base de datos Medline entre 2014 y 2019, mediante los términos ischemic stroke prognosis o outcome; sleep apnea o sleep disordered breathing o apnea-hipopnea índex, y pathophysiology mechanistic o endothelial dysfunction o inflammation. Fueron encontrados 41 artículos originales, 5 metaanálisis y 4 revisiones sistemáticas.
RESULTADOS: Por cada unidad que aumente el índice de apnea-hipopnea, el riesgo de infarto cerebral se incrementa en un 6 %. Los episodios de apnea agravan la hipoperfusión en el área cerebral lesionada mediante un mecanismo de robo de flujo sanguíneo. Después de un primer accidente cerebrovascular, por cada una unidad adicional de índice de apnea-hipopnea, aumenta en un 5 % el riesgo de mortalidad. La escala NIHSS aumenta en 17,6 % en el grupo de pacientes apneicos con infarto cerebral en comparación con 12,5 % en pacientes no apneicos. La apnea del sueño severa se asocia independientemente a puntuaciones en la escala de Ranquin ≥2 a los 6 meses del ictus (OR: 9,7; 95 % CI: 1,3-73,8; p= 0,03).
CONCLUSIONES: Los principales mecanismos fisiopatológicos involucrados en la relación entre la apnea-hipopnea del sueño y el infarto cerebral fueron la hipoxemia e hipercapnia intermitente, la descarga catecolaminérgica, la disfunción autonómica, el estrés oxidativo, la disfunción endotelial y la inflamación sistémica. Por dicha razón, la apnea del sueño favorece el desarrollo de factores de riesgo vascular y predice resultados adversos después de un ictus isquémico en términos de mortalidad, severidad del déficit neurológico, complicaciones y recuperación funcional.
Palabras clave
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