Vulnerabilidad intrínseca del miocardio auricular como mecanismo de génesis de fibrilación auricular en el síndrome de Wolff-Parkinson-White
Palabras clave:
vulnerabilidad auricular, síndrome de WPW, electrograma auriculares anormalesResumen
Los investigadores que describieron por primera vez el síndrome de Wolff-Parkinson-White (WPW) ya reconocieron la existencia de una asociación de ésta entidad con la fibrilación auricular (FA). Se han documentado episodios de FA hasta en un 30% de los pacientes con síndrome de WPW. Diversas modificaciones histológicas y electrofisiológicas del miocardio auricular, tales como, cambios fibrodegenerativos, aumento en la dispersión de los períodos refractarios, retardo en la conducción de los impulsos, conducción anisotrópica, e interacción con el sistema nervioso autonómico, se encuentran asociadas a la inducción, generación y persistencia de la FA. Mediante la estimulación auricular programada con extraestímulo simple durante el estudio electrofisiológico se pueden inducir varios parámetros de vulnerabilidad auricular aumentada. Por ejemplo, la actividad auricular repetitiva, la actividad auricular fragmentada, y el retardo en la conducción interauricular inducidos por un extraestímulo temprano en diástole en pacientes que poseen anormalidades electrofisiológicas del miocardio auricular, han sido utilizados como indicadores de vulnerabilidad auricular y como requisitos importantes para la génesis de la reentrada, y por ende, de la FA. Los pacientes con síndrome de WPW y FA paroxística poseen un número significativamente mayor de electrogramas auriculares anormalmente fragmentados y prolongados y una anormalidad electrofisiológica del músculo auricular significativamente mayor que los pacientes con síndrome de WPW sin FA paroxística. Estos resultados claramente demuestran que el miocardio auricular patológico y la vulnerabilidad intrínseca del miocardio auricular juegan un papel muy importante en el desarrollo de la FA en pacientes con el síndrome de WPW.
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