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Disfunción autónoma cardíaca en el síndrome de Brugada
Thomas Wichter1, Peter Matheja, Lars Eckardt
1Hospital of the Westfälische Wilhelms-University, Department of Cardiology and Angiology, Münster, Germany. wichtet@uni-muenster.de
Circulation
|February 13, 2002
Resumen
Los pacientes con síndrome de Brugada muestran una reabsorción cardíaca anormal de norepinefrina, lo que sugiere una disfunción del nervio simpático presináptico. Este hallazgo puede afectar la comprensión de la fisiopatología del síndrome de Brugada y el desarrollo de la arritmia.
Área de la Ciencia:
- Cardiología Cardiología.
- Investigación del sistema nervioso autónomo.
- Imágenes moleculares de imágenes.
Sus antecedentes:
- El síndrome de Brugada se caracteriza por anomalías en el ECG y arritmias potencialmente mortales en corazones estructuralmente normales.
- La implicación del sistema nervioso autónomo se sugiere por arritmias que ocurren en reposo y signos alterados de ECG con modulación autónoma.
Objetivo del estudio:
- Para investigar la recaptación presináptica cardíaca neuronal de norepinefrina (recaptación 1) en pacientes con síndrome de Brugada.
- Para comparar la recaptación de norepinefrina entre pacientes con síndrome de Brugada y controles sanos utilizando técnicas avanzadas de imagen.
Principales métodos:
- Utilizado [123I]m-iodobenzylguanidine (123I-MIBG) para la obtención de imágenes de la función del nervio simpático cardíaco presináptico.
- Utilizó CT de emisión de un solo fotón (SPECT) y análisis cuantitativo de ojo de toros de 33 segmentos.
- Se estudiaron 17 pacientes con síndrome de Brugada y 10 controles de la misma edad.
Principales resultados:
- Se observó una reducción regional de la absorción de 123I-MIBG en el 47% de los pacientes con síndrome de Brugada, pero en ninguno de los controles.
- El análisis cuantitativo reveló una reducción segmental en las paredes ventriculares izquierda inferior y septal en pacientes con síndrome de Brugada.
- No se encontró correlación entre los hallazgos de 123I-MIBG-SPECT y las características clínicas del paciente.
Conclusiones:
- Se ha demostrado una absorción anormal de 123I-MIBG en el síndrome de Brugada, lo que indica una disfunción simpática presináptica cardíaca.
- Los hallazgos sugieren un papel potencial para la disfunción simpática en la fisiopatología del síndrome de Brugada y la arritmogénesis.
- Se necesita más investigación para explorar el equilibrio del sistema nervioso simpático y parasimpático en el síndrome de Brugada.
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