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La activación epicárdica de la pared ventricular izquierda prolonga el intervalo QT y la dispersión transmural de la
Jeffrey M Fish1, José M Di Diego, Vladislav Nesterenko
1Masonic Medical Research Laboratory, Utica, NY 13501-1787, USA.
Circulation
|April 14, 2004
Resumen
El ritmo epicárdico del ventrículo izquierdo prolonga el intervalo QT y aumenta la dispersión de repolarización, creando un sustrato para arritmias peligrosas. Este estudio celular explica los mecanismos aritmogénicos detrás de la reversión de la activación epicárdica.
Área de la Ciencia:
- Cardiología Cardiología.
- Electrofisiología y electrofisiología.
- Las arritmias cardíacas son arritmias cardíacas.
Sus antecedentes:
- Se sabe que el ritmo epicárdico del ventrículo izquierdo (LV) prolonga el intervalo QT y aumenta el riesgo de arritmias torsade de pointes.
- Los mecanismos celulares subyacentes a la prolongación del intervalo QT y la arritmogénesis debido a la dirección inversa de activación de LV requieren más investigación.
Objetivo del estudio:
- Para investigar la base celular de la prolongación del intervalo QT y la arritmogénesis cuando la dirección de la activación de LV se invierte.
- Para dilucidar el impacto del ritmo epicárdico versus endocardiano en la repolarización transmural y la conducción.
Principales métodos:
- Registro simultáneo de electrocardiogramas transmurales (ECG) y potenciales de acción transmembrana de las preparaciones caninas de cuña de LV.
- Se tomaron medidas de las células epicárdicas, M y endocárdicas en condiciones de perfusión arterial.
- Se realizaron experimentos con y sin activación rápida de bloqueadores de corriente de potasio de rectificador retrasado (por ejemplo, E-4031, cisaprida).
Principales resultados:
- El cambio de ritmo del endocardio al epicardio aumentó significativamente el intervalo QT y la dispersión transmural de repolarización (TDR).
- El tiempo de conducción entre las células M y las epicárdicas aumentó con el ritmo epicárdico.
- La amplificación de la TDR fue mejorada aún más por los bloqueadores de corriente de potasio, y las arritmias de torsade de pointes fueron inducibles durante el ritmo epicárdico en estas condiciones.
Conclusiones:
- La activación inversa de LV, como se ve en el ritmo biventricular, aumenta notablemente QT y TDR debido a la repolarización diferencial entre las células epicárdicas y M.
- El TDR elevado crea un sustrato electrofisiológico propicio para las arritmias de torsade de pointes en el contexto de intervalos QT prolongados.
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