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La refractariedad postrepolarización frente a la desaceleración de la conducción causada por los medicamentos
P F Kirchhof1, C L Fabritz, M R Franz
1Cardiology Division, Veterans National Administration Center, Washington, DC 20422, USA.
Circulation
|July 10, 1998
Resumen
La refractividad por posrepolarización inducida por fármacos (PRR) protege contra la fibrilación ventricular (VF). Sin embargo, la propafenona puede promover la taquicardia ventricular monomórfica lenta (VT) al afectar la conducción y la longitud de onda.
Área de la Ciencia:
- Electrofisiología y electrofisiología.
- Farmacología cardíaca farmacología cardíaca.
Sus antecedentes:
- El bloqueo de conducción puede ser antiarrítmico y proarrítmico.
- La refractividad postrepolarizada (PRR) inducida por el fármaco puede prevenir la taquiarritmia.
- Se investigaron los efectos antiarrítmicos y proarrítmicos de la propafenona y la procainamida.
Objetivo del estudio:
- Para investigar los efectos de la propafenona y la procainamida en la electrofisiología cardíaca.
- Para determinar las consecuencias antiarrítmicas o proarrítmicas de estos medicamentos.
- Evaluar el papel de la refractariedad postrepolarización en las arritmias inducidas por fármacos.
Principales métodos:
- Se utilizaron corazones de conejo aislados con perfusión de Langendorff.
- Se registraron potenciales de acción monofásicos (MAP) y ECG.
- La taquicardia ventricular (VT) y la fibrilación (VF) fueron inducidas por estimulación eléctrica antes y después de la administración de fármacos.
Principales resultados:
- Tanto la propafenona como la procainamida prolongaron la duración del potencial de acción e indujeron PRR.
- La procainamida redujo la inducibilidad de la FV en un 70%, mientras que la propafenona eliminó la FV.
- La propafenona ralentizó significativamente la conducción y acortó la longitud de onda, lo que condujo a la inducción de VT en el 57% de las estimulaciones de ráfaga.
Conclusiones:
- La PRR inducida por fármacos protege eficazmente contra la fibrilación ventricular (VF).
- La propafenona, a pesar de prevenir la fibrilación venosa, puede promover un VT monomórfico lento.
- La desaceleración de la conducción dependiente del uso y el acortamiento de la longitud de onda por propafenona probablemente subyacen a la promoción de VT.
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