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Pruebas de respuesta a fármacos para el estentamiento de la arteria carótida electiva: Prevalencia de la falta de
Farzaneh Yousefi1, Dimah Hasan1, Frederic De Beukelaer1
1Department of Neuroradiology, University Hospital RWTH Aachen, Aachen, Germany.
The neuroradiology journal
|August 29, 2025
Resumen
La falta de respuesta antiplaquetaria al clopidogrel (CPG) y a la aspirina (ASS) es común en pacientes sometidos a estenting de la arteria carótida (CAS). Sin embargo, el uso de tirofibán durante el CAS anula el impacto de la falta de respuesta en el infarto cerebral post-procedural.
Área de la Ciencia:
- Cardiología
- Neurología
- Farmacología
Sus antecedentes:
- No se conoce bien la prevalencia de la falta de respuesta al clopidogrel (CPG) y a la aspirina (ASS) en pacientes sometidos a stenting de la arteria carótida (CAS).
- El impacto de la respuesta antiplaquetaria en la isquemia cerebral post-intervencionista después del CAS no está claro.
Objetivo del estudio:
- Investigar la influencia del estado de respuesta CPG y ASS en la isquemia cerebral posterior al CAS.
- Determinar la prevalencia de CPG y no respuesta de ASS en pacientes sometidos a CAS.
Principales métodos:
- Análisis retrospectivo de pacientes sometidos a CAS electivo entre 2010 y 2024 con resonancia magnética pre y post CAS.
- Los pacientes se agruparon en función de la respuesta ASS y CPG.
- Comparación de los patrones de isquemia cerebral y asociación de las comorbilidades con la resistencia a los fármacos o el infarto.
Principales resultados:
- El 73,5% de los pacientes mostró una respuesta adecuada tanto a la ASS como a la GPC.
- La falta de respuesta al clopidogrel (14,8%) fue más frecuente que la falta de respuesta a la aspirina (9,2%).
- Con el puente de tirofibano durante el CAS, el estado de respuesta no influyó en el infarto cerebral post-intervencionista.
Conclusiones:
- La falta de respuesta antiplaquetaria, particularmente a la GPC, es frecuente en pacientes con SAE.
- El puente de tirofibano durante el CAS mitiga el efecto de la falta de respuesta antiplaquetaria en los patrones de infarto cerebral.
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