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El ensayo de inhibición de sPLA2 para disminuir la liberación de enzimas después de la intervención coronaria

Vladimír Džavík1, Shahar Lavi, Kevin Thorpe

  • 1Interventional Cardiology Program, Division of Cardiology, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada. vlad.dzavik@uhn.on.ca

Circulation
|November 25, 2010
PubMed
Resumen
Este resumen es generado por máquina.

Varespladib, un inhibidor de la fosfolipasa A2 secretora, no redujo la liberación de biomarcadores cardíacos después de la intervención coronaria percutánea. Este estudio no encontró ningún beneficio significativo de la inhibición de sPLA para prevenir la mionecrosis en pacientes con ICP.

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Área de la Ciencia:

  • Cardiología Cardiología.
  • La bioquímica es la bioquímica.
  • Farmacología Farmacología.

Sus antecedentes:

  • La fosfolipasa secretora A(2) (sPLA(2) está implicada en la mionecrosis después de la intervención coronaria percutánea (PCI).
  • La inhibición de sPLA(2) puede ofrecer un beneficio terapéutico en la reducción del daño cardíaco después de la ICP.
  • Varespladib es un inhibidor de moléculas pequeñas dirigido a la sPLA.

Objetivo del estudio:

  • Investigar la eficacia de varespladib en la reducción de la liberación de biomarcadores cardíacos post-procedural después de la ICP electiva.
  • Para comprobar la hipótesis de que la inhibición de sPLA(2) con varespladib mitiga la mionecrosis asociada con la ICP.

Principales métodos:

  • Un ensayo de fase II, aleatorizado y controlado con placebo que involucró a 144 pacientes estables sometidos a ICP electiva.
  • Los pacientes recibieron varespladib (500 mg PO BID) o placebo durante 3-5 días antes y 5 días después del procedimiento.
  • El objetivo primario: elevación de la troponina I o la creatina quinasa-MB por encima del límite superior de la normalidad a las 6-8 o 18-24 horas después de la ICP.

Principales resultados:

  • El criterio de valoración primario se produjo en el 75% de los pacientes con varespladib frente al 63% de los pacientes con placebo (P = 0,14), lo que no indica una reducción significativa.
  • El aumento de la troponina I (3x ULN) se observó en el 57% frente al 50% (P = 0,39), y el aumento de la CK-MB (2x ULN) en el 14% frente al 3% (P = 0,018).
  • Varespladib redujo significativamente la actividad de sPLA, pero no afectó los niveles de proteína C reactiva de alta sensibilidad.

Conclusiones:

  • La administración de varespladib durante 3-5 días antes de la ICP electiva no redujo la mionecrosis periprocedural.
  • La inhibición de sPLA ((2) con varespladib no demostró un beneficio significativo en esta población de pacientes.
  • Es posible que se necesite más investigación para explorar otras estrategias terapéuticas para prevenir la mionecrosis relacionada con la ICP.