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Prehospital Thrombolysis: A Manual from Berlin
Published on: November 27, 2013
Eficacia relativa de la antitrombina en comparación con los agentes antiplaquetarios para acelerar la trombólisis
E J Haskel1, N A Prager, B E Sobel
1Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
Circulation
|March 1, 1991
Resumen
La hirudina recombinante inhibe efectivamente la trombina, mejorando la trombólisis coronaria con el activador de plasminógeno de tipo tisular (t-PA) y previniendo la reoclusión. Este efecto anticoagulante también reduce la activación plaquetaria para la permeabilidad arterial sostenida.
Área de la Ciencia:
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
- Farmacología Farmacología.
- La trombosis y la hemostasis.
Sus antecedentes:
- La trombólisis coronaria rápida y persistente es crucial para obtener resultados óptimos.
- La activación plaquetaria y la actividad de la trombina están implicadas en el retraso de la trombólisis y la reoclusión.
- Los distintos roles de las plaquetas y la trombina en estos procesos requieren una mayor aclaración.
Objetivo del estudio:
- Investigar el impacto de la inhibición de la función plaquetaria frente a la actividad de la trombina en la velocidad de la trombolisis y las tasas de reoclusión.
- Para comparar la eficacia de los agentes antiplaquetarios (antagonista de la glicoproteína IIb / IIIa, aspirina) y los anticoagulantes (hirudina recombinante, heparina) cuando se usan con el activador de plasminógeno de tipo tisular (t-PA).
Principales métodos:
- Los perros conscientes con trombosis coronaria inducida eléctricamente recibieron t-PA. por vía intravenosa.
- Los tratamientos complementarios incluían inhibidores de las plaquetas (antagonista de la glicoproteína IIb/IIIa, aspirina) o inhibidores de la trombina (hirudina recombinante, heparina).
- Se evaluó el tiempo de trombolisis y la incidencia de reoclusión.
Principales resultados:
- La aspirina acortó el tiempo de trombolisis con t-PA; el antagonista de la glicoproteína IIb/IIIa no lo hizo.
- Ambos agentes antiplaquetarios retrasaron pero no impidieron consistentemente la reoclusión.
- La hirudina recombinante aceleró significativamente la trombolisis y evitó la reoclusión en todos los perros.
- La heparina no mejoró la trombolisis ni impidió la reoclusión.
Conclusiones:
- La inhibición de la trombina con hirudina recombinante es altamente efectiva para facilitar la trombólisis coronaria y mantener la permeabilidad de los vasos después del tratamiento con t-PA.
- Los beneficios de la hirudina pueden deberse a su actividad anticoagulante y a la reducción secundaria de la activación plaquetaria.
- Dirigir la trombina ofrece una estrategia superior para mejorar la terapia trombolítica en comparación con la inhibición exclusiva de las plaquetas o el uso de heparina.
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