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La formación de trombos en placas ateroscleróticas rotas y la retrombosis en el desarrollo de trombos
L Badimon1, J H Chesebro, J J Badimon
1Cardiovascular Biology Research, Massachusetts General Hospital, Harvard Medical School, Boston 02114.
Circulation
|December 1, 1992
Resumen
La ruptura de la placa en la enfermedad de la arteria coronaria conduce a la formación de trombos. Los factores locales y sistémicos influyen en este proceso, y el trombo residual puede causar reoclusión, incluso con anticoagulación.
Área de la Ciencia:
- Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular
- La trombosis y la hemostasis.
- La patogénesis y la patogénesis de la aterosclerosis.
Sus antecedentes:
- La angina inestable y el infarto de miocardio a menudo implican estenosis coronarias excéntricas con bordes irregulares, lo que indica placas ateroscleróticas rotas y trombosis.
- La angioscopia y la autopsia confirman la ruptura de la placa y la formación de trombos como eventos clave en los síndromes coronarios agudos.
Objetivo del estudio:
- Investigar los factores locales y sistémicos que influyen en la trombogenicidad después de la ruptura de la placa aterosclerótica.
- Comprender el papel del trombo residual en la reoclusión y la eficacia de la anticoagulación.
Principales métodos:
- Simulación de la ruptura de la placa y la trombosis utilizando una cámara de perfusión ex vivo.
- Procesos trombóticos estudiados en un modelo porcino in vivo.
- Se utilizó la hirudina recombinante para investigar el papel de la trombina en la retrombosis.
Principales resultados:
- La ruptura de la placa expone sustratos, lo que lleva a la formación de trombos proporcional al daño.
- Las altas tasas de cizallamiento en las lesiones estenoticas mejoran la deposición de plaquetas y el crecimiento de trombos.
- Los factores sistémicos como la epinefrina, el colesterol y el deterioro de la fibrinólisis pueden aumentar la trombogenicidad.
- El trombo residual contribuye significativamente a la reoclusión, incluso en sangre heparinizada.
- La trombina unida a la fibrina dentro del trombo original juega un papel en la retrombosis.
Conclusiones:
- Los factores locales de la pared vascular (sustrato expuesto, dinámica de fluidos) y los factores sistémicos (hormonas, lípidos, fibrinólisis) modulan críticamente la trombogenicidad después de la ruptura de la placa.
- El trombo residual es una potente superficie trombogénica, que contribuye a la reoclusión.
- Dirigirse a la trombina unida a la fibrina puede ser una estrategia para prevenir la reoclusión.
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