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Glicoproteína plaquetaria IIIa Pl ((a) polimorfismo, fibrinógeno y agregabilidad plaquetaria: El estudio del corazón
D Feng1, K Lindpaintner, M G Larson
1Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Boston, MA, USA. dfeng2@caregroup.harvard.edu
Circulation
|July 12, 2001
Resumen
Los niveles plasmáticos de fibrinógeno aumentan la agregación plaquetaria, pero este efecto depende del genotipo Pl(A). Esta interacción entre el gen y el entorno puede explicar los hallazgos contradictorios sobre el riesgo de enfermedad cardiovascular asociado con el alelo Pl(A2).
Área de la Ciencia:
- Genética cardiovascular genética cardiovascular
- Biología de las plaquetas Biología de las plaquetas
- Interacciones entre genes y medio ambiente.
Sus antecedentes:
- El alelo Pl(A2) del receptor de la glicoproteína IIIa plaquetaria es un factor de riesgo potencial de enfermedad cardiovascular.
- Los hallazgos anteriores sobre Pl(A2) y la agregabilidad plaquetaria son contradictorios, ya que algunos muestran un aumento de la agregación y otros una reducción de la unión al fibrinógeno.
- El fibrinógeno es un mediador clave de la agregación plaquetaria.
Objetivo del estudio:
- Para investigar la hipótesis de que los niveles plasmáticos de fibrinógeno interactúan con el genotipo Pl(A) en la modulación de la agregabilidad plaquetaria.
- Para aclarar la relación entre el genotipo Pl(A), los niveles de fibrinógeno y la función plaquetaria en el riesgo de enfermedad cardiovascular.
Principales métodos:
- Se evaluó el genotipo Pl(A), los niveles plasmáticos de fibrinógeno y la agregabilidad plaquetaria en 1340 participantes del Framingham Offspring Study.
- Se midió la agregabilidad plaquetaria utilizando el método Born, evaluando la agregación inducida por epinefrina y ADP.
- Se analizó la interacción entre los niveles de fibrinógeno y el genotipo Pl(A) en la agregación plaquetaria.
Principales resultados:
- Los niveles más altos de fibrinógeno en plasma se correlacionaron con un aumento de la agregación plaquetaria inducida por epinefrina (P=0,002) y una tendencia a la agregación inducida por ADP (P=0,07).
- Esta asociación entre el fibrinógeno y la agregación plaquetaria fue específica para el genotipo Pl(A1/A1) (P=0.0005 para la epinefrina, P=0.03 para la ADP).
- No se observó una asociación significativa entre los niveles de fibrinógeno y la agregación plaquetaria en individuos positivos para PlA2 (P>0,90).
Conclusiones:
- Los niveles elevados de fibrinógeno en plasma mejoran la agregabilidad plaquetaria.
- El efecto del fibrinógeno en la agregación plaquetaria depende del genotipo Pl (A) del individuo.
- Esta interacción genético-ambiental específica del genotipo puede conciliar hallazgos contradictorios sobre el alelo Pl (A) y la función plaquetaria, ofreciendo información sobre la patogénesis de las enfermedades cardiovasculares.
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