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Farmacología Cardiovascular 17

  • Text
  • Tept
  • Cardiovascular
  • Endotelial
  • Niveles
  • Controles
  • Factor
  • Pacientes
  • Marcadores
  • Vascular
  • Dmla
Publicación independiente de Farmacología y Fisiopatología cardiovascular aplicada.

farmacología

farmacología cardiovascular 17 | Julio de 2012 que a su vez son inhibidas por activación de receptores de proliferación de peroxisomas, se genera una situación de equilibrio que limita la inflamación crónica mediada por v-CAM-1 e ICAM- 1, sin afectar los fenómenos de inflamación agudos mediados por e-Selectina y la aglutinación de leucocitos (72) (figura 13), pero el balance se rompe en condiciones de estrés crónico como en TEPT a través de una elevación de niveles de e-Selectina, fvW y tPA (73). Dado que estas modificaciones pueden responder a múltiples desencadenantes, como factores de riesgo cardiovascular, artritis reumatoidea, trastornos endocrinos y metabólicos, incluso hábitos de salud como tabaquismo, sedentarismo, consumo de alcohol y obesidad, además de edad y género (74), se tuvo en cuenta aparear la muestra clínica por edad y género con controles sanos. Por otra parte, la asociación de MMP-9, TEPT y ateromatosis, pareciera representar un proceso más tardío, ya que alteran la estabilidad de la placa fibrosa, disolviendo los puentes de colágeno y disminuyendo su síntesis, con el riesgo subsecuente de formación de trombos y eventos isquémicos agudos (75). Esto podría explicar en parte los valores bajos de estos marcadores, así como de TIM-1, y la ausencia de significación estadística para las diferencias entre ambos grupos de TEPT y controles. Las limitaciones del estudio surgen de la muestra relativamente pequeña, la falta de seguimiento longitudinal, y omisión de posibles factores de confusión derivados de comportamientos de riesgo no evaluados en el estudio (ej.: número de cigarrillos consumidos o ingesta de comidas con alto tenor de lípidos y sal), pero que podrían estar asociados con el comienzo de los síntomas de TEPT. Conclusiones Se puede concluir del presente estudio que hay una relación continua entre la severidad de los síntomas de TEPT y los niveles plasmáticos de marcadores de disfunción endotelial. Este vínculo puede explicar la asociación entre la probabilidad de desarrollar enfermedades cardiovasculares y aterogénesis y los eventos traumáticos conducentes a desarrollar TEPT en el nivel de la respuesta vascular inflamatoria común. Son necesarios más estudios de tipo longitudinal para valorar el posible rol antecedente del evento traumático o TEPT en el desarrollo de patología cardiovascular, así como investigar la relación de los cambios neuro-hormonales como hiperactividad simpática adrenal, disfunción del eje hipotálamo-hipófiso-suprarrenal e hipercortisolemia en la disfunción endotelial de pacientes con TEPT, ya que estos factores neuroendócrinos podrían afectar la función endotelial de manera directa o indirecta. Referencias bibliográficas 1. López-Ibor AJJ, Valdés-Miyar, M (dir.) 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