La congestión, tanto sistémica como pulmonar, juega un papel determinante en la mediación del daño o disfunción orgánica, durante las descompensaciones de la insuficiencia cardiaca (IC). La activación inmune o de mecanismos inflamatorios puede generar concentraciones circulantes detectables de algunos biomarcadores que podrían estar relacionados con el daño tisular y por consiguiente con el pronóstico.
La congestión pulmonar podría estimular la actividad macrofágica alveolar y la sistémica generar una pérdida de eficacia de la mucosa intestinal y permitir el paso de endotoxinas al torrente circulatorio con la consiguiente activación inmune.
Postulamos que la Enzima Conversora de Angiotensina (ECA) procedente de los macrófagos alveolares y la Procalcitonina (PCT) como expresión de la pérdida de la función de barrera del epitelio intestinal, son marcadores subrogados de gravedad durante los episodios de descompensación de IC.
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