farmacología cardiovascular 60 | mayo de 2024servó regresión de la placa en el 50% de los sujetos con EPAmás estatinas frente al 24% en el grupo de estatinas solas(55). Por el contrario, cuando se utilizó una mezcla de ácidosgrasos omega-3 (EPA + DHA) en diversos ensayos clínicos, nose observaron los beneficios (56-57).Se han revisado las posibles diferencias mecanísticas entreEPA y DHA: la longitud más corta y posiblemente el menornúmero de dobles enlaces de EPA permite una mayor intercalaciónde EPA en la bicapa de membrana de las células delmúsculo liso vascular, lo que resulta en más efectos antioxidantesy menos fluidez/inestabilidad de la membrana, inhibiendoasí la formación excesiva de colesterol en la membranacelular. Por el contrario, una mayor longitud de hidrocarburodel DHA provoca una intercalación deficiente en la bicapa dela membrana celular, y conduce a la formación de cristales decolesterol, que pueden dañar los macrófagos y la integridadde la membrana celular. En un modelo murino reciente sedemostró que el EPA reducía el espesor de la íntima-media delas placas ricas en macrófagos y estaba más concentrado enlas placas de capa delgada que en las de capa gruesa, mientrasque el DHA se distribuía más uniformemente en ambostipos de placas. Estas diferencias pueden, al menos en parte,explicar los hallazgos dispares entre los desenlaces CV observadosen los ensayos clínicos de EPA puro (IPE) y ensayos similarespero que usaron ácidos grasos omega-3 que contienenDHA y EPA (58-61).ConclusionesHemos revisado las características del icosapento de etilo, ycomprobamos que presenta características diferentes al restode las estrategias basadas en omega-3 para la reducción deeventos CV. 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