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• W2015390056 abstract "Las estatinas mejoran la estabilidad de la placa al disminuir la actividad inflamatoria. Hemos analizado el efecto de un ciclo corto de tratamiento con altas dosis de atorvastatina sobre la inflamación de la placa de ateroma carotídea humana. Veinte pacientes programados para endarterectomía carotídea electiva, y sin tratamiento previo con estatinas, fueron asignados aleatoriamente en el momento de la indicación quirúrgica para recibir atorvastatina 80 mg/día (n = 11) o no estatinas (n = 9) hasta el día de la cirugía (1 mes). En las placas extraídas durante la endarterectomía se analizaban el infiltrado de macrófagos, y la expresión de MCP-1 (monocyte chemoattractant protein-1) y ciclooxigenasa-2 (COX-2) por inmunohistoquímica. La activación de NF-?B se estudió con la técnica de Southwestern. La atorvastatina disminuyó las concentraciones de colesterol total (118 ± 10 frente a 191 ± 10 mg/dl; p = 0,016) y de lipoproteínas de baja densidad (LDL) (63 ± 9 frente a 125 ± 9 mg/dl; p = 0,038), mientras que no hubo cambios en el grupo control. Los triglicéridos y las lipoproteínas de alta densidad (HDL) no variaron significativamente en ningún grupo. Las placas ateroscleróticas del grupo de atorvastatina presentaron una reducción significativa del infiltrado de macrófagos (2,5 ± 1% frente a 9,3 ± 2,4%; p < 0,05), y de la expresión de MCP-1 (11 ± 1% frente a 24 ± 4%; p < 0,05) y COX-2 (16 ± 2,3% frente a 34 ± 4,4%; p < 0,05). El número de núcleos con actividad de NF-κB era menor en las placas de los pacientes que recibieron atorvastatina que en los que no recibieron tratamiento (5.706 ± 1.260 frente a 8.063 ± 1.308; p < 0,05). El tratamiento intensivo con atorvastatina disminuye la inflamación en las placas de aterosclerosis carotídea humana en sólo 1 mes. Statins improve plaque stability by diminishing inflammatory activity. We analyzed the effect of short-term high-dose atorvastatin on plaque inflammation in human carotid atherosclerosis. Twenty patients scheduled to undergo elective carotid endarterectomy without previous statin treatment were randomized at the time of surgical indication to receive either atorvastatin 80 mg/day (n = 11) or no statins (n = 9) until surgery (1 month later). Atherosclerotic plaques were analyzed by immunohistochemistry to investigate macrophage infiltrate, and expression of monocyte chemoattractant protein-1 (MCP-1) and cyclooxygenase-2 (COX-2). In addition, nuclear factor-κB (NF-κB) activity was studied by Southwestern histochemistry. Atorvastatin decreased serum levels of total cholesterol (118 ± 10 versus 191 ± 10 mg/dl; p = 0.016) and low-density lipoprotein (63 ± 9 versus 125 ± 9 mg/dl; p = 0.038), while no changes were noted in the control group. Triglycerides and highdensity lipoprotein showed no significant changes in either of the two groups. Carotid atherosclerotic plaques from the atorvastatin group demonstrated a significant reduction in macrophage infiltration (2.5 ± 1% versus 9.3 ± 2.4%; p < 0.05) and expression of MCP-1 (11 ± 1% versus 24 ± 4%; p < 0.05) and COX-2 (16 ± 2.3% versus 34 ± 4.4%; p < 0.05). The number of nuclei active for NF-?B was lower in plaques from patients that received atorvastatin than in those from the non-treated group (5,706 ± 1,260 versus 8063 ± 1,308; p < 0.05). Intensive atorvastatin therapy decreases inflammatory activity in human carotid atherosclerotic plaques in as little as 1 month." @default.
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• W2015390056 date "2006-02-01" @default.
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• W2015390056 title "El tratamiento con dosis altas de atorvastatina disminuye la inflamación en la aterosclerosis carotídea humana" @default.
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• W2015390056 doi "https://doi.org/10.1016/s0214-9168(06)73648-8" @default.
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