血脂醇和普伐他汀对老年高胆固醇血症患者血脂、血小板聚集和内皮的影响。

G Castaño, R Más, M L Arruzazabala, M Noa, J Illnait, J C Fernández, V Molina, A Menéndez
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引用次数: 0

摘要

这项随机、双盲研究比较了10 mg/天给药的胆甾醇和普伐他汀对老年II型高胆固醇血症和高冠状动脉风险患者血脂、血小板聚集和内皮素水平的影响。在降脂饮食6周后,低密度脂蛋白(LDL)胆固醇水平> 3.4 mmol/l的患者在双盲条件下随机接受10 mg的糖醇或普伐他汀片,随晚餐服用,为期8周。低密度脂蛋白胆固醇(LDL-cholesterol, 19.3%)、总胆固醇(total cholesterol, 13.9%)、低密度脂蛋白胆固醇/高密度脂蛋白胆固醇(HDL -cholesterol, 28.3%)、总胆固醇/高密度脂蛋白胆固醇(total cholesterol, HDL-cholesterol, 24.4%)比值显著降低(p < 0.00001)。普伐他汀显著(p < 0.00001)降低ldl -胆固醇(15.6%)、总胆固醇(11.8%)和ldl -胆固醇/ hdl -胆固醇(18.9%)、总胆固醇/ hdl -胆固醇(15.7%)的比值(p < 0.0001)。而非普伐他汀显著提高(p < 0.001)高密度脂蛋白胆固醇水平(18.4%),降低(p < 0.01)甘油三酯水平(14.1%)。甘草甾醇对所有激动剂诱导的血小板聚集的抑制作用均优于普伐他汀(p < 0.05),其中花生四烯酸1.5和3 mmol/l诱导的血小板聚集分别显著降低42.2%和69.5% (p < 0.0001),胶原0.5微克/ml诱导的血小板聚集(p < 0.05)(16.6%)和二磷酸腺苷1 μ mol/l诱导的血小板聚集(p < 0.01)(20.3%)。普伐他汀仅能显著降低花生四烯酸3 mmol/l诱导的血小板聚集(p < 0.001)(27%)。两种药物均显著降低(p < 0.00001)内皮水平,但终值显著低于普伐他汀组(p < 0.001)。两种治疗方法都是安全且耐受性良好的。普伐他汀显著(p < 0.01)提高了血清丙氨酸胺转移酶水平,但个体水平维持在正常范围内。两名服用普伐他汀的患者因不良经历(分别为心肌梗死和黄疸)而停止研究。综上所述,与相同剂量普伐他汀诱导的老年II型高胆固醇血症和冠状动脉高危患者相比,10 mg/天的胆甾醇对其血脂、血小板聚集和内皮素水平的影响更有利。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of policosanol and pravastatin on lipid profile, platelet aggregation and endothelemia in older hypercholesterolemic patients.

This randomized, double-blind study was undertaken to compare the effects of policosanol and pravastatin administered at 10 mg/day on lipid profile, platelet aggregation and endothelemia in older patients with type II hypercholesterolemia and high coronary risk. After 6 weeks on a lipid-lowering diet, patients with low-density lipoprotein (LDL) cholesterol levels > 3.4 mmol/l were randomized to receive, under double-blind conditions, policosanol or pravastatin 10 mg tablets that were taken with the evening meal for 8 weeks. Policosanol significantly (p < 0.00001) lowered LDL-cholesterol (19.3%), total cholesterol (13.9%) and the ratios of LDL-cholesterol/high-density lipoprotein (HDL)-cholesterol (28.3%) and total cholesterol/HDL-cholesterol (24.4%). Pravastatin significantly (p < 0.00001) lowered LDL-cholesterol (15.6%), total cholesterol (11.8%) and the ratios (p < 0.0001) of LDL-cholesterol/HDL-cholesterol (18.9%) and total cholesterol/HDL-cholesterol (15.7%). Policosanol, but not pravastatin, significantly increased (p < 0.001) levels of HDL-cholesterol (18.4%) and reduced (p < 0.01) triglycerides (14.1%). Policosanol was more effective (p < 0.05) than pravastatin in inhibiting platelet aggregation induced by all agonists and it significantly reduced (p < 0.0001) platelet aggregation induced by arachidonic acid at 1.5 and 3 mmol/l by 42.2% and 69.5%, respectively, platelet aggregation induced by collagen 0.5 microgram/ml (p < 0.05) (16.6%) and that induced by adenosine diphosphate 1 mumol/l (p < 0.01) (20.3%). Pravastatin significantly reduced (p < 0.001) (27%) only platelet aggregation induced by arachidonic acid 3 mmol/l. Both drugs significantly decreased (p < 0.00001) endothelemia levels but final values were significantly lower (p < 0.001) in the policosanol than in the pravastatin group. Both treatments were safe and well tolerated. Pravastatin significantly (p < 0.01) increased serum levels of alanine amine transferase but individual values remained within normal. Two patients on pravastatin discontinued the study because of adverse experiences (myocardial infarction and jaundice, respectively). In conclusion, the effects of policosanol (10 mg/day) on lipid profile, platelet aggregation and endothelemia in older patients with type II hypercholesterolemia and high coronary risk are more favorable than those induced by the same doses of pravastatin.

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