Lye M, Valacio R, Reckless J P, Ghosh A K, Findlay I N, Ghosh M K, Passmore A P, Fulcher R A
University Clinical Department of Geriatric Medicine, Royal Liverpool Hospital, UK.
Coron Artery Dis. 1998;9(9):583-90.
Coronary heart disease is a major cause of morbidity and mortality in the elderly, a rapidly growing section of the population. Elderly patients have been excluded from most preventative risk factor trials.
We evaluated fluvastatin, a fully synthetic hydroxymethyl glutaryl coenzyme A reductase inhibitor, in white patients older than 60 years, in seven hospital centres. After an 8-week cholesterol-decreasing diet phase, patients were allocated to groups to receive fluvastatin 40 mg daily (n = 33) or placebo (n = 36) given for 12 weeks. All patients had low-density lipoprotein cholesterol concentrations > or = 4.1 mmol/l 1 week before they were allocated to a treatment at random. After receiving randomised treatment for 12 weeks, 50 patients then received fluvastatin 40 mg daily on an open basis for a further 12 weeks.
Mean +/- SD age was 70.7 +/- 5.2 years for fluvastatin patients and 68.3 +/- 5.6 years for placebo. Mean +/- SD percentage changes in lipid concentrations from randomisation to the end of 12 weeks were calculated (n = 63) by intent-to-treat analysis. Total cholesterol decreased by 21.64 +/- 8.7% in the fluvastatin group and by 2.91 +/- 7.25% in the placebo group (P < 0.01); high-density lipoprotein cholesterol increased by 4.98 +/- 10.84% in the fluvastatin group and decreased by 0.05 +/- 8.68% in the placebo group (P = 0.05); low-density lipoprotein cholesterol decreased by 27.14 +/- 8.45% in the fluvastatin group and by 2.16 +/- 9.68% in the placebo group (P < 0.01); very-low-density lipoprotein cholesterol decreased by 30.70 +/- 30.65% in the fluvastatin group and by 9.80 +/- 28.6% in the placebo group (P < 0.01); triglyceride decreased by 18.13 +/- 17.35% in the fluvastatin group and by 2.97 +/- 21.85% in the placebo group (P < 0.01). There were no statistically significant differences between treatment groups for any other biochemical or haematological parameters. Adverse events were mainly mild, diminishing with continued treatment, and no event was serious by standard criteria. Patient-assessed tolerability after randomised treatment was 'very good' for 18 fluvastatin patients and for 26 placebo patients (P = 0.79). Seven patients withdrew from the 12-week follow-up (four from the fluvastatin group and three from the placebo group).
We conclude that fluvastatin decreases lipid concentrations effectively and safely in elderly patients, producing clinically significant decreases in total cholesterol, low-density lipoprotein cholesterol, triglyceride and, especially, very-low-density lipoprotein cholesterol, while increasing high-density lipoprotein cholesterol moderately.
冠心病是老年人发病和死亡的主要原因，而老年人群数量正在迅速增长。大多数预防性危险因素试验都将老年患者排除在外。
我们在7个医院中心对60岁以上的白人患者评估了氟伐他汀，一种完全合成的羟甲基戊二酰辅酶A还原酶抑制剂。在经过8周的降低胆固醇饮食阶段后，患者被随机分组，分别接受每日40毫克氟伐他汀治疗（n = 33）或安慰剂治疗（n = 36），为期12周。所有患者在随机分配接受治疗前1周的低密度脂蛋白胆固醇浓度均≥4.1毫摩尔/升。在接受随机治疗12周后，50名患者随后以开放方式继续接受每日40毫克氟伐他汀治疗，为期12周。
氟伐他汀组患者的平均±标准差年龄为70.7±5.2岁，安慰剂组为68.3±5.6岁。通过意向性分析计算了从随机分组到12周结束时脂质浓度的平均±标准差百分比变化（n = 63）。氟伐他汀组总胆固醇下降了21.64±8.7%，安慰剂组下降了2.91±7.25%（P < 0.01）；氟伐他汀组高密度脂蛋白胆固醇增加了4.98±10.84%，安慰剂组下降了0.05±8.68%（P = 0.05）；氟伐他汀组低密度脂蛋白胆固醇下降了27.14±8.45%，安慰剂组下降了2.16±9.68%（P < 0.01）；氟伐他汀组极低密度脂蛋白胆固醇下降了30.70±30.65%，安慰剂组下降了9.80±28.6%（P < 0.01）；氟伐他汀组甘油三酯下降了18.13±17.35%，安慰剂组下降了2.97±21.85%（P < 0.01）。治疗组之间在任何其他生化或血液学参数上均无统计学显著差异。不良事件主要为轻度，随着持续治疗而减轻，按照标准标准没有严重事件。随机治疗后患者评估的耐受性，18名氟伐他汀患者和26名安慰剂患者为“非常好”（P = 0.79）。7名患者退出了12周的随访（4名来自氟伐他汀组，3名来自安慰剂组）。
我们得出结论，氟伐他汀在老年患者中能有效且安全地降低脂质浓度，使总胆固醇、低密度脂蛋白胆固醇、甘油三酯尤其是极低密度脂蛋白胆固醇出现具有临床意义的下降，同时适度增加高密度脂蛋白胆固醇。
