Sacks F M, Pasternak R C, Gibson C M, Rosner B, Stone P H
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
Lancet. 1994 Oct 29;344(8931):1182-6. doi: 10.1016/s0140-6736(94)90506-1.
Lipid-lowering therapy ameliorates coronary atherosclerosis in patients with raised concentrations of low-density-lipoprotein (LDL) cholesterol. We have investigated whether a similar benefit can be obtained in normocholesterolaemic patients. We studied 79 normocholesterolaemic patients with coronary heart disease (70 male, 9 female), mean age 58 years, all non-smokers, with mean total cholesterol concentration 5.5 mmol/L. All patients received diet therapy and were randomly assigned placebo (39) or active treatment (40) with pravastatin, nicotinic acid, cholestyramine, and gemfibrozil stepwise as needed to reach the specified goal (total cholesterol < or = 4.1 mmol/L, ratio of LDL/high-density-lipoprotein [HDL] cholesterol < or = 2.0). Coronary angiograms at baseline and after 2.5 years of treatment were analysed by computer-assisted quantitative techniques. There was no significant difference in coronary atherosclerosis during follow-up between the active treatment and placebo groups; the mean minimum diameter narrowed significantly but to the same extent in both groups (change baseline to 2.5 years 0.14 [SD 0.42] and 0.15 [0.42] mm, respectively, both p < 0.001). Similarly, the change in percentage stenosis did not differ between the groups (2.1 [10.6] vs 2.4 [10.3]%). By multiple regression analysis, the adjusted difference between the groups was a 0.04 mm (95% CI -0.04 to 0.12 mm) increase in minimum diameter and a 0% (-1.7 to 1.7) change in percentage stenosis. The groups differed significantly in plasma lipids (% change in active minus % change in placebo group: -28% total cholesterol, -41% LDL-cholesterol, 13% HDL-cholesterol, -26% triglycerides, -31% apolipoprotein B, all p < 0.001). Thus, intensive pharmacological treatment of normocholesterolaemic patients has significant effects on plasma lipid concentrations but no angiographically measurable benefit on the coronary arteries.
降脂治疗可改善低密度脂蛋白（LDL）胆固醇浓度升高患者的冠状动脉粥样硬化。我们研究了在血脂正常的患者中是否也能获得类似益处。我们研究了79例血脂正常的冠心病患者（70例男性，9例女性），平均年龄58岁，均不吸烟，平均总胆固醇浓度为5.5 mmol/L。所有患者均接受饮食治疗，并随机分配接受安慰剂治疗（39例）或使用普伐他汀、烟酸、考来烯胺和吉非贝齐进行积极治疗（40例），根据需要逐步调整治疗，以达到规定目标（总胆固醇≤4.1 mmol/L，LDL/高密度脂蛋白[HDL]胆固醇比值≤2.0）。采用计算机辅助定量技术分析治疗2.5年前后的冠状动脉造影。积极治疗组和安慰剂组在随访期间冠状动脉粥样硬化无显著差异；两组平均最小直径均显著缩小，但缩小程度相同（基线至2.5年的变化分别为0.14[标准差0.42]和0.15[0.42]mm，均p<0.001）。同样，两组狭窄百分比的变化也无差异（2.1[10.6]%对2.4[10.3]%）。通过多元回归分析，两组间经调整后的差异为最小直径增加0.04 mm（95%可信区间-0.04至0.12 mm），狭窄百分比变化为0%（-1.7至1.7）。两组血浆脂质有显著差异（积极治疗组变化百分比减去安慰剂组变化百分比：总胆固醇-28%，LDL胆固醇-41%，HDL胆固醇13%，甘油三酯-26%，载脂蛋白B-31%，均p<0.001）。因此，对血脂正常的患者进行强化药物治疗对血浆脂质浓度有显著影响，但对冠状动脉造影无明显可测量的益处。
