Ericsson C G, Hamsten A, Nilsson J, Grip L, Svane B, de Faire U
Division of Cardiology, Department of Medicine, Danderyd Hospital, Stockholm, Sweden.
Lancet. 1996 Mar 30;347(9005):849-53. doi: 10.1016/s0140-6736(96)91343-4.
Bezafibrate has effects on lipid metabolism and haemostatic function. We undertook a double-blind, placebo-controlled intervention trial, the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT), to establish whether bezafibrate (200 mg three times daily) could retard or prevent the progression of atherosclerotic lesions in dyslipidaemic male survivors of myocardial infarction who were younger than 45 years at the time of the event.
92 patients completed an initial 3-month period of dietary intervention and were randomly assigned to treatment with bezafibrate or placebo. Dietary intervention continued throughout the trial. Coronary angiography was done at baseline and after 2 and 5 years. 81 patients (42 bezafibrate treated and 39 placebo treated) who underwent baseline angiography and at least one post-treatment angiogram were included in the efficacy analysis. The primary endpoint was change in mean minimum lumen diameter.
The mean minimum lumen diameter decreased from baseline to the last angiographic assessment (2 or 5 years) by 0.06 mm (95% CI 0.15 reduction to 0.01 increase) in the bezafibrate group and by 0.17 mm (0.33 reduction to 0.09 increase) in the placebo group. The treatment effect was therefore 0.13 mm (95% CI 0.10 to 0.15; p=0.049). Parallel treatment effects, although not statistically significant, were observed for the secondary angiographic endpoints (mean segment diameter 0.02 mm [0.01-0.04] and percentage stenosis -3.41% [-4.00 to -2.98]). The cumulative coronary event rate was significantly lower among bezafibrate-treated than among placebo-treated patients (three vs 11 patients; p=0.02). There were significant treatment effects of bezafibrate for serum concentrations of cholesterol (-9%; p<0.001), very-low-density-lipoprotein (VLDL) cholesterol (-35%; p<0.001), serum triglycerides (-31%; p<0.001), VLDL triglycerides (-37%; p<0.001), and plasma fibrinogen (-12%; p=0.001), whereas low-density (LDL) cholesterol concentrations did not change. High density lipoprotein (HDL) cholesterol increased significantly with bezafibrate (9%; p=0.02).
The results show that bezfibrate improves dyslipidaemia, lowers plasma fibrinogen, slows the progression of focal coronary atherosclerosis, and reduces coronary events in young survivors of myocardial infarction.
苯扎贝特对脂质代谢和止血功能有影响。我们开展了一项双盲、安慰剂对照干预试验，即苯扎贝特冠状动脉粥样硬化干预试验（BECAIT），以确定苯扎贝特（每日三次，每次200毫克）是否能延缓或预防心肌梗死血脂异常男性幸存者（事件发生时年龄小于45岁）动脉粥样硬化病变的进展。
92例患者完成了初始3个月的饮食干预，并被随机分配接受苯扎贝特或安慰剂治疗。整个试验期间饮食干预持续进行。在基线时以及2年和5年后进行冠状动脉造影。81例患者（42例接受苯扎贝特治疗，39例接受安慰剂治疗）接受了基线血管造影和至少一次治疗后血管造影，纳入疗效分析。主要终点是平均最小管腔直径的变化。
从基线到最后一次血管造影评估（2年或5年），苯扎贝特组平均最小管腔直径减少了0.06毫米（95%CI为减少0.15至增加0.01），安慰剂组减少了0.17毫米（减少0.33至增加0.09）。因此，治疗效果为0.13毫米（95%CI为0.10至0.15；p=0.049）。对于次要血管造影终点（平均节段直径0.02毫米[0.01 - 0.04]和狭窄百分比 - 3.41%[-4.00至 - 2.98]）观察到了平行的治疗效果，尽管无统计学意义。苯扎贝特治疗组的累积冠状动脉事件发生率显著低于安慰剂治疗组（3例对11例患者；p=0.02）。苯扎贝特对血清胆固醇浓度（-9%；p<0.001）、极低密度脂蛋白（VLDL）胆固醇（-35%；p<0.001）、血清甘油三酯（-31%；p<0.001）、VLDL甘油三酯（-37%；p<0.001）和血浆纤维蛋白原（-12%；p=0.001）有显著治疗效果，而低密度（LDL）胆固醇浓度未改变。高密度脂蛋白（HDL）胆固醇在苯扎贝特治疗后显著升高（9%；p=0.02）。
结果表明，苯扎贝特可改善血脂异常，降低血浆纤维蛋白原，减缓局灶性冠状动脉粥样硬化的进展，并减少心肌梗死年轻幸存者的冠状动脉事件。
