Ruotolo G, Ericsson C G, Tettamanti C, Karpe F, Grip L, Svane B, Nilsson J, de Faire U, Hamsten A
Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Hospital, Stockholm, Sweden.
J Am Coll Cardiol. 1998 Nov 15;32(6):1648-56. doi: 10.1016/s0735-1097(98)00442-2.
To investigate the mechanisms by which bezafibrate retarded the progression of coronary lesions in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT), we examined the relationships of on-trial lipoproteins and lipoprotein subfractions to the angiographic outcome measurements.
BECAIT, the first double-blind, placebo-controlled, randomized serial angiographic trial of a fibrate compound, showed that progression of focal coronary atherosclerosis in young survivors of myocardial infarction could be retarded by bezafibrate treatment.
A total of 92 dyslipoproteinemic men who had survived a first myocardial infarction before the age of 45 years were randomly assigned to treatment for 5 years with bezafibrate (200 mg three times daily) or placebo; 81 patients underwent baseline and at least one post-treatment coronary angiography.
In addition to the decrease in very low density lipoprotein (VLDL) cholesterol (-53%) and triglyceride (-46%) and plasma apolipoprotein (apo) B (-9%) levels, bezafibrate treatment resulted in a significant increase in high density lipoprotein-3 (HDL3) cholesterol (+9%) level and a shift in the low density lipoprotein (LDL) subclass distribution toward larger particle species (peak particle diameter +032 nm). The on-trial HDL3 cholesterol and plasma apo B concentrations were found to be independent predictors of the changes in mean minimum lumen diameter (r=-0.23, p < 0.05), and percent (%) stenosis (r = 0.30, p < 0.01), respectively. Decreases in small dense LDL and/or VLDL lipid concentrations were unrelated to disease progression.
Our results suggest that the effect of bezafibrate on progression of focal coronary atherosclerosis could be at least partly attributed to a rise in HDL3 cholesterol and a decrease in the total number of apo B-containing lipoproteins.
为研究在苯扎贝特冠状动脉粥样硬化干预试验(BECAIT)中苯扎贝特延缓冠状动脉病变进展的机制,我们检测了试验期间脂蛋白及脂蛋白亚组分与血管造影结果测量值之间的关系。
BECAIT是第一项关于贝特类化合物的双盲、安慰剂对照、随机系列血管造影试验,结果显示苯扎贝特治疗可延缓年轻心肌梗死幸存者局灶性冠状动脉粥样硬化的进展。
共有92名45岁之前首次发生心肌梗死的血脂异常男性被随机分配接受苯扎贝特(每日三次,每次200mg)或安慰剂治疗5年;81名患者接受了基线及至少一次治疗后的冠状动脉造影。
除极低密度脂蛋白(VLDL)胆固醇(-53%)、甘油三酯(-46%)和血浆载脂蛋白(apo)B(-9%)水平降低外,苯扎贝特治疗还使高密度脂蛋白3(HDL3)胆固醇水平显著升高(+9%),并使低密度脂蛋白(LDL)亚类分布向更大颗粒类型转变(峰值颗粒直径+0.32nm)。试验期间的HDL3胆固醇和血浆apo B浓度分别被发现是平均最小管腔直径变化(r=-0.23,p<0.05)和狭窄百分比(%)(r=0.30,p<0.01)的独立预测因素。小而密LDL和/或VLDL脂质浓度的降低与疾病进展无关。
我们的结果表明,苯扎贝特对局灶性冠状动脉粥样硬化进展的影响可能至少部分归因于HDL3胆固醇的升高和含apo B脂蛋白总数的减少。