Farrer M, Game F L, Albers C J, Neil H A, Winocour P H, Laker M F, Adams P C, Alberti K G
Department of Cardiology, Royal Victoria Infirmary, Newcastle upon Tyne.
BMJ. 1993 Oct 2;307(6908):832-6. doi: 10.1136/bmj.307.6908.832.
To examine whether impaired glucose tolerance and raised Lp(a) lipoprotein concentrations are associated in subjects with coronary artery disease.
Study of two subject populations, one with and one without symptomatic coronary artery disease. Case-control analysis of patients with impaired glucose tolerance and normal glucose tolerance performed in each subject population independently.
A general practice and a hospital ward in Newcastle upon Tyne.
517 apparently healthy subjects, 13 with impaired glucose tolerance, and 245 patients who had undergone coronary artery bypass graft surgery 12 months before, 51 with impaired glucose tolerance.
Serum Lp(a) lipoprotein concentration, plasma glucose concentration before and after oral challenge with 75 g glucose monohydrate, and Lp(a) lipoprotein isoforms.
In both the asymptomatic subjects and the subjects with coronary artery disease there was no significant difference between subjects with impaired glucose tolerance and subjects with normal and body mass index in serum Lp(a) lipoprotein concentrations (geometric mean 61 (geometric SD 4) mg/l v 83 (5) mg/l for asymptomatic subjects, 175 (3) v 197 (2) for subjects with heart disease), nor was there any difference in the proportion of subjects who had Lp(a) lipoprotein concentrations > 300 mg/l (31% v 23% for asymptomatic subjects, 37% v 37% for subjects with heart disease). For both subject groups there was no significant correlation between Lp(a) lipoprotein concentration and plasma glucose concentration after a glucose tolerance test, nor did Lp(a) lipoprotein concentration vary by quintile of glucose concentration after the test. Examination of Lp(a) lipoprotein isoforms in the subjects with coronary artery disease revealed an inverse relation between isoform size and plasma Lp(a) lipoprotein concentration, but there was no evidence that impaired glucose tolerance was associated with particular Lp(a) lipoprotein isoforms.
Raised Lp(a) lipoprotein concentrations are not responsible for the association between impaired glucose tolerance and coronary artery disease.
研究糖耐量受损与升高的脂蛋白(a)[Lp(a)]浓度在冠心病患者中是否相关。
对两组研究对象进行研究,一组有症状性冠心病,另一组无。在每组研究对象中独立地对糖耐量受损和糖耐量正常的患者进行病例对照分析。
泰恩河畔纽卡斯尔的一家普通诊所和一个医院病房。
517名表面健康的研究对象,其中13名糖耐量受损;245名在12个月前接受过冠状动脉搭桥手术的患者,其中51名糖耐量受损。
血清Lp(a)脂蛋白浓度、口服75 g一水葡萄糖前后的血浆葡萄糖浓度以及Lp(a)脂蛋白亚型。
在无症状研究对象和冠心病患者中,糖耐量受损的研究对象与糖耐量正常且体重指数正常的研究对象相比,血清Lp(a)脂蛋白浓度无显著差异(无症状研究对象的几何均数为61(几何标准差4)mg/L,而糖耐量正常者为83(5)mg/L;心脏病患者为175(3)mg/L,而糖耐量正常者为197(2)mg/L),Lp(a)脂蛋白浓度>300 mg/L的研究对象比例也无差异(无症状研究对象中为31%,而糖耐量正常者中为23%;心脏病患者中为37%,而糖耐量正常者中为37%)。对于两组研究对象,糖耐量试验后Lp(a)脂蛋白浓度与血浆葡萄糖浓度之间均无显著相关性,且试验后Lp(a)脂蛋白浓度也不会因葡萄糖浓度的五分位数不同而有所变化。对冠心病患者的Lp(a)脂蛋白亚型进行检测发现,亚型大小与血浆Lp(a)脂蛋白浓度呈负相关,但没有证据表明糖耐量受损与特定的Lp(a)脂蛋白亚型相关。
升高的Lp(a)脂蛋白浓度并非糖耐量受损与冠心病之间关联的原因。