Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev Hospital, Copenhagen University Hospital, Denmark; The Copenhagen City Heart Study, Frederiksberg Hospital, Copenhagen University Hospital, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
Atherosclerosis. 2014 May;234(1):95-101. doi: 10.1016/j.atherosclerosis.2014.01.049. Epub 2014 Feb 12.
There are no recommendations in guidelines on measuring lipoprotein(a) in the fasting or nonfasting state, or on the influence of inflammation. We tested the hypotheses that lipoprotein(a) levels change only minimally in response to normal food intake, and to inflammation. Also, we tested whether normal food intake or inflammation influenced lipoprotein(a)'s ability to predict ischemic heart disease.
We studied 34 829 individuals from the Danish general population using the Copenhagen General Population Study and the Copenhagen City Heart Study.
Lipoprotein(a) levels did not change in response to normal food intake: median fasting levels were 17.3 mg/dL, while median levels at 3-4 h since last meal were 19.4 mg/dL(p = 0.38). Lipoprotein(a) levels increased minimally with increasing levels of C-reactive protein(CRP): median lipoprotein(a) levels at CRP <1 mg/L were 18.0 mg/dL, while median levels at CRP >10 mg/L were 21.1 mg/dL(p < 0.001). Furthermore, highest versus lowest tertile of lipoprotein(a) at <3 h and ≥3 h since last meal was associated with a 1.4(95%CI:1.2-1.6) and 1.4(1.2-1.6) fold increased risk of ischemic heart disease(p = 0.82), and a 1.8(1.5-2.2) and 1.4(1.1-1.7) fold increased risk of myocardial infarction(p = 0.05). The corresponding odds ratios at CRP levels of <2 mg/L and ≥2 mg/L were 1.3(1.2-1.5) and 1.4(1.2-1.6)(p = 0.80) for ischemic heart disease, and 1.5(1.2-1.8) and 1.7(1.4-2.0)(p = 0.38) for myocardial infarction.
Lipoprotein(a) levels did not change in response to normal food intake, but were minimally increased at increased levels of CRP. The ability of elevated lipoprotein(a) levels to predict ischemic heart disease and myocardial infarction in the general population was not affected by normal food intake or inflammation.
目前，指南中并未就空腹或非空腹状态下脂蛋白(a)的检测，以及炎症对其的影响提出建议。我们假设脂蛋白(a)水平仅会发生微小变化以应对正常饮食摄入，以及炎症。此外，我们还检测了正常饮食摄入或炎症是否会影响脂蛋白(a)预测缺血性心脏病的能力。
我们使用哥本哈根普通人群研究和哥本哈根城市心脏研究对来自丹麦普通人群的 34829 名个体进行了研究。
脂蛋白(a)水平并未因正常饮食摄入而发生变化：禁食时的中位数水平为 17.3mg/dL，而末次进食后 3-4 小时的中位数水平为 19.4mg/dL（p=0.38）。脂蛋白(a)水平随 C 反应蛋白（CRP）水平的升高而略有升高：CRP<1mg/L 时的脂蛋白(a)中位数水平为 18.0mg/dL，而 CRP>10mg/L 时的脂蛋白(a)中位数水平为 21.1mg/dL（p<0.001）。此外，末次进食后<3 小时和≥3 小时时脂蛋白(a)水平最高与最低三分位数相比，缺血性心脏病的风险分别增加了 1.4（95%CI：1.2-1.6）和 1.4（1.2-1.6）倍（p=0.82），心肌梗死的风险分别增加了 1.8（1.5-2.2）和 1.4（1.1-1.7）倍（p=0.05）。CRP 水平<2mg/L 和≥2mg/L 时，缺血性心脏病的比值比分别为 1.3（1.2-1.5）和 1.4（1.2-1.6）（p=0.80），心肌梗死的比值比分别为 1.5（1.2-1.8）和 1.7（1.4-2.0）（p=0.38）。
脂蛋白(a)水平不会因正常饮食摄入而发生变化，但在 CRP 水平升高时会略有增加。在普通人群中，升高的脂蛋白(a)水平预测缺血性心脏病和心肌梗死的能力不受正常饮食摄入或炎症的影响。
