Lipoprotein(a): fasting and nonfasting levels, inflammation, and cardiovascular risk

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.