2023 Volume 30 Issue 1 Pages 1-2
See article vol. 30: 3-14
Dyslipidemia is one of the most important risk factors for atherosclerotic disorders. Traditionally, dyslipidemia treatment strategy is decided based on fasting serum lipid profiles. However, recent clinical guidelines in the U.S.A., Europe, and Canada endorse dyslipidemia screening using nonfasting blood samples. It is well known that triglyceride (TG) concentration increases significantly after food intake but declines gradually thereafter1). Although the cutoff value for hypertriglyceridemia is set at a higher value for nonfasting samples than for fasting samples in recent guidelines, it is likely that the interval from the last food intake to blood sampling actually affects the sensitivity of dyslipidemia.
Unlike TG, total cholesterol, low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C) are stable during the day2, 3). In any of these parameters, however, lipid test results are significantly affected by the changes in plasma volume and vascular tone3). To minimize such effects, blood samples should be taken in a sitting position after a 15-min rest2). Another option is to correct lipid concentrations with simultaneously measured albumin concentrations3). Using the data excluding the aforementioned factors, LDL-C and HDL-C concentrations were found to be the highest in the morning; the concentrations decreased significantly by 2%–6% during the day2, 3). Homogeneous assays are so reproducible that we can detect such clinically negligible reductions.
Accumulating evidence suggest that small dense LDL is more atherogenic than large buoyant LDL4). Small dense LDL can be separated from large buoyant LDL by different factors such as density, electrophoretic mobility, and particle size. However, there is no clear consensus on the definition of small dense LDL4). Among various methods, the homogeneous assay for small dense LDL-C is a highly reproducible method. It can be used to measure various samples on an automated analyzer. In this issue, Hayashi et al. clearly showed that small dense LDL-C concentration does not exhibit significant within-day variation in both controls and patients with diabetes5). Therefore, nonfasting small dense LDL-C concentration can be considered for fasting.
Recent large cohort studies in Japan and the U.S.A. have confirmed that fasting small dense LDL-C concentration is an excellent predictor of coronary heart disease, independent of LDL-C concentration6, 7). Moreover, we previously reported that casual small dense LDL-C concentration was significantly higher in patients with acute coronary syndrome (ACS) than in controls although LDL-C and TG concentrations were similar in the two groups8). Patients with ACS often receive a bolus injection of heparin and undergo emergent coronary angioplasty. Heparin injection markedly reduces not only TG but also total cholesterol concentrations9). Therefore, lipid profiles should be evaluated immediately on admission in patients with ACS. It is highly likely that small LDL-C concentration on admission may reflect the baseline fasting level before the onset of ACS.
Although small dense LDL is a subfraction of LDL, it is closely related to TG metabolism and insulin resistance4). Postprandial hypertriglyceridemia is another important risk factor for atherosclerotic disorders. It is diagnosed via serial TG measurement during oral fat loading test. Although fasting concentrations of remnant-like protein-cholesterol (RLP-C) and apolipoprotein B-48 (ApoB48) are significantly correlated with the incremental area under the curve of TG1, 10), both RLP-C and ApoB48 concentrations increase significantly after food intake. It is of great interest whether postprandial hypertriglyceridemia can be predicted with nonfasting small dense LDL-C concentration. This question should be addressed in future studies.
Takashi Miida was supported by Denka, Co. Ltd.