Regular paperMeasurement issues related to lipoprotein heterogeneity
Section snippets
Prevalence and metabolic origins of low-density lipoprotein cholesterol compositional variability
LDL cholesterol has been used for so long as the basis of quantifying LDL that physicians and patients rarely bother to note the distinction. For example, it is common for someone to express concern about “my LDL of 160 mg/dL” without worrying about the fact that it is a cholesterol concentration they are talking about, not an LDL concentration. Why is this distinction important? Because LDL particles from different individuals vary tremendously in the amount of cholesterol they contain. As a
Lipoprotein quantification by NUCLEAR MAGNETIC RESONANCE spectroscopy
NMR spectroscopic analysis of lipoprotein subclasses is considerably more efficient than traditional electrophoretic or ultracentrifugal methods, because no physical fractionation of the lipoproteins is required. However, potentially more important in terms of clinical utility is the fact that NMR provides direct access for the first time to lipoprotein particle data. Instead of basing lipoprotein quantification on cholesterol or apolipoprotein measurements, the NMR method employs the
Clinical implications of the disconnect between LDL cholesterol and LDL particles in patients with low HDL cholesterol
NMR analyses conducted on >3,400 frozen plasma samples from the Framingham Offspring Study cohort26 provide an opportunity to take a fresh look at the reasons for the enhanced CAD risk of patients whose primary lipid abnormality is not high LDL cholesterol, but low HDL cholesterol. Prospective epidemiologic studies have consistently shown low HDL cholesterol to be a strong CAD risk factor, independent of the level of LDL cholesterol.4 With clinical trial support coming from the recent VA-HIT
Prevalence of the disconnect between LDL cholesterol and LDL particles
The ATP III guidelines recommend LDL cholesterol targets of <100 mg/dL for patients with CAD or CAD risk equivalents, <130 mg/dL for patients with ≥2 risk factors and a 10-year Framingham risk ≤20%, and <160 mg/dL for patients with 0 to 1 risk factors.30 As shown in Figure 5, these targets correspond to the 20th, 50th, and 80th percentile values in the Framingham Offspring population. The LDL particle concentration distribution, also given in Figure 5, shows that the corresponding 20th, 50th,
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