Low Density Lipoprotein Cholesterol (LDL-C)
LDL cholesterol has been, and will continue to be the focus of risk reduction intervention strategies. Despite the usefulness of total LDL cholesterol for CVD prediction on a population level, the measurement has significant limitations for individual risk assessment. LDL is not present in the circulation as one well-defined structure, but rather as particles in a continuum of size and density. Knowing LDL cholesterol breakdown is consistent with the recommendation outlined by the Working Group on Lipoprotein Measurments.
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LDL Size/Density Pattern.
Small, dense LDL occurs in 40% to 50% of patients with CAD; this information is not provided by the routine lipid panel. Dense LDL (Pattern B) is associated with a 4 fold increased risk for CAD and a 6.9 fold risk for myocardial infarction. By contrast, even very high total cholesterol and total LDL are associated with only a 2-fold increase in risk for CAD. Small dense LDL is a risk factor for CAD even in patients with normal cholesterol.
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LDL component Lipoprotein (a).
Lp(a) has been proven to be an independent and critical risk factor for CAD. It is highly correlated with risk of premature coronary artery disease and appears to have strong negative synergies when other lipid abnormalities are present. The prevalence of elevated Lp(a) has been reported to be 16–32% in the offspring of patients with premature myocardial infarction. High Lp(a) plus low HDL was recently found in PROCAM to increase risk 8.3 times. When the atherogenic dyslipidemia (low HDL2, small dense LDL, etc.) is present then Lp(a) contributes a relative risk of 25 times normal. Lp(a) is also a powerful and independent predictor of stroke. In type 2 diabetics, elevated Lp(a) levels were independently associated with coronary heart disease with an increased risk of 3.5. Lp(a) levels are under strong genetic control, with minimal environmental influences.
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LDL component Intermediate density lipoprotein (IDL)
IDL, represents a lipoprotein transition between VLDL and LDL particles. Data from a number of angiographic trials, show IDL is significantly more atherogenic than LDL alone. IDL concentration is under strong genetic control, and diet and exercise have little effect on IDL levels.
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It is important to note that in the traditional lipid profile “LDL cholesterol concentration” actually represents the sum of real LDL-C, IDL-C, and Lp(a)-C concentrations.
