Apolipoprotein B and Cardiovascular Disease Risk
The key role of low-density lipoprotein (LDL) in the development of atherosclerosis and cardiovascular disease (CVD) is well known. Following
entry into the artery wall, LDL particles promote the development of atherosclerosis, which increases an individual’s risk for heart attack and
stroke.1 Because of the difficulty in directly “counting” LDL particles, measurement of cholesterol carried by LDL particles (ie, LDL cholesterol or
LDL-C) has been used for many decades as a surrogate to estimate LDL quantity for the purpose of risk assessment and as a principal target of
therapy. The establishment of LDL-C treatment goals by the National Cholesterol Education Program Adult Treatment Panel guidelines and the
success of lipid-lowering therapies in achieving those goals have reduced CVD morbidity and mortality2 and, in so doing, further entrenched
LDL-C into medical decision making.
In recent years, numerous studies have evaluated the association of apolipoprotein B (apo B) levels as a predictor of heart disease in patients.3 At
the same time, a deeper understanding has also emerged regarding the relationship of LDL particle measurement along the continuum of CVD risk
assessment. These two developments, along with the facts presented below, may shift the CVD risk paradigm from exclusive reliance on LDL-C.
• The cholesterol content of lipoproteins varies widely in a single individual as well as between individuals.3,4
• Although lipid-lowering therapies are effective in reducing CV events, many individuals with cardiometabolic (CMR) factors (such as age,
abdominal obesity, insulin resistance, elevated blood pressure, low HDL-C levels, elevated triglycerides, and increased numbers of small
dense LDL particles) harbor residual risk.2 In many individuals, this combination of factors is characterized by a discordance between
“normal” LDL-C and increased numbers of LDL particles (LDL-P).1,2,5
• When LDL particle number is elevated, risk of coronary heart disease events has been shown to increase.4 If LDL-C and LDL particle
number measures are discordant, CHD risk has been found to track with LDL particle number, and LDL-C may be less predictive.2,4,5
• The dramatic increase in the prevalence of obesity has contributed to a shift in the overall CVD risk profile toward individuals with
CMR factors.2
Apo B is the main protein component of LDL particles, and each particle contains a single apo B molecule (as does each intermediate-density
lipoprotein [IDL] and each very low density lipoprotein [VLDL]). Since more than 90% of total plasma apo B is associated with LDL particles4 and
automated, routine immunochemical methods are commercially available for apo B measurement, apo B may be a good surrogate for LDL-P.3
There is a linear relationship between LDL-P and apo B values such that the higher the values, the higher the level of risk assigned to the patient.
If a clinical judgement places a patient in the high-risk category, it has been suggested that the target level of therapy be more aggressively
lowered, regardless of the measurement method used.2
Expert panels have established suggested treatment goals, including LDL-P targets (either NMR LDL-P or apo B), in addition to LDL-C and nonHDL-C goals to optimize the management of moderate- and high-risk individuals.1,2,3,6,7,8 For high-risk individuals, optimal particle levels have
been expressed as follows:
Method
Test
Units
Optimal Goal
NMR
LDL particle
nmol/L
< 1000
Immunochemical
Apo B
mg/dL
< 80
In addition to providing Lipid Cascade With Reflex to Lipoprotein Particle Assessment by NMR (361946), LabCorp now offers Lipid Cascade With
Reflex to Apolipoprotein B (363676) as another option for lipoprotein measurement.
Test Name
Test Number
Lipid Cascade With Reflex to Lipoprotein Particle Assessment by NMR 361946
Lipid Cascade With Reflex to Apolipoprotein B 363676
Visit the online Test Menu at www.LabCorp.com for full test information, including CPT codes and specimen collection requirements.
References
1. Brunzell JD, Davidson M, Furberg CD, et al. Lipoprotein management in patients with cardiometabolic risk. Consensus statement from the
American Diabetes Association and the American College of Cardiology Foundation. Diabetes Care. 2008 April; (31)4:811-822.
2. Davidson MH, Ballantyne CM, Jacobson TA, et al. Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an
expert panel of lipid specialists. J Clin Lipidol. 2011; (5):338-367.
3. Contois JH, McConnell JP, Sethi AA, et al. Apolipoprotein B and cardiovascular disease risk: position statement from the AACC lipoproteins
and vascular diseases division working group on best practices. Clin Chem. 2009;(55)3:407-419.
4. Cromwell WC, Berringer TA. Low-density lipoprotein and Apolipoprotein B: clinical use in patients with coronary heart disease. Curr Cardiol
Rep. 2009;(11):468-475.
5. Otvos JD, Mora S, Shalaurova I, et al. Clinical implications of discordance between low-density lipoprotein cholesterol and particle number.
J Clin Lipidol. 2011; (5): 105-113.
6. Genest J, McPherson R, Frohlich, et al. 2009 Canadian Cardiovascular Society/Canadian guidelines for the diagnosis and treatment of
dyslipidemia and prevention of cardiovascular disease in the adult – 2009 recommendations. Can J Cardiol. 2009;25(10):567-579.
7. Jellinger PS, Smith DA, Mehta AE, et al. American Association of Clinical Endocrinologists’ Guidelines for Management of Dyslipidemia and
Prevention of Atherosclerosis. Endocr Pract. 2012;18(Suppl 1): 1-78.
8. Perk J, De Backer G, Gohlke H, et al. European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). Euro Heart
J. 2012;33:1635-1701.
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