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University of Lynchburg DMSc Doctoral Project Assignment Repository

University of Lynchburg DMSc Doctoral Project Assignment Repository

Abstract

ABSTRACT

This review examines the clinical utility of apolipoprotein B as a marker of atherogenic lipoprotein particle burden compared with LDL cholesterol in cardiovascular risk assessment and lipid management.. ApoB is the structural protein present on all atherogenic lipoprotein particles, including low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and lipoprotein(a). Because each atherogenic particle contains one ApoB molecule, ApoB directly reflects total particle number, a primary driver of plaque formation. Although LDL cholesterol (LDL-C) remains the principal therapeutic target in current clinical guidelines, accumulating evidence suggests ApoB more accurately represents atherogenic burden. Atherosclerosis is driven more by the number of circulating atherogenic particles penetrating the arterial wall than by the cholesterol mass they contain, making particle number, measured by ApoB, more strongly associated with disease progression than LDL-C concentration alone. While LDL-C and ApoB are often correlated, discordance frequently occurs in patients with obesity, diabetes, hypertriglyceridemia, or metabolic syndrome. In these populations, LDL-C may underestimate true atherogenic burden, leaving residual cardiovascular risk despite achievement of guideline-recommended LDL-C targets. ApoB measurement addresses this limitation by capturing all atherogenic particles not fully reflected by LDL-C. Additionally, ApoB offers practical advantages, including reliability at low LDL-C levels, accuracy in elevated triglyceride states, and no requirement for fasting. Despite these benefits, ApoB remains underutilized, as current guidelines lack clearly defined ApoB thresholds for treatment initiation or titration. Incorporating ApoB into lipid management has the potential to improve risk stratification and better address residual atherosclerotic risk beyond LDL-C alone.

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