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To ApoB or Not to ApoB: New Arguments, but Basis for Widespread Implementation Remains Elusive

Paul Welsh, Naveed Sattar

Link to Paper

Introduction

How best should we measure circulating lipoproteins to facilitate the prevention of atherosclerotic cardiovascular disease (ASCVD)? Cholesterol was first identified in human blood in 1833 by Félix-Henri Boudet (1), and in 1913, Anitschkow showed cholesterol caused atherosclerosis in rabbits (2). Interest in LDL-cholesterol (LDLc) per se began in 1955, when Gofman used ultracentrifugation to separate cholesterol-carrying lipoproteins in plasma according to density, identifying low and high density (LDLc and HDLc) fractions (3). The idea that not all lipoproteins were the same in terms of ASCVD transformed our understanding of atherosclerosis.

Over time, technological advances have driven ever-expanding options for measuring different lipid fractions or lipoproteins, including by physical properties (such as ultracentrifugation techniques, gel electrophoresis, nuclear magnetic resonance) and biochemical characteristics (total cholesterol, HDLc, and direct LDLc). Advances in understanding have also led to multiple options for calculating different fractions including non-HDLc (total cholesterol minus HDLc) or LDLc (Friedewald, Sampson, and the Martin/Hopkins equations). Adding to this complex mix, apolipoprotein B (apoB) immunoassays have been around since the 1970s (4) but, to date, have been little used in clinical practice. As such, our definition of what is the best measure of “bad” cholesterol to measure lipid-associated ASCVD risk continues to be debated.

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First published: 11 January 2023