The inflammatory events leading to atherosclerosis are due to the presence of LDL particles that diffuse through the endothelium and into the vessel wall. It makes sense that the more LDL particles there are, the more risk there would be for LDL depositing in the vessel wall. It would seem therefore that measuring the number of LDL particles could be more useful than measuring the cholesterol content of the particles.
Traditional measurements of LDL-C quantify the amount of cholesterol associated with all the LDL in a patient sample; they don't tell us how many LDL particles there are. It would seem intuitive that the more LDL-C there is, the greater the number of LDL particles there must be. In that sense, LDL particle number should correlate to LDL cholesterol, and this is indeed true... most of the time.
Studies now show that measurement of the number of LDL particles is a more powerful predictor of cardiovascular risk. Patients with diseases like diabetes, or patients who have metabolic syndrome or hyperlipemia often have different sized lipoproteins. This skews the predictive power of simply measuring cholesterol content in these particles. Instead, particle counts may be a better estimate of risk in these patients. The exact relationship between LDL particle number and cholesterol content varies due to the fact that the lipoproteins vary in size and in their ratio of triglycerides to cholesterol. So, although cholesterol is related to LDL particle number, it is not in perfect proportion and the proportion seems to change in some disease states.
How can we then measure LDL particle number? The most obvious way would be to measure apolipoprotein B100 (often abbreviated ApoB). Each LDL particle has one molecule of ApoB attached to it. Therefore, if we measured ApoB, we would be measuring the number of LDL particles, not the contents of those particles, and number appears to be more important with regard to adverse outcomes.