Should we measure routinely the LDL peak particle size?

Low density lipoproteins (LDL) do not show in humans a normal distribution and comprise two different main fractions: large, buoyant (phenotype pattern A) and small, dense (phenotype pattern B) particles, that differ not only in size and density but also in physicochemical composition, metabolic behaviour and atherogenicity. The prevalence of small, dense LDL changes with age (30–35% in adult men, 5–10% in men < 20 years and in pre-menopausal women, 15–25% in postmenopausal women) and is genetically influenced, with a heritability ranging from 35% to 45%. Small, dense LDL correlate negatively with plasma HDL levels and positively with plasma triglyceride levels and are associated with the metabolic syndrome and with increased risk for cardiovascular disease and diabetes mellitus. LDL size seems also to be an important predictor of cardiovascular events and progression of coronary artery disease and the predominance of small dense LDL has been accepted as an emerging cardiovascular risk factor by the National Cholesterol Education Program Adult Treatment Panel III. In addition, patients with acute myocardial infarction show an early reduction of LDL size, which persists during hospitalization and seems to precede all other plasma lipoprotein modifications. However, it is still on debate whether to measure the LDL size routinely and in which categories of patients. Since the therapeutic modulation of small, dense LDL particles is of great benefit in reducing the atherosclerotic risk, the LDL size measurement should be extended to patients at high risk of coronary artery disease as much as possible.