Lipoprotein(a), is a highly heterogeneous lipoprotein, due to variations in the size of apolipoprotein(a), and the density of the apoB100-containing particles to which apo(a) is linked. Although high plasma levels of Lp(a) have been associated with an increased risk for atherosclerotic cardiovascular disease, the mechanism underlying this association is still largely undetermined, as is the potential role played by the particle's heterogeneity. Lp(a) pathogenicity may also be influenced by the action of environmental factors and post-translational events relating to oxidative processes, and the action of lipolytic and proteolytic enzymes. Complicating the study of Lp(a) are the competing methods for its quantification due to its complex structure, and the lack of standardized methodologies. The recognition that Lp(a) particles may not all be alike in atherogenic potential should encourage studies to identify genetic and nongenetic factors underlying its heterogeneity, in order to reach a better understanding of its actual impact on atherosclerotic cardiovascular disease.