Lipoprotein(a) (Lp(a)) resembles a low-density lipoprotein (LDL) particle, but with the addition of apolipoprotein(a). Apolipoprotein(a) (apo(a)) is homologous to plasminogen, and its similarity to plasminogen indicates a prothrombogenic role for Lp(a), whereas the similarity of Lp(a) to LDL suggests a proatherogenic role. Thus, Lp(a) is a link between atherosclerosis and thrombosis. The apo(a) gene is highly polymorphic, and a relationship exists between the different apo(a) alleles and plasma Lp(a) levels. There is also evidence to suggest an association between serum Lp(a) concentration and the frequency of cardiovascular atherosclerosis, particularly myocardial infarction in men, although some of the recently published epidemiological studies have been controversial. The heightened awareness of increased Lp(a) levels being a risk factor for coronary artery disease has led to the evaluation of the effects of lipid-lowering agents on Lp(a) levels. The data that have emerged, however, are conflicting, and are derived mostly from short-term studies involving the use of statins. Our group has studied the short- and long-term effect of fluvastatin on Lp(a) in hypercholesterolaemic patients; fluvastatin was found to have no effect in such patients as observed in the short-term studies, but significant reductions in Lp(a) levels were noted during long-term treatment. Although our findings are in agreement with those of a previously published report, there is still a great need to confirm the data that have been reported in separate studies.