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BackgroundLipoprotein(a) [Lp(a)] is a genetically determined lowdensity lipoprotein (LDL) particle that is comprised of apolipoprotein(a) [apo(a)] and apolipoprotein B-100 (apoB) moieties. It is well-established that elevated Lp(a) is an independent risk factor for cardiovascular disease (CVD). It is associated with an increased risk of myocardial infarction, aortic valve stenosis, ischemic stroke and peripheral vascular disease [1,2].The structure of Lp(a) is similar to plasminogen and competes for the same binding site, which reduces fibrinolysis resulting in secretion of plasminogen activator inhibitor-1 and thrombogenesis. Reduction in LDL-C is widely recognized as a means of reducing cardiovascular events. As a form of LDL-C, Lp(a) similarly binds atherogenic proinflammatory oxidized phospholipids, which attract a cascade of inflammatory cells to the vessel wall [3]. It is not entirely clear which of these specific mechanisms contributes to increased CVD risk.