Over the last decades, numerous studies have demonstrated that elevated lipoprotein (Lp)(a) is a powerful and independent risk factor for coronary heart disease,^, ischemic stroke, and calcific aortic stenosis. Even in patients treated with statins who achieve LDL-cholesterol goals below 70 mg/dL, elevated Lp(a) levels remain independently related to an increased risk of atherosclerotic events.

The LDL particle has a unique molecular structure, as exemplified by its covalent bond with an apolipoprotein(a) that bears resemblance to plasminogen and may well represent an evolutionary deviation of this well-known plasmin precursor. Lp(a) is synthesized by the liver and the amount of circulating particles in the bloodstream is almost exclusively determined by inheritance, leaving very little space for environmental influence. The distribution of Lp(a) levels in the population is highly skewed with approximately 80% of people exhibiting plasma concentrations below 50 mg/dL, and the remaining 20% with a wide range of values above that limit.

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