Abstract
Elevated levels of lipoprotein (a), a complex between apolipoprotein (a) and LDL, indicate an increased risk of atherosclerosis and cardiovascular disease. The important genetic regulation of lipoprotein (a) is now relatively well understood, but the progress in finding ways of influencing plasma lipoprotein (a) has been disappointingly slow. Nicotinic acid, pharmacological doses of sex hormones and anabolic steroids, as well as LDL apheresis may provide sufficient lowering of lipoprotein (a) for the evaluation of clinical response. Presently, the most important aspect is to take an evaluated lipoprotein (a) level into consideration when deciding to institute particularly aggressive lipid lowering treatment in a given individual.
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