**1. Introduction**

Lipoprotein (a) [Lp(a)], first described in 1963 is an inherited cholesterol-rich particle found in a density range of 1.055-1.120 g/ml. The suggestion that Lp(a) might be a risk factor for cardiovascular diseases was first made by Dahlen et al. [1] who found out that individuals with angina pectoris exhibit an "extra pre--band" in lipid electrophoresis. In whites the concentration of Lp(a) in plasma varies from undetectable up to 200 mg/dl in different individuals but seems to be rather constant in the same person [2]. Chemical and physicochemical properties of Lp(a) in comparison with LDL are summarized in table 1.

Plasma Lp(a) concentrations above 30 mg/dl, as measured in about 20 percent of white people, are associated with an approx. two-fold relative risk of coronary atherosclerosis [3] rising to the range of five-fold when LDL and Lp(a) are both elevated [4]. Interestingly, blacks with high levels of Lp(a) do not experience greatly increased atherosclerotic progression and mortality. In those cases it is assumed that the atherogenicity of Lp(a) must be decreased or counterbalanced by other factors [5].

Till now the site and mechanism of Lp(a) synthesis are quite unclear. Measurements of serum Lp(a) levels of patients suffering from liver disease or from cholestasis who showed significantly lower concentrations than healthy controls gave indications that Lp(a) might be synthesized by the liver [6]. On the other hand there are studies which suggest that apo-a is associated with the postprandial d < 1.006 lipoproteins induced by fat feeding [7] but it is not yet clear however whether apo-a determined in this fraction is really of intestinal origin or whether it originates from free apo-a in serum which might bind to freshly secreted chylomicrons [8]. Because of the chemical similarities between Lp(a) and LDL it is possible that Lp(a) is formed during the metabolic catabolism of chylomicrons, VLDL or LDL. As Lp(a) levels stay nearly constant within one individual and as lipid-rich diet as well as fasting have no influence on Lp(a) concentrations it is assumed that Lp(a) exhibits a

© 2012 Gries, licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

metabolic behaviour completely different from other apo-B containing lipoproteins. Turnover studies in vivo performed with labelled VLDL confirmed these assumptions. Nearly all the activity of labelled VLDL could be detected in LDL whereas only trace amounts could be found in Lp(a) [9] confirming the hypothesis that unlike LDL, Lp(a) probably has no triglyceride-rich lipoproteins as precursors but seems to be secreted directly by the liver [10]. On the other hand the site of catabolism of Lp(a) in humans is unknown so far although the kidney is favourized to be implicated [11].

Despite extensive work on Lp(a) its possible physiological function remains unclear till now.


**Table 1.** Chemical and physicochemical properties of LDL and Lp(a)
