**1. Introduction**

Lipoprotein(a) [Lp(a)] was uncovered in 1963, and its role in atherogenesis has been a matter of debate for many years. This was caused to a certain extent by the fact that the function of Lp(a) was—and still is—unknown. Also, there exists no specific therapy for reducing elevated blood levels of Lp(a). Lp(a) consists of an LDL-like core and a specific antigen, apo(a). Apo(a) exhibits a great homology to plasminogen. For this reason, it was long believed that Lp(a) may play a role in hemostasis and fibrinolysis. There are numerous publications dealing with the role of Lp(a) in hemostasis (reviewed in ref. [1]) providing evidence that the atherogenicity of Lp(a) in fact might be due to a certain extent to pathophysiological effects in fibrinolysis. These findings, however, appear to be of little relevance for practical considerations. Of much greater importance is the causal relationship of elevated plasma Lp(a) with the incidence of athero‐ sclerosis, coronary heart diseases and stroke [2–4]. Of note, on the other hand, are the findings that plasma Lp(a) levels rise with age, i.e. that nonagenarians exhibit significantly higher Lp(a) plasma levels than younger generations [5].
