Increased levels of lipoprotein(a) are known as an independent risk factor for atherosclerosis, heart disease, and stroke in man. Even in children it could show that elevated levels of Lp(a) are an independent thromboembolic risk factor. Levels of Lp(a) are influenced by several factors like nutrition, kidney or liver function, or acute-phase reaction. But the most important factors are genetically determined. About 45% of genetic variation depends on polymorphisms and mutations in the promotor region. About 50% are dependent on the size polymorphism of Lp(a). The number of Kringle 4 domains varies between 12 and over 40. The number of Kringle 4 repeats correlates negatively with the level of Lp(a) in plasma. The determination of apo(a) phenotype is able to estimate thromboembolic risk due to this risk factor.