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Lipoprotein (a) is a low-density lipoprotein (LDL)
structure-like lipoprotein

Its height is inherited, does not change significantly
the whole life and can not be influenced by diet or medicaments.

A one-time determination is therefore sufficient.

If the lipoprotein (a) is increased to more than 100 mg / dl,
life expectancy is shortened by about 10 years.

Therapy of choice is on the one hand a particularly pronounced one
LDL reduction or - in individual cases - LDL apheresis.




Lp-Apheresis or. PCSK9 – Inhibitors




The therapy of fat metabolism is always a step therapy.

Firstly, an assessment of nutritional and lifestyle habits as well as a consultation on necessary changes is appropriate. If these measures are not sufficient, a therapy is started with lipid-lowering medications (usually from the family of statins). If this is not sufficient too, a combination with other lipid nuclei can lead to a further improvement in the blood fat values.

If the drug combination therapy is not sufficient or if these side effects occur, a PCSK9 inhibitor therapy is indicated.


Therapy with PCSK9-Inhibitors

  • monoclonal antibodies against PCSK9 (Evolocumab, Alirocumab)
  • each subcutaneously

Metabolic Control

  • under a lipid-lowering therapy (usually statins) together with PCSK9 inhibitors an approx. 50-60% additional reduction of LDL-C is achieved
  • Reduction of the lipoprotein (a) (Lp [a]) by approx. 25%
  • Reduction of triglycerides by 12-17%

Reduction of cardiovascular events

  • First results (post-hoc analyzes for evolocumab and alirocumab) show an approx. 50% reduction in cardiovascular events.
  • Final evaluation possible only after publication of the large clinical endpoint studies (expected in 2017).

Side effects

  • with the exception of muscle complaints, are not significantly different from the control groups
  • local reaction at the injection site (up to 6% of the affected population)
  • Upper respiratory infections (up to 5%)
  • flu-like symptoms (up to 3%)
  • muscle complaints (up to 5 %)


Modifiziert aus J f Kardiologie 2016; 23 (1-2), 30-34 „Clinical Shortcuts: PCSK9-Hemmer“



Lp-Apheresis Therapy


However, if the lipoprotein (a) is elevated above the corresponding limit of 100 mg / dl, either isolated or in combination with the increase in other blood fats, only liporprotein apheresis is a measure assured by studies.


Primary prevention

  • Homozygote FH (Start of treatment in childhood)
  • Heterozygote FH, despite maximum drug combination therapy LDL-C > 190 mg/dl

Cardiovascular (first) event - secondary prevention

  • Lp(a) > 100 mg/dl (>~ 250 nmol/L), At first, LDL-C should be reduced by LDL-C <70mg / dL by means of drug combination therapy, if necessary, additional PCSK9 inhibitors. In case of therapy failure, LP-apheresis.
  • In the case of progressive atherosclerosis, LDL-C <70 mg / dl and / or non-HDL-C <100 mg / dl and / or non-HDL-Lp <130 mg / dl and / or increased Lp(a) > 100 mg/dl (>~ 250 nmol/L)
  • Documented intolerance of all available statins, LDL-C treatment target is not achieved and Lp (a) > 100mg/dl (>~ 250 nmol/L)

Aus J f Kardiologie 2016, im Druck







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