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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
? WHEN - WHAT ?
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.
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Therapy with PCSK9-Inhibitors
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- monoclonal antibodies against PCSK9 (Evolocumab, Alirocumab)
- each subcutaneously
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Metabolic Control
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- 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%
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Reduction of cardiovascular events
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- 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).
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Side effects
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- 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 %)
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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.
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Primary prevention
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- Homozygote FH (Start of treatment in childhood)
- Heterozygote FH, despite maximum drug combination therapy LDL-C > 190 mg/dl
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Cardiovascular (first) event - secondary prevention
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- 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)
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Aus J f Kardiologie 2016, im Druck
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