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2017 ; 12
(Suppl 1
): 12-17
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Hyperlipoproteinaemia(a) - apheresis and emerging therapies
#MMPMID28185213
Vogt A
Clin Res Cardiol Suppl
2017[Mar]; 12
(Suppl 1
): 12-17
PMID28185213
show ga
A high level of lipoprotein(a) (Lp(a)) is recognized as an independent and
additional cardiovascular risk factor contributing to the risk of early onset and
progressive course of cardiovascular disease (CVD). All lipid lowering
medications in use mainly lower low density lipoprotein-cholesterol (LDL-c) with
no or limited effect on levels of Lp(a). Niacin, the only component lowering
Lp(a), is firstly often poorly tolerated and secondly not available anymore in
many countries. A level of <50?mg/dl was recommended recently as the cut off
level for clinical use and decision making. Since lipoprotein apheresis (LA)
lowers not only LDL-c but also Lp(a) significantly, its use is recommended in
some countries in very high-risk patients with early or progressive CVD.
Retrospective analyses show that regular LA improves the course of CVD. This is
supported by a recent prospective observational trial and data of the German
Lipoprotein Apheresis Registry. Despite many treatment options, all too often it
is not possible to reduce LDL-c levels to target and to reduce Lp(a) levels
sustainably at all. Therefore, new drug therapies are awaited. Some of the lipid
modifying drugs in development lower Lp(a) to some extent in addition to LDL-c;
the only specific approach is the apoprotein(a) antisense oligonucleotide.
Currently LA is the standard of care as a last resort treatment in high-risk
patients with elevated Lp(a) and severe CVD despite optimal control of all other
cardiovascular risk factors.
|*Blood Component Removal
[MESH]
|Animals
[MESH]
|Biomarkers/blood
[MESH]
|Cardiovascular Diseases/*prevention & control
[MESH]