Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Clinical Trial
. 2015 Apr;10(Suppl 1):46-50.
doi: 10.1007/s11789-015-0068-y.

Lipoprotein apheresis results in plaque stabilization and prevention of cardiovascular events: comments on the prospective Pro(a)LiFe study

Reinhard Klingel  1 , Andreas Heibges, Cordula Fassbender
Affiliations
Clinical Trial

Lipoprotein apheresis results in plaque stabilization and prevention of cardiovascular events: comments on the prospective Pro(a)LiFe study

Reinhard Klingel et al. Clin Res Cardiol Suppl. 2015 Apr.

Abstract
in English, German

Elevated lipoprotein(a) (Lp(a)) has emerged as an important independent cardiovascular risk factor, and causal association has been accepted with adverse outcome in atherosclerotic disease. Lipoprotein apheresis (LA) can lower low-density lipoprotein (LDL)-cholesterol and Lp(a) by 60-70 % and is the final escalating therapeutic option in patients with hyperlipoproteinemias (HLP) involving LDL or Lp(a) particles. Major therapeutic effect of LA is preventing cardiovascular events. Stabilizing plaque morphology might be an important underlying mechanism of action. In Germany, since 2008, a reimbursement guideline has been implemented to establish the indication for LA not only for familial or severe forms of hypercholesterolemia but also for Lp(a)-HLP associated with a progressive course of cardiovascular disease, that persists despite effective treatment of other concomitant cardiovascular risk factors, i.e. isolated Lp(a)-HLP. The Pro(a)LiFe-study confirmed with a prospective multicenter design that LA can effectively reduce Lp(a) plasma levels and prevent cardiovascular events.

Ein erhöhter Spiegel von Lipoprotein(a) (Lp(a)) ist ein bedeutender unabhängiger und kausal zu wertender kardiovaskulärer Risikofaktor. Die Lipoprotein-Apherese (LA) kann LDL-Cholesterin und Lp(a) um 60–70 % absenken und ist die ultima ratio der Therapie-Eskalation bei Hypercholesterinämie und Lp(a)-Hyperlipoproteinämie (Lp(a)-HLP). Der wesentliche therapeutische Effekt der LA besteht in der Prävention kardiovaskulärer Ereignisse. Die Stabilisierung der Plaquemorphologie könnte hierbei ein wichtiger Wirkmechanismus sein. Die deutschen Erstattungsrichtlinien für die LA umfassen seit 2008 nicht nur die familäre und schwere Hypercholesterinämie sondern auch die Lp(a)-HLP mit progredienter Gefäßerkrankung, die persistiert trotz effektiver Behandlung aller bestehenden kardiovaskulären Risikofaktoren und dann als isolierte Lp(a)-HLP bezeichnet wird. Die Pro(a)LiFe-Studie bestätigte mit prospektivem Multicenter-Design, daß die LA zur effektiven Reduktion der Lp(a)-Spiegel und Prävention kardiovaskulärer Ereignisse führte.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Mean plasma concentrations of lipoprotein(a) (Lp(a)) and LDL-cholesterol (LDL-C) before and after commencing chronic lipoprotein apheresis (LA) (modified according to [7]). Sawtooth-like pattern of Lp(a) and LDL-C levels illustrates weekly changes during chronic LA with approximately > 60–70 % reduction after a single treatment: a Lp(a), b LDL-C, c LDL-C after correction for Lp(a) cholesterol estimated as 45 % of measured LDL-C according to [8, 19]
Fig. 2
Fig. 2
Annual percentage change of mean annual cardiovascular events during the Pro(a)LiFe study. MACE major adverse cardiac event, i.e., cardiovascular death, nonfatal myocardial infarction, coronary bypass surgery, percutaneous coronary intervention or stent. ACVE adverse cardiac or vascular events, i.e., the sum of all documented cardiac or vascular events in arterial and venous vascular beds including MACE, cerebrovascular event, peripheral vascular event, venous thrombotic event (deep venous thrombosis or pulmonary embolism) (modified from [7])
See this image and copyright information in PMC

References

    1. Nordestgaard BG, Chapman MJ, Ray K, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010;31:2844–2853. doi: 10.1093/eurheartj/ehq386. - DOI - PMC - PubMed
    1. Ridker PM, Hennekens CH, Stampfer MJ. A prospective study of lipoprotein(a) and the risk of myocardial infarction. JAMA. 1993;270:2195–2199. doi: 10.1001/jama.1993.03510180065035. - DOI - PubMed
    1. Edelstein C, Hinman J, Marcovina S, et al. Properties of human free apolipoprotein(a) and lipoprotein(a) after either freezing or lyophilization in the presence and absence of cryopreservatives. Anal Biochem. 2001;288:201–208. doi: 10.1006/abio.2000.4904. - DOI - PubMed
    1. Rifai N, Ma J, Sacks FM, et al. Apolipoprotein(a) size and lipoprotein(a) concentration and future risk of angina pectoris with evidence of severe coronary atherosclerosis in men: the physicians. Clin Chem. 2004;50:1364–1371. doi: 10.1373/clinchem.2003.030031. - DOI - PubMed
    1. German Federal Ministry of Health (2008) Publication of a decision of Federal Joint Committee on apheresis for isolated Lp(a)-elevation with progressive cardiovascular disease. Transactions Ger Fed Ministries (BAnz) 138:3321