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Updated: Dec 8, 2025

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Therapeutic Apheresis for Management of Lp(a) Hyperlipoproteinemia
Sergei N Pokrovsky1, Olga I Afanasieva2, Marat V Ezhov2
1"National Medical Research Center of Cardiology" of Ministry of Health of the Russian Federation, Institute of Clinical Cardiology, 15A, 3d Cherepkovskaya street, Moscow, 121552, Russia. Dr.Pokrovsky@mail.ru.
Insights
High lipoprotein(a) (Lp(a)) levels are a cardiovascular risk. Lipoprotein apheresis (LA) effectively reduces Lp(a), decreasing cardiovascular event risk. This review covers optimal LA management for Lp(a) hyperlipoproteinemia.
Area of Science:
- Cardiology
- Lipidology
- Vascular Medicine
Background:
- Elevated lipoprotein(a) (Lp(a)) is a significant cardiovascular risk factor, particularly in atherosclerotic cardiovascular disease (ASCVD) patients.
- Current lipid-lowering drugs are largely ineffective at reducing Lp(a) pathogenicity.
- Lipoprotein apheresis (LA) is an effective, though not universally approved, method for removing atherogenic lipoproteins like Lp(a).
Purpose of the Study:
- To review and present current information on the optimal management of Lp(a) hyperlipoproteinemia using lipoprotein apheresis (LA).
- To discuss recent findings on the efficacy and application of LA in reducing cardiovascular risk associated with high Lp(a).
Main Methods:
- Review of recent clinical studies and real-world data on various LA systems for Lp(a) reduction.
- Analysis of the impact of Lp(a) elimination on inflammatory and thrombotic processes.
- Evaluation of long-term outcomes and cardiovascular event rates in patients treated with LA.
Main Results:
- LA effectively reduces Lp(a) levels by 60-80%, leading to decreased inflammation and plaque regression.
- Sustained Lp(a) reduction via LA over 2-5 years is associated with a proportional decrease in cardiovascular event rates.
- Specific Lp(a) apheresis targets Lp(a) exclusively, while non-specific LA is used for high-risk ASCVD patients. PCSK9 inhibitors show only modest effects on significantly elevated Lp(a).
Conclusions:
- Lipoprotein apheresis is a crucial therapeutic option for managing Lp(a) hyperlipoproteinemia, especially in progressive ASCVD.
- Sustained and significant reduction of Lp(a) levels is necessary to mitigate major adverse cardiovascular events.
- Further research and broader approval of LA are warranted for optimal patient management.
Purpose Of Review:
High lipoprotein(a) (Lp(a)) level is an independent cardiovascular risk factor with higher prevalence among patients with atherosclerotic cardiovascular disease (ASCVD). The actual problem is that most currently available lipid-lowering drugs are unable to abolish Lp(a) pathogenicity. Lipoprotein apheresis (LA) is an effective method for elimination of atherogenic lipoproteins, but it is approved only in some countries for treatment of elevated Lp(a) level in the presence of progressive ASCVD. In recent years, new studies on LA were published and the purpose of this review is to present the information on optimal management of Lp(a) hyperlipoproteinemia by LA in the modern era.
Recent Findings:
Most clinical studies designed to treat Lp(a) hyperlipoproteinemia with different LA systems are small in size but demonstrate that the elimination of Lp(a) from bloodstream leads to reduction of inflammatory and prothrombotic process in a few months and to atherosclerotic plaques regression in 1.5 years. Treatment with LA for 2 to 5 years in terms of clinical trials and in real-world setting provides further evidence that Lp(a) reduction by 60-80% is associated with proportional decreasing of rate and risk of cardiovascular events. Specific Lp(a) apheresis is the only possible method that solely targets Lp(a). In most countries, non-specific LA is used for treatment Lp(a) hyperlipoproteinemia in very high-risk subjects with progressive ASCVD. PCSK9 inhibitors have only modest effect on significantly elevated Lp(a), whereas large population-based studies requested sustained and prolonged reduction of Lp(a) levels by 50-100 mg/dL to gain proportional decreasing of major adverse cardiovascular events.
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