A selective extracorporeal lipid removal procedure that targets LDL cholesterol and lipoprotein(a) for patients with familial hypercholesterolemia who cannot achieve adequate LDL reduction through diet and maximum tolerated pharmacological therapy. FDA-approved and covered by Medicare for qualifying patients.
ACE inhibitors must be held for at least 24 hours before LDL apheresis. This warning applies to all LDL apheresis systems, particularly those using negatively charged dextran sulfate columns. Contact of blood with these columns generates bradykinin; ACE inhibitors prevent bradykinin degradation, allowing levels to rise to concentrations that cause severe anaphylactoid reactions — including profound hypotension, flushing, and bronchospasm. This interaction is well-documented and potentially life-threatening. Confirm medication hold status before every procedure, as patients may restart medications between sessions.
LDL apheresis is a selective extracorporeal lipid removal procedure. Unlike TPE, which removes the entire plasma fraction, LDL apheresis uses specialized adsorption columns or precipitation techniques to selectively capture LDL cholesterol, VLDL, and lipoprotein(a) from plasma while returning other plasma proteins to the patient.
The procedure begins with plasma separation from cellular blood components using centrifugation or membrane filtration. The separated plasma is then passed through the selective removal system, and the treated plasma is recombined with the cellular components and returned to the patient.
A single session can reduce LDL cholesterol by 60–75%, with a corresponding reduction in lipoprotein(a) — a particularly valuable effect since Lp(a) is not effectively lowered by most pharmacological agents. LDL levels rebound over the following 1–2 weeks as the liver resynthesizes lipoproteins, which is why biweekly treatment is the standard protocol.
Dextran Sulfate Adsorption (Liposorber®): Plasma passes through columns packed with dextran sulfate cellulose beads. Apolipoprotein B-containing lipoproteins (LDL, VLDL, IDL, Lp(a)) bind to the negatively charged dextran sulfate. The columns are regenerated with saline and reused during the same session.
Heparin-Induced Extracorporeal LDL Precipitation (H.E.L.P.®): Plasma is acidified with acetate buffer and heparin is added, causing LDL, VLDL, and Lp(a) to precipitate. The precipitate is removed by filtration, and the plasma is treated to remove excess heparin and acetate before return.
Lp(a) Benefit: Elevated lipoprotein(a) is an independent cardiovascular risk factor that is largely genetically determined and resistant to most lipid-lowering medications. LDL apheresis is one of the few interventions that can substantially reduce Lp(a) levels, making it particularly valuable for patients with combined LDL and Lp(a) elevation.
Patients with confirmed HoFH are eligible for LDL apheresis regardless of LDL level, given the severity of the condition and inadequate response to pharmacological therapy alone.
Patients with HeFH and documented coronary artery disease (CAD) who have LDL ≥200 mg/dL despite maximum tolerated pharmacological therapy for at least 6 months.
Patients with HeFH without documented CAD who have LDL ≥300 mg/dL despite maximum tolerated pharmacological therapy for at least 6 months.
Patients with significantly elevated Lp(a) and progressive cardiovascular disease despite optimal LDL management. This is an emerging indication with growing evidence base.
| Condition | Category | Grade | Notes |
|---|---|---|---|
| Familial Hypercholesterolemia — Homozygous | I | 1A | FDA-approved; Medicare-covered; reduces cardiovascular events |
| Familial Hypercholesterolemia — Heterozygous with CAD | I | 1B | LDL ≥200 mg/dL despite maximum pharmacotherapy |
| Elevated Lp(a) with Progressive CVD | II | 2C | Emerging indication; Lp(a) not reducible by most drugs |