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Lipoprotein apheresis

Lipoprotein apheresis

Lipoprotein apheresis

The challenge of familial hypercholesterolaemia

Familial hypercholesterolaemia (FH) is the most common inherited cause of premature cardiovascular disease and atherosclerosis. Between 14 and 34 million people suffer from FH worldwide. This genetic disorder is characterized by high to extremely high blood levels of low-density lipoprotein cholesterol (LDL-C or "bad cholesterol"). There are two genetically distinct forms of FH: homozygous (HoFH) and heterozygous (HeFH). Typically, LDL-C concentrations range from 310 to 580 mg/dL (8–15 mmol/L) in heterozygous cases and from 460 to 1,160 mg/dL (12–30 mmol/L) in homozygous cases.1

An effective reduction in LDL-C levels in homozygous patients is not possible through dietary measures or pharmacological treatment alone. Extracorporeal lipoprotein apheresis, when performed regularly in conjunction with dietary measures and drug treatment, is currently the state-of-the-art approach to effectively reducing LDL-C in these patients.

Therapy stages - hypercholesterolaemia

Above: Adapted from: “Harefield Hospital, Information about LDL apheresis”, © Royal Brompton & Harefield NHS Foundation Trust 2012.

The new perspective on elevated Lp(a) levels

High levels of lipoprotein(a) [Lp(a)] also advance the development of atherosclerosis.

Lp(a) is structurally similar to LDL-C, with an additional apolipoprotein (apolipoprotein (a)) on the surface. The blood concentration is mainly genetically determined. The function and metabolism of Lp(a) are to date not fully understood.

However, there is a clear link between cardiovascular (CV) risk and Lp(a):

Lp(a) is a proven independent CV risk factor.2 Elevated Lp(a) levels cannot be efficiently managed through dietary measures or drug treatment.

Lipoprotein apheresis is the most effective method for removing Lp(a) in patients with Lp(a) levels of more than 60 mg/dL (120 mmol/L)3 and concomitant cardiovascular disease.

Lipoprotein apheresis - how it works
Lipoprotein apheresis – how it works

In lipoprotein apheresis, the removal of lipoproteins (e.g., low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a)) takes place in an extracorporeal circuit. The patient's blood is removed from a vein in their arm and passed to the apheresis device, which monitors the extracorporeal circulation. After the removal of LDL-C and Lp(a), the purified blood is returned via a vein in the other arm. Depending on the method used, lipoprotein apheresis takes 60 to 150 minutes on average.

Since the concentration of lipids starts to increase again after a certain time, lipoprotein apheresis must be repeated at regular intervals. Frequency of treatment ranges from once a fortnight to twice a week and depends on national treatment guidelines and the patient’s clinical condition. Target levels for patients with very high CV risk are less than 70 mg/dL (1.8 mmol/L) for LDL-C and less than 50 mg/dL for Lp(a), according to European (ESC/EAS) guidelines.4, 5

LDL/Lp(a) target levels according to EAS/ESC guidelines.4,5

Risk category4 

Recommended target levels

Very high cardiovascular risk

  • Documented cardiovascular disease
  • Diabetes mellitus (DM) with target organ damage or with a major risk factor such as smoking, hypertension or dyslipidaemia
  • Severe CKD (GFR <30 mL/min/1.73 m2)
  • SCORE ≥10% for 10-year risk of fatal CVD
  • LDL-C <70 mg/dL (1.8 mmol/L)4
  • Lp(a) <50 mg/dL5

High cardiovascular risk

  • Markedly elevated single risk factors, in particular cholesterol >310 mg/dL (8 mmol/L) or BP ≥180/110 mmHg
  • Most other people with DM
  • Moderate CDK (GFR <30–59 mL/min/1.73 m2)
  • SCORE ≥5% and <10% for 10-year risk of fatal CVD
  • LDL-C <100 mg/dL (<2.6 mmol/L)

Moderate cardiovascular risk

  • SCORE ≥1% and <5% for 10-year risk of fatal CVD
  • LDL-C <115 mg/dL (<3.0 mmol/L)

Low cardiovascular risk

  • SCORE <1% for 10-year risk of fatal CVD
  • LDL-C <115 mg/dL (<3.0 mmol/L)

BP = blood pressure; CKD = chronic kidney disease; DM = diabetes mellitus; GFR = glomerular filtration rate; SCORE = systemic coronary risk estimation

In lipoprotein apheresis, a distinction is made between whole-blood therapy and the plasma method. Fresenius Medical Care offers an adsorption system for whole-blood therapy (DALI®) and a cascade filtration system for the plasma method (MONET®). Both systems run on the ART Universal device.

Related products
DALI lipoprotein apheresis

DALI

 

MONET lipoprotein filtration

MONET

 

1 Nordestgaard BG et al.; European Heart Journal Dec. 2013; 34(45): 3478–90a

2 Nordestgaard BG, Langsted A.; Journal of Lipid Research Nov. 2016; 57(11): 1953–1975

3 Richtlinie Methoden vertragsärztliche Versorgung, 16 May 2015.

4 Catapano AL et al.; Atherosclerosis Journal. Oct. 2016; 253: 281–344.

5 Nordestgaard BG et al.; Lipoprotein(a): EAS Recommendations for Screening, Desirable Levels and Management, A Handbook for Clinicians, 2012.