State of the art of low-density lipoprotein apheresis in the year 2003.
Low-density lipoprotein (LDL) apheresis is a last-resort treatment for hypercholesterolemic patients resistant to conservative lipid-lowering therapy. In the extracorporeal circuit, LDL, Lp(a) and coagulation factors are selectively eliminated, while the beneficial proteins like high-density lipoprotein, albumin and immunoglobulins are returned to the patient. Clinical effects of LDL apheresis comprise improvement of symptoms like angina and exercise tolerance, reduction of clinical coronary events like unstable angina, need for angioplasty or bypass operation, myocardial infarction and ultimately coronary mortality. The reduction of atherogenic lipoproteins and of coagulation factors by LDL apheresis (LA) positively influences hemorheology, endothelial function and coronary reserve. In the controlled LAARS, LA significantly improved the electrocardiographic signs of myocardial ischemia in the treadmill test. In angiographically controlled trials such as LARS and L-CAPS, a reduction of progression of coronary lesions was observed; in favorable cases, regression of the stenoses could be documented. In addition, in the LDL apheresis coronary morphology trial, LA decreased the coronary plaque area. The Hokuriku trial documented a 72% decrease of coronary events (MACE) in the LA group vs. controls treated only by statins. In longitudinal studies, the incidence of MACE after regular LA decreased compared with the preapheresis period in the same patients. Apart from coronary heart disease, recent studies indicate a positive effect of LA also on carotid artery stenoses and peripheral vascular disease. Prospective randomized studies showed the beneficial effects of cascade filtration on age-related macular degeneration and of heparin-induced LDL precipitation apheresis on acute inner ear deafness.
Bosch
Thomas
T
Nephrology Division, Department I of Internal Medicine, University Hospital Munich-Grosshadern, Munich, Germany. thomas.bosch@med.uni-muenchen.de
Wendler
Thorsten
T
D000208:Acute Disease; D000327:Adsorption; D001781:Blood Component Removal / Q000379:methods*; D001783:Blood Flow Velocity / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000493:pharmacokinetics; D008078:Cholesterol, LDL / Q000493:pharmacokinetics*; D003327:Coronary Disease / Q000209:etiology / Q000517:prevention & control*; D034381:Hearing Loss / Q000628:therapy; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000628:therapy*; D008055:Lipids / Q000493:pharmacokinetics; D008268:Macular Degeneration / Q000628:therapy; D010956:Plasmapheresis / Q000379:methods; D013997:Time Factors
D015815:Cell Adhesion Molecules; D008078:Cholesterol, LDL; D008055:Lipids