title: The effects of three different LDL-apheresis methods on the plasma concentrations of E-selectin, VCAM-1, and ICAM-1.
abstract: Plasma concentrations of cellular adhesion molecules are associated with atherosclerotic diseases and major cardiovascular risk factors. It was shown that LDL-apheresis with dextran sulfate lowers the levels of E-selectin and ICAM-1 in patients with familial hypercholesterolemia. The effects of different LDL-apheresis methods have not been studied yet. Cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, fibrinogen, and the adhesion molecules E-selectin, VCAM-1, and ICAM-1 were measured in 20 patients with coronary heart disease and severe hyperlipoproteinemia immediately before and after regular LDL-apheresis. Treatment was performed by different apheresis methods (direct absorption, DA, n = 6; dextran sulfate adsorption, DS, n = 7; heparin precipitation, HP, n = 7). Rebound data of adhesion molecule levels were obtained from 2 patients of each group. Lipids were reduced similarly in all groups. The concentrations of all adhesion molecules were lowered during apheresis. The reduction of E-selectin (-31 +/- 7 vs. -6 +/- 5 and -6 +/- 5%, respectively, P < 0.001) was most prominent in the patients treated by heparin precipitation. Depending on the method of LDL-apheresis, the concentrations of VCAM-1 and E-selectin in the outlets of the LDL-apheresis columns were significantly lower compared to the concentration in the inlets. Plasma concentrations of adhesion molecules increased to their pre-apheresis values within 2 to 4 days following LDL-apheresis. The reductions of adhesion molecule levels observed during LDL-apheresis are at least partly due to adsorption to the LDL-apheresis column. The extent of absorption depends on the principle of extracorporeal LDL elimination.
authors.affiliation: Medical Department II, Ludwig-Maximilians-University, Klinikum Grosshadern, D-81366 Munich, Germany. Klaus.Empen@t-online.de
authors.forename: Klaus
authors.initials: K
authors.lastname: Empen
authors.forename: Carsten
authors.initials: C
authors.lastname: Otto
authors.forename: Uli C
authors.initials: UC
authors.lastname: Brödl
authors.forename: Klaus G
authors.initials: KG
authors.lastname: Parhofer
mesh_terms: D000327:Adsorption; D000328:Adult; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D000925:Anticoagulants / Q000494:pharmacology; D000069059:Atorvastatin; D001781:Blood Component Removal / Q000379:methods*; D002448:Cell Adhesion; D002614:Chelating Agents / Q000494:pharmacology; D011232:Chemical Precipitation; D003131:Combined Modality Therapy; D003327:Coronary Disease / Q000097:blood / Q000150:complications; D016264:Dextran Sulfate; D019040:E-Selectin / Q000097:blood*; D004492:Edetic Acid / Q000494:pharmacology; D005260:Female; D006400:Hematocrit; D006493:Heparin / Q000494:pharmacology; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D006951:Hyperlipoproteinemias / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000628:therapy*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D011758:Pyrroles / Q000627:therapeutic use; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D000924:Anticholesteremic Agents; D000925:Anticoagulants; D002614:Chelating Agents; D019040:E-Selectin; D006538:Heptanoic Acids; D008055:Lipids; D008077:Lipoproteins, LDL; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D006493:Heparin; D016264:Dextran Sulfate; D004492:Edetic Acid; D000069059:Atorvastatin