LOW-DENSITY LIPOPROTEIN-APHERESIS DECREASES OXIDIZED LOW-DENSITY LIPOPROTEINS AND MONOCYTE ADHESION TO ENDOTHELIAL-CELLS

The mutual interaction between monocytes and low density lipoprotein ( LDL) in atherogenesis prompted a test of the hypothesis that LDL-apher esis could reduce the adhesive properties of monocytes to endothelium; and therefore interfere with a key mechanism in atheroma formation. F ive patients affected by heterozygous familial hypercolesterolemia wer e studied. All patients received LDL-apheresis treatment with selectiv e adsorption of LDL-cholesterol on dextran-sulphate columns. Low densi ty lipoprotein particles were isolated by sequential preparative ultra centrifugation and subfractionated by ion exchange high performance li quid chromatography. Thiobarbituric acid reacting products of lipid pe roxidation were measured fluorometrically. Vitamin E was estimated by high performance liquid chromatographic technique. Monocytes were isol ated from patients blood before and 1 day after LDL-apheresis by Perco ll gradient. The blood samples for monocyte adhesion were drawn from c ontrol subjects for 2 consecutive days. The adhesion of monocytes to a n endothelial monolayer was evaluated by assaying the peroxidase conte nt of the adherent monocytes. Low density lipoprotein-apheresis reduce d total cholesterol (-65%; p < 0.01), LDL-cholesterol (-75%; p < 0.01) , triglycerides (-51%; p < 0.05), and fibrinogen (-28%; p < 0.01). Wit h LDL-apheresis treatment, a reduction of 54% in oxidized LDLs was obs erved; vitamin E concentration significantly increased in LDLs (+14.2% ; p < 0.05). The monocyte adhesion decreased by approximately 61% afte r apheresis; the variation became statistically significant (-65%; p < 0.01) when endothelial cells were stimulated by lipopolysaccaride.