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(Circulation. 1997;96:1381-1385.)
© 1997 American Heart Association, Inc.

Articles

Plasma Cholesterol Regulates Soluble Cell Adhesion Molecule Expression in Familial Hypercholesterolemia

T. Sampietro, MD; M. Tuoni, MD; M. Ferdeghini, MD; A. Ciardi, MD; P. Marraccini, MD; C. Prontera, PhD; G. Sassi, MD; M. Taddei, MD; ; A. Bionda, MD

From the CNR Institute of Clinical Physiology and S. Chiara Hospital (T.S., P.M.), Institute of 2° Medical Clinic (M. Tuoni, A.C., G.S., M. Taddei, A.B.), and Institute of Nuclear Medicine (M.F., C.P.) University of Pisa, Italy.

Correspondence to T. Sampietro, MD, CNR Institute of Clinical Physiology, Via Savi, 8, 56110 Pisa, Italy.

Background Hypercholesterolemia is associated with endothelial dysfunction. On the basis of the hypothesis that high plasma cholesterol per se may be a sufficient stimulus to upregulate endothelial adhesiveness and that this phenomenon might be reversible, soluble endothelial leukocyte adhesion molecules (sELAMs) were studied in patients with familial hypercholesterolemia undergoing LDL apheresis.

Methods and Results Selective LDL absorption by dextran sulfate columns was used to treat plasma volumes of 6.5 to 9.2 L; after LDL apheresis, total cholesterol, LDL cholesterol, apolipoprotein B, triglycerides, and lipoprotein(a) levels were reduced by 74%, 82%, 79%, 56%, and 86%, respectively. Soluble intercellular adhesion molecule-1 (sICAM-1) and sELAM-1 were measured before, immediately after, and 2 and 6 days after LDL apheresis. Basal sICAM-1 and sELAM-1 values were higher than in healthy control subjects. After LDL apheresis, they decreased (P<.0001 and P<.0004, respectively); their removal by extracorporeal circulation components was excluded. Individual pretreatment and posttreatment values of sICAM-1 and sELAM-1 were positively correlated (P<.0001 and P<.001, respectively) with total cholesterol; their rebound curves showed patterns similar to the total cholesterol rebound curve but not to the triglyceride and lipoprotein(a) curves.

Conclusions In the absence of changes in clinical chemical parameters, tumor necrosis factor-, interleukin-6, and acute-phase reactant proteins, these results confirm in a clinical setting the upregulation of endothelial adhesiveness observed in experimental hypercholesterolemia and suggest a direct role for cholesterol in regulating this phenomenon, at least in familial hypercholesterolemia.

Key Words: hypercholesterolemia • cholesterol • endothelium • atherosclerosis

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