Statins reduce oxidized low-density lipoprotein levels, but do not alter soluble intercellular cell-adhesion molecule-1 and vascular cell-adhesion molecule-1 levels in subjects with hypercholesterolaemia Available to Purchase

ICAM-1 (intercellular cell-adhesion molecule-1) and VCAM-1 (vascular cell-adhesion molecule-1) are cell-adhesion molecules that have an essential role in monocyte recruitment. In the present study we have investigated (i) whether statins reduce soluble levels of ICAM-1 (sICAM-1) and VCAM-1 (sVCAM-1), and the relationship between resistance of LDL (low-density lipoprotein) to in vitro oxidation and sICAM-1 and sVCAM-1 levels. Whole blood samples were obtained from 55 healthy non-smoking adults (aged 35–65 years) with moderate (LDL-cholesterol, 3.4–4.9 mmol/l) hypercholesterolaemia participating in a randomized double-blinded, 8-week trial comparing pravastatin (40 mg), simvastatin (20 and 80 mg) and placebo. sICAM-1 levels (means±S.D.) increased slightly from 12.2±4.2 to 13.6±4.2 ng/ml with statin therapy, whereas, among placebo-assigned subjects, levels were unchanged (11.8±5.0 and 11.8±3.9 ng/ml). sVCAM-1 increased from 18.9±10.1 to 21.1±7.4 ng/ml among those on active therapy and slightly declined with placebo assignment (19.8±8.8 to 19.4±6.4 ng/ml). Lag times increased with statin therapy from 74.3±39.8 min to 98.3±57.8 min (P=0.003), and were unchanged in the placebo group (from 103.1±61.1 to 90.8±65.9 min; P=0.48). There were no significant changes between statin and placebo therapy for sICAM-1, sVCAM-1 or lag times (P=0.09, 0.16 and 0.067 respectively). Changes in sICAM-1 and sVCAM-1 were not correlated with the change in lag times. In contrast with the known effects of oxidized LDL on gene activation of ICAM-1 and VCAM-1, lag times did not correlate with sICAM-1 and sVCAM-1. Statin therapy improved lag times, but has no effect on sICAM-1 or sVCAM-1 levels.