Net mass transfer of plasma cholesteryl esters and lipid transfer proteins in normolipidemic patients with peripheral vascular disease.

The role of plasma cholesteryl ester transfer and lipid transfer proteins in atherosclerosis is unclear. Recent data suggest both antiatherogenic and atherogenic properties for cholesteryl ester transfer protein (CETP). The overall effect of CETP on atherosclerosis may thus vary depending on individual lipid metabolism. To test whether lipid transfer parameters are of importance even in patients without major lipid risk factors for atherosclerosis, CETP mass and activity, net mass transfer of cholesteryl esters between endogenous lipoproteins (CET), and phospholipid transfer protein (PLTP) activity were determined in plasma from 18 normolipidemic male patients with peripheral vascular disease and 21 controls. Furthermore, lecithin: cholesterol acyltransferase (LCAT) activity was tested. The results show that CETP mass, CETP activity, and LCAT activity are not different between patients and controls. However, specific CETP activity (CETP activity/CETP mass) is lower in the patients (P < .02). On the contrary, higher CET is observed in patients' plasma (P < .001). Increased plasma PLTP activity (P = .052) is demonstrable in the patients. If the data of all subjects are combined, CET correlates positively with triglycerides ([TG], r = .45, P < .001) and with PLTP activity (r = .32, P < .05) but negatively with specific CETP activity (r = -.37 P < .05). CET and specific CETP activity remain significantly different in TG-matched patients and controls and are more strongly interrelated (r = -.71, P < .001), suggesting a higher and selective influence of lipid transfer inhibitor(s) on CET and CETP activity in the patients. CET allows the best discrimination between patients and controls in univariate and multivariate analysis. Eighty-eight percent of the subjects are correctly classified by CET as a single parameter. The results suggest that increased CET in the patients may reflect atherogenic alterations in TG metabolism and/or in lipid transfer protein activities despite normal fasting lipoprotein levels.