Introduction: The role of lipids in atherogenesis is now well established. However, the exact mechanisms by which different lipoproteins affect endothelial function and induce atherogenesis are still not well understood. In the present study we examined the effect of lipid profile on forearm vasodilatory response to reactive hyperemia, an index of endothelial function, in a cohort of young, low-risk adults.
Methods: One hundred sixty seven healthy subjects were included in the study. The effect of total cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides, apolipoprotein (apo)-A1, apo-B and apo-E on endothelial function and inflammatory process was examined. Endothelial function was evaluated by determining forearm vasodilatory response to reactive hyperemia (RH%) using gauge-strain plethysmography. RH% was defined as the % change of forearm blood flow from baseline to the maximum flow during post-ischemic hyperemia. Endothelium independent dilatation in response to nitroglycerin (NTG%) was defined as the % change of forearm blood flow from baseline to the maximum flow after sublingual nitroglycerin administration.
Results: RH% was correlated with HDL (r = 0.267, p = 0.001), LDL (r = 0.355, p = 0.0001), triglycerides (rho = -0.366, p = 0.0001), apo-Al (r = 0.240, p = 0.004) and apo-B (r = -0.277, p = 0.005). NTG% was not affected by serum lipid levels. In multivariate linear regression, LDL (beta = -0.217 [SE: 0.098], p = 0.028), apo-A1 (beta = 0.277 [SE: 0.124], p = 0.027) and age (beta = 0.916 [SE:0.369], p = 0.015) were independent predictors for RH% in this population (R2 for the model: 0.243, p = 0.0001).
Conclusions: Elevated lipid levels decrease forearm vasodilatory response to reactive hyperemia. Apolipoproteins, and especially apo-Al, are important determinants of endothelial function in these subjects, independently of LDL, HDL and triglycerides, implying that full measurement of the lipid profile may be of great importance in risk stratification of young individuals.