No evidence of impaired endothelial function or altered inflammatory state in patients with familial hypercholesterolemia treated with statins

BackgroundFamilial hypercholesterolemia (FH) is associated with an increased risk of premature atherosclerosis. Central in this aspect is enhanced inflammation and endothelial dysfunction.ObjectiveWe sought to examine inflammatory cytokines and endothelial dysfunction in patients with FH treated with statins (n = 14) compared with healthy control patients (n = 11).MethodsEndothelial function was evaluated by the use of the Endo-PAT® system which measured mean reactive hyperemia index. Fasting blood samples were drawn, and 27 biomarkers in addition to standard laboratory tests were analyzed.ResultsThere were no statistically significant differences between the FH group and the control group regarding age, weight, blood pressure, or body mass index. Endothelial function given as RHI was 1.58 and 1.93 (P = NS) in the control and FH groups, respectively. There were no differences between the groups in tumor necrosis factor-alpha, interleukin (IL-1) beta, IL-1 receptor antagonist, IL-6, IL-10, monocyte chemoattractant protein 1, high-sensitivity C-reactive protein, or any of the other inflammatory markers tested. Furthermore, no significant differences between the groups in high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, apolipoprotein A, apolipoprotein B, lipoprotein (a), homocysteine, HbA1c, platelets, and fibrinogen were found.ConclusionEndothelial function assessed by reactive hyperemia index-peripheral arterial tonometry or inflammatory state assessed by soluble inflammatory biomarkers were not different in FH patients on statins compared with healthy control patients.