In a study of 60 asymptomatic patients, 21 with a confirmed FH-causing mutation, 19 with an elevated LDL-C level but no FH-causing mutation and 20 healthy controls, brachial artery flow-mediated dilation was significantly lower in all patients with a raised LDL-C level compared with the healthy group, but arterial stiffness parameters were similar.42 This suggests that the FH mutation by itself is not a main indicator of endothelial dysfunction and that other factors are involved. The gene discussed is FH; the disease is familial hyperaldosteronism.