Changes in the compliance of the radial artery in normotensive subjects with familial hypercholesterolemia]

Recent studies have shown that in normotensive hypercholesterolemic subjects endothelial dependent dilatation of arterioles is impaired.We studied the effects of hypercholesterolemia on arterial compliance in normotensive subjects of both sexes, with a normal serum cholesterol (n = 8, total serum cholesterol = 209 +/- 7 mg/dl, means +/- SEM), an elevated serum cholesterol (n = 8, 285 +/- 8 mg/dl) and familial hypercholesterolemia (n = 8, 393 +/- 20 mg/dl). All subjects were normotensive and devoid of clinical and laboratory evidence of atherosclerotic lesions. The mean age of the 3 groups was 46.7 +/- 2.5, 51.5 +/- 2.9 and 49.8 +/- 2.9 years respectively. In hypercholesterolemic subjects use of hypolipidemic drugs was stopped 2 months before the study. Arterial compliance was measured from the radial artery by an echo-tracking device capable of providing radial artery diameter and, with the addition of a Finapres device, diameter/pressure and compliance/pressure curves continuously over the systolic-diastolic blood pressure range.Mean arterial pressure was similar in the three groups (84.5 +/- 6.1, 79.8 +/- 2.4 and 73.1 +/- 4.4 mm Hg). Arterial compliance was similar in normocholesterolemic and non familial hypercholesterolemic subjects but it was strikingly reduced (50%) in familial hypercholesterolemic subjects. The reduction was even more evident following prolonged local ischemia because while in the first two groups arterial compliance increased after ischemia, in familial hypercholesterolemia no increase occurred.Thus, familial hypercholesterolemia is accompanied by a strikingThus, familial hypercholesterolemia is accompanied by a striking reduction in radial artery compliance, i.e. a marked increase in arterial wall stiffness. This may increase the traumatic effect of blood pressure on the arterial wall, favouring atherosclerosis. The lack of compliance alterations in non familial hypercholesterolemia suggests that this hemodynamic disturbance either occurs when serum cholesterol is more markedly increased or it has a genetic origin.