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Objective To investigate whether individuals affected by familial combined hyperlipidemia, a common lipid disorder increasing the cardiovascular risk, had different carotid ultrasound parameters compared to control subjects without this family disorders. Methods 127 cases and 127 controls matched for age and gender were enrolled. Serum glucose, total cholesterol, high-density lipoprotein-cholesterol, triglycerides, ApoB, insulinemia were measured by standard laboratory techniques. All the subjects underwent B-mode ultrasonography to measure the end-diastolic and end-systolic diameter of the common carotid artery and, successively, to calculate distensibility, compliance, Young's elastic modulus and distension. Results Carotid diameter and Young's elastic modulus were significantly greater among FCH subjects than among controls, and carotid distensibility, compliance, distension and score distension were significantly lower than control, also after analysis of covariance in order to adjust all the carotid indexes for confounding variables. A multiple regression analysis confirmed that familial combined hyperlipidemia status was correlated to carotid indexes. In a model including the lipid parameters, triglycerides was the only lipid variable correlated with distensibility but not with distension. Conclusion This hyperlipidemia, particularly hypertrigliceridemia, could be the direct responsibility of carotid modification leading to the impairment of the distension/distensibility that, in turn, makes the patients prone to atherosclerosis.

It is recognized that arteries can enlarge to compensate atherosclerosis. The role of diameter enlargement of unaffected arteries is not well known. We hypothesized that brachial and common carotid arteries diameters were larger in subjects with carotid atherosclerosis compared to subjects without these lesions.We measured diameters in the common carotid and brachial arteries. Intimal medial thickness (IMT) of carotid arteries and carotid atherosclerosis were also evaluated using ultrasound in 83 cases and 83 disease-free control subjects.Common carotid and brachial diameter was greater in cases (subjects with carotid atherosclerosis) than controls (subjects without carotid atherosclerosis) after adjustment for confounding variables (P0.02). Common carotid diameter was also larger in individuals with greater IMT (P0.0001), whereas brachial artery diameter was not. Subjects with more than one carotid plaque had larger arterial diameters than those with one or without plaques.Common carotid and brachial artery diameters are both larger in cases than controls. This result suggests that vascular remodeling is a systemic process and not only a local response to atherosclerosis. The relationship between diameters and burden of disease could also suggest a link between vascular remodeling and severity of disease. Finally, if confirmed in prospective studies, brachial artery diameter could help to identify subjects at high cardiovascular risk, at least in postmenopausal women.

Objective To investigate on Brachial Artery Diameter enlargement in postmenopausal women with Metabolic Syndrome. Methods 294 women were admitted and classified in two groups according to the presence of Metabolic Syndrome. Serum glucose, insulin, lipid profile, carotid arteries and Brachial Artery Diameter were measured. Results Subjects with Metabolic Syndrome had the following different parameters in comparison to subjects without Metabolic Syndrome: Brachial Artery Diameter, Common Carotid Artery Diameter, IMT, and age. In a multivariate regression analysis Brachial Artery Diameter resulted correlated to age and presence of Metabolic Syndrome, among the Metabolic Syndrome components HDL was the only one to be associated to artery diameter. Furthermore, artery diameters increased with the increasing number of Metabolic Syndrome components. Conclusion Brachial Artery Diameter enlargement was found in postmenopausal women with Metabolic Syndrome. Arterial enlargement seems to be a systemic process occurring in response to some factors involved in atherosclerosis and not a focal change.