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(Hypertension. 2006;47:371.)
© 2006 American Heart Association, Inc.
Original Articles |
From the Department of Pharmacology (A.P., P.B., B.L., S.L.), Hôpital Européen Georges Pompidou, INSERM U652, and Université Paris-Descartes, Faculté de Médecine, Paris, France; Internal Medicine (A.P.), University of Brescia, Brescia, Italy; Neurology Department (D.C.), Hopital Sainte-Anne, Paris, France; Pharmacology Department (A.-I.T.), Hopital Henri Mondor, Creteil, France.
Correspondence to Stéphane Laurent, Department of Pharmacology and INSERM U652, Hôpital Européen Georges Pompidou, Assistance Publique - Hôpitaux de Paris, Université Paris-Descartes, Faculté de Médecine, 20, rue Leblanc, 75015 Paris, France. E-mail stephane.laurent{at}egp.ap-hop-paris.fr
Several studies have shown that aortic stiffness was an independent predictor for cardiovascular events. However, data are less consistent concerning carotid stiffness. We analyzed the determinants of the discrepancies between aortic and carotid stiffness in different populations with contrasting cardiovascular risk factors: 94 healthy normotensives (NT), 243 nondiabetic hypertensives (HT), and 126 patients with hypertension and type 2 diabetes (T2D). Aortic stiffness was measured with carotid-femoral pulse wave velocity. Common carotid stiffness was determined from the relative stroke change in diameter (measured with a high-resolution echotracking system) and carotid pulse pressure (measured with applanation tonometry) and was expressed in the same dimensions as pulse wave velocity (m/s). We identified the various factors explaining the discrepancies between aortic and carotid stiffness by multivariate analysis of the residuals of the correlation between aortic and carotid stiffness. The strength of the correlation between aortic and carotid stiffness became weaker as the number of cardiovascular risk factors increased (NT, r2=0.41; HT, r2=0.16; and T2D, r2=0.11), whereas we observed the opposite for the discrepancies (residuals) between aortic and carotid stiffness, of which an increasing part was explained (11% in NT, 22% in HT, and 45% in T2D) primarily by aging. In conclusion, although carotid-femoral pulse wave velocity and carotid stiffness provided similar information on the impact of aging on large artery stiffness in normal subjects, this was not the case for high blood pressure and/or diabetes. In these cases, the aorta stiffened more than the carotid artery with age and other cardiovascular risk factors.
Key Words: aorta carotid arteries elasticity diabetes mellitus arteriosclerosis
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