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(Hypertension. 2009;54:3.)
© 2009 American Heart Association, Inc.
Brief Reviews |
From the Department of Clinical Sciences (P.M.N.), Lund University, University Hospital, Malmö, Sweden; Université Paris-Descartes (P.B., S.L.), Paris, France; Department of Pharmacology (P.B., S.L.), Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris France; and the Institut National de la Santé et de la Recherche Médicale U 970 (P.B., S.L.), Paris, France.
Correspondence to Peter M. Nilsson, Department of Clinical Sciences, Lund University, University Hospital, S-205 02 Malmö, Sweden. E-mail Peter.Nilsson@med.lu.se
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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It has been shown that target organ damage (TOD) represents a mediating step between risk factors and CVD events. Examples of well-established TOD categories include left ventricular hypertrophy and albumin excretion. In addition, substantial evidence has accumulated to show that arterial stiffness and increased pulse wave velocity (PWV), as well as central aortic pulse pressure, are important independent predictors of CVD events.2 These are in fact not only examples of TOD but also of the underlying pathological process, because increased PWV might determine the degree of left ventricular hypertrophy through increased arterial pulse wave reflection, central pulse pressure, and postload.2
Because aging is a common denominator to many chronic disease manifestations, eg, CVD, type 2 diabetes mellitus, or cancer, we propose that early vascular aging (EVA) could be a useful concept to better guide clinical investigations in subjects at increased cardiovascular (CV) risk. This could be the case in individuals with marginal elevation of classic risk factors or with
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