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Validity of pulse pressure and augmentation index as surrogate measures of arterial stiffness during beta-adrenergic stimulation

Lemogoum, Daniela; Flores, Gabriellaa; Van den Abeele, Wouterb; Ciarka, Agnieszkac; Leeman, Marca; Degaute, Jean Paula; van de Borne, Philippea; Van Bortel, Lucb

Original papers: Blood vessels

Objective Increased arterial stiffness is a determinant of cardiovascular mortality. Pulse wave velocity (PWV) is a direct measure of arterial stiffness. Aortic augmentation index (AI) and pulse pressure (PP) are surrogate measures of arterial stiffness. Both PWV, AI and PP increase with cardiovascular risk factors. The aim of this study was to test the validity of AI and PP as surrogate measures of arterial stiffness compared with PWV, during beta-adrenergic stimulation with Isoprenaline (Iso).

Design and methods A total of 41 healthy volunteers entered a randomized, double-blind, placebo-controlled, cross-over study. In random order, subjects were given intravenous infusion in equal volume of Iso 8 μg/kg per min (dissolved in glucose 5%) and placebo (glucose 5%). A wash-out period of 25 min was observed between the infusions. Measurements included blood pressure (BP), heart rate (HR), PWV, and AI. PWV were determined using complior (Complior, Artech-Medical, Paris, France). AI and aortic PP were obtained from pulse wave analysis of radial applanation tonometry, using transfer function (SphygmoCor Windows software).

Results Baseline AI increased (P< 0.05) with aging, a lower height and a larger diastolic BP (DBP). Iso increased (P< 0.0001) HR, brachial SBP, brachial and aortic PP as compared with placebo. In contrast, Iso decreased (P< 0.05) AI, brachial DBP, peripheral PWV, but not aortic PWV. Decrease of AI induced by Iso was not related to PWV. In stepwise multiple regression changes in HR, brachial SBP and DBP were independent determinants of AI response to Iso (r = 0.78, P< 0.0001).

Conclusions Our findings show that AI and PP fail as surrogate measures of arterial stiffness during beta-adrenergic stimulation.

aDepartment of Cardiology, Erasme Hospital, Brussels, bHeymans Institute of Pharmacology, Ghent, Belgium and cDepartment of Experimental and Clinical Physiology, Medical University of Warsaw, Poland.

Sponsorship: Material and financial supports of this study have been provided by Astra Zeneca (D.L.), Sankyo (A.C.), the Foundation for cardiac Surgery (P.vdB.) and the Heymans Institute of Pharmacology (W.vdA., L.V.B.).

Correspondence and requests for reprints to Daniel Lemogoum, Hypertension Clinic, Department of Cardiology, Erasme Hospital, 808 Lennik Road, 1070 Brussels, Belgium. Tel: +32 25553381; fax: +32 25556713; e-mail:

Received 16 June 2003 Revised 24 September 2003 Accepted 17 November 2003

See editorial commentary on page 447

© 2004 Lippincott Williams & Wilkins, Inc.