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Augmentation index is associated with cardiovascular risk

Nürnberger, Jensa; Keflioglu-Scheiber, Aytena; Opazo Saez, Anabelle Mb; Wenzel, Rene Ra; Philipp, Thomasa; Schäfers, Rafael Fa

Original papers: Blood vessels
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Objectives  Augmentation index is a parameter measured by pulse wave analysis (PWA) and is used as a surrogate measure of arterial stiffness. The aim of this study was to assess whether augmentation index is associated with cardiovascular risk, as well as to evaluate whether the determinants of augmentation index are different in patients with cardiovascular disease compared to healthy subjects.

Design and methods  We related augmentation index to risk scores in 216 subjects with or without a cardiovascular disease. Subjects without cardiovascular disease were classified according to the ‘coronary risk chart’ of the European Society of Cardiology (ESC), and those with cardiovascular disease were classified using the SMART (Second Manifestations of ARTerial disease) score and the EPOZ (Epidemiological Prevention study Of Zoetermeer) function. Augmentation index was derived by PWA using carotid applanation tonometry. Augmentation index was also correlated to age, blood pressure, heart rate, smoking history, cholesterol, height, body mass index and gender in subjects categorized as healthy or with cardiovascular disease.

Results  Augmentation index significantly increased with increasing risk scores (P < 0.0001) and was significantly correlated to cardiovascular risk (ESC: P < 0.0001; SMART: P < 0.0001; EPOZ: P < 0.0001). In subjects with and without cardiovascular disease, augmentation index was correlated with diastolic blood pressure, heart rate, height and gender. Age was found to be significantly correlated with augmentation index only in healthy subjects but not in those with atherosclerotic disease.

Conclusions  Our findings suggest that augmentation index may be a useful marker of cardiovascular risk. Further studies are required to investigate the relationship between age and augmentation index in subjects with atherosclerotic disease.

aDepartment of Nephrology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany and bDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Sponsorship: This study has been supported by the intramural research program of the University of Essen Medical School (IFORES).

Correspondence and requests for reprints to Dr R.F. Schäfers, Department of Nephrology, University of Essen, Hufelandstraße 55, 45122 Essen, Germany. Tel: +49 201 723 3852; fax: +49 201 723 3855; e-mail: rafael.schaefers@uni-essen.de

Received 30 April 2002 Revised 5 August 2002 Accepted 21 August 2002

See editorial commentary page 2337

Part of this work was presented in a poster at the tenth European meeting on hypertension (Goteborg, Sweden, 29 May–3 June 2000).

© 2002 Lippincott Williams & Wilkins, Inc.