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Long-term reduction in aortic stiffness: a 5.3-year follow-up in routine clinical practice

Ait-Oufella, Hafida,b,c; Collin, Cédrica,b,c; Bozec, Erwana,b,c; Laloux, Brigrittea,b,c; Ong, Kim-Thanha,b,c; Dufouil, Caroled,e; Boutouyrie, Pierrea,b,c; Laurent, Stéphanea,b,c

doi: 10.1097/HJH.0b013e32833da2b2
Original papers: Therapeutic aspects
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Background Whether a direct blood pressure-independent reduction in aortic stiffness can occur after several years of antihypertensive treatment has never been unequivocally demonstrated.

Method In this observational study, performed under conditions of routine clinical practice, we included 97 patients (age 63 ± 11 years) with treated essential hypertension who attended the outpatient hypertension clinic of a university hospital, had a significant blood pressure (BP) lowering under treatment before the first measurement of aortic stiffness, and had at least one additional measurement of aortic stiffness during follow-up. Aortic stiffness and carotid pulse pressure (PP) were determined through carotid–femoral pulse wave velocity (PWV) and applanation tonometry, respectively.

Results A linear mixed model showed that the reduction in PWV (from 14.2 ± 4.2 to 11.0 ± 2.4 m/s; P < 0.0001) over a long follow-up (mean delay 5.3 ± 1.3 years) was associated with a significant reduction in central SBP (from 132 ± 22 to 122 ± 16 mmHg; P < 0.0001) and central PP (from 59 ± 22 to 54 ± 14; P < 0.001), contrasting with a smaller change in brachial SBP (from 132 ± 17 to 129 ± 16 mmHg; P < 0.02) and no change in brachial PP. In multivariate analysis, the decrease in PWV (−0.70 ± 0.07 m/s per year; P < 0.0001) was only slightly explained by the reduction in mean blood pressure. By contrast, the decrease in central PP (−0.83 ± 0.41 mmHg per year; P = 0.043) was largely explained by the reduction in PWV.

Conclusion These results indicate that a large and sustained decrease in aortic stiffness can be obtained in treated hypertensive patients under conditions of routine clinical practice. These changes likely represent a delayed response to the long-term normalization of BP and cardiovascular risk factors, through arterial remodeling.

aDepartment of Pharmacology, European Hospital Georges Pompidou, France

bUniversité René Descartes-Paris 5, France

cINSERM U 970, France

dINSERM U 708, France

eUniversité Pierre et Marie Curie-Paris 6, Paris, France

Received 22 December, 2009

Revised 28 April, 2010

Accepted 28 June, 2010

Correspondence to Pr Stéphane Laurent, Department of Pharmacology and INSERM U 970, Hôpital Européen Georges Pompidou, Assistance Publique – Hôpitaux de Paris, Université Paris Descartes, 20 rue Leblanc, 75015 Paris, France E-mail: stephane.laurent@egp.aphp.fr

© 2010 Lippincott Williams & Wilkins, Inc.