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. 2010 Nov;28(11):2336-41.
doi: 10.1097/HJH.0b013e32833da2b2.

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

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

Hafid Ait-Oufella et al. J Hypertens. 2010 Nov.

Abstract

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.

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