Literature DB >> 19179203

Blood pressure response under chronic antihypertensive drug therapy: the role of aortic stiffness in the REASON (Preterax in Regression of Arterial Stiffness in a Controlled Double-Blind) study.

Athanase Protogerou1, Jacques Blacher, George S Stergiou, Apostolos Achimastos, Michel E Safar.   

Abstract

OBJECTIVES: We sought to evaluate the role of arterial stiffness on blood pressure (BP) response to drug treatment.
BACKGROUND: Increased arterial stiffness (pulse wave velocity [PWV]) is associated with increased systolic blood pressure (SBP). Antihypertensive drug therapy achieves better control of diastolic blood pressure (DBP) than SBP does, implying that increased PWV might be a predictor of the SBP response to treatment.
METHODS: The REASON (Preterax in Regression of Arterial Stiffness in a Controlled Double-Blind) study is a randomized, double-blind trial comparing atenolol versus perindopril/indapamide; 375 patients with hypertension, with BP and PWV measurements at baseline and after 12 months of treatment, were divided into 3 tertiles according to baseline PWV and included in a post-hoc analysis.
RESULTS: After 12 months of treatment, BP differed significantly between PWV tertiles (the third having the lowest response, p < 0.05). Factors related to smaller BP decline were low baseline BP, high baseline PWV, need for a double dose of treatment, use of atenolol (only for SBP response), and age (only for DBP). Although DBP control did not differ in the PWV tertiles, SBP control was significantly associated with PWV level (p = 0.001) as well as with the use of perindopril/indapamide (p < 0.001). The predictive value of PWV on BP response was independent of age, sex, mean BP, and cardiovascular risk factors.
CONCLUSIONS: Baseline PWV is a significant predictor of BP response to antihypertensive treatment, independent from age, the need for increasing drug dosage, and the presence of cardiovascular risk factors. Achievement of SBP control appears to be influenced by aortic stiffness as well as by angiotensin-converting enzyme inhibition.

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Year:  2009        PMID: 19179203     DOI: 10.1016/j.jacc.2008.09.046

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


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