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      Azelnidipine plus olmesartan versus amlodipine plus olmesartan on arterial stiffness and cardiac function in hypertensive patients: a randomized trial

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          To compare the long-term effects of olmesartan combined with either azelnidipine or amlodipine on central blood pressure (CBP), left ventricular (LV) mass index (LVMI), LV diastolic function (e′ velocity, E/e′ ratio, E/A ratio) and arterial stiffness (brachial-ankle pulse wave velocity [baPWV] and augmentation index normalized for a heart rate of 75 bpm [AIx]).

          Patients and methods

          Patients with systolic BP ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg received olmesartan monotherapy (20 mg/day) for 12 weeks. They were then randomly assigned to fixed-dose add-on therapy with azelnidipine (16 mg/day; n = 26) or amlodipine (5 mg/day; n = 26) for a further 2 years. CBP, LVMI, e′ velocity, E/e′ ratio, E/A ratio, baPWV, and AIx were measured at baseline, 6 months, and 2 years.


          Baseline characteristics of both groups were similar. The decrease in brachial BP over 2 years was similar in both groups. CBP, LVMI, E/e′ ratio, baPWV, and AIx decreased significantly, and the E/A ratio and e′ velocity increased significantly in both groups. The decreases in CBP ( P < 0.001), AIx ( P < 0.001), baPWV ( P < 0.001), LVMI ( P < 0.001), and E/e′ ( P = 0.002) as well as the increase in E/A ratio ( P = 0.03) over 2 years were significantly greater in the olmesartan/azelnidipine group than in the olmesartan/amlodipine group. Multivariate linear regression analyses showed that the changes in baPWV (β = 0.41, P < 0.001) and CBP (β = 0.47, P = 0.01) were independently associated with the change in LVMI, the change in baPWV (β = 0.25, P < 0.001) was independently associated with the change in E/e′ ratio, and the changes in baPWV (β = 0.21, P = 0.001) and AIx (β = 0.25, P = 0.03) were independently associated with the change in E/A ratio.


          Treatment with olmesartan/azelnidipine for 2 years resulted in greater improvements in CBP, LVMI, and LV diastolic function, and arterial stiffness compared with olmesartan/amlodipine. Improvements in LV diastolic function were associated with improvements in arterial stiffness.

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          Most cited references 28

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          The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009).

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            Noninvasive estimation of left ventricular filling pressure by E/e' is a powerful predictor of survival after acute myocardial infarction.

            The aim of this study was to assess the prognostic value of a noninvasive measure of left ventricular diastolic pressure (LVDP) early after acute myocardial infarction (MI). The early diastolic velocity of the mitral valve annulus (e') reflects the rate of myocardial relaxation. When combined with measurement of the early transmitral flow velocity (E), the resultant ratio (E/e') correlates well with mean LVDP. In particular, an E/e' ratio >15 is an excellent predictor of an elevated mean LVDP. We hypothesized that an E/e' ratio >15 would predict poorer survival after acute MI. Echocardiograms were obtained in 250 unselected patients 1.6 days after admission for MI. Patients were followed for a median of 13 months. The end point was all-cause mortality. Seventy-three patients (29%) had an E/e' >15. This was associated with excess mortality (log-rank statistic 21.3, p 15 improved the prognostic utility of a model containing clinical variables and conventional echocardiographic indexes of left ventricular systolic and diastolic function (p = 0.001). E/e' is a powerful predictor of survival after acute MI. An E/e' ratio >15 is superior, in this respect, to other clinical or echocardiographic features. Furthermore, it provides prognostic information incremental to these parameters.
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              Relationship between radial and central arterial pulse wave and evaluation of central aortic pressure using the radial arterial pulse wave.

              Since a decrease of central aortic pressure contributes to the prevention of cardiovascular events, simple measurement of not only brachial blood pressure but also central aortic pressure may be useful in the prevention and treatment of cardiovascular diseases. In this study, we simultaneously measured radial artery pulse waves non-invasively and ascending aortic pressure invasively, before and after the administration of nicorandil. We then compared changes in central aortic pressure and radial arterial blood pressure calibrated with brachial blood pressure in addition to calculating the augmentation index (AI) at the aorta and radial artery. After nicorandil administration, the reduction in maximal systolic blood pressure in the aorta (Deltaa-SBP) was -14+/-15 mmHg, significantly larger than that in early systolic pressure in the radial artery (Deltar-SBP) (-9+/-12 mmHg). The reduction in late systolic blood pressure in the radial artery (Deltar-SBP2) was -15+/-14 mmHg, significantly larger than Deltar-SBP, but not significantly different from Deltaa-SBP. There were significant relationships between Deltaa-SBP and Deltar-SBP (r=0.81, p<0.001), and between Deltaa-SBP and Deltar-SBP2 (r=0.91, p<0.001). The slope of the correlation regression line with Deltar-SBP2 (0.83) was larger and closer to 1 than that with Deltar-SBP (0.63), showing that the relationship was close to 1:1. Significant correlations were obtained between aortic AI (a-AI) and radial AI (r-AI) (before nicorandil administration: r=0.91, p<0.001; after administration: r=0.70, p<0.001). These data suggest that the measurement of radial artery pulse wave and observation of changes in the late systolic blood pressure in the radial artery (r-SBP2) in addition to the ordinary measurement of brachial blood pressure may enable a more accurate evaluation of changes in maximal systolic blood pressure in the aorta (a-SBP).

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Dove Medical Press
                22 March 2013
                : 7
                : 175-183
                [1 ]Department of Internal Medicine, Clinic Jingumae, Kashihara, Japan
                [2 ]First Department of Internal Medicine, Nara Medical University, Kashihara, Japan
                Author notes
                Correspondence: Takeshi Takami, Department of Internal Medicine, Clinic Jingumae, 5-4-41 Naizencho, Kashihara, Nara 634-0804, Japan, Tel +81 744 23 8568, Fax +81 744 23 6818, Email takami66@ 123456m5.kcn.ne.jp
                © 2013 Takami and Saito, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                Original Research


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