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      Fimasartan for independent reduction of blood pressure variability in mild-to-moderate hypertension

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          The angiotensin receptor antagonist fimasartan lowered blood pressure (BP) in a previous large population study. The purpose of this study was to evaluate whether fimasartan treatment for 3 months affects clinical and home BP variability in addition to reducing BP.


          The study enrolled 1,396 patients (mean age 56.2±10.0 years; males 53.6%) with mild-to-moderate hypertension who had a complete set of home BP measurements (morning and evening) and metabolic risk evaluation. During the 3 months of study, fimasartan alone was used to control BP at a daily dose of 30–120 mg. Clinical and home BP measurements were performed before and after the 3-month treatment. BP variability included beat-to-beat variability (clinical) and day-to-day variability (home).


          Fimasartan reduced BP after 3 months of treatment. The average reduction of clinical systolic BP (c-SBP) was 15.08±18.36 mmHg ( P<0.0001), and the average reduction of morning home SBP (m-SBP) was 11.49±19.33 mmHg ( P<0.0001). Beat-to-beat variability as standard deviation (SD) of c-SBP was reduced from 4.56±3.22 to 4.24±3.11 mmHg ( P=0.0026). Day-to-day variability as SD of m-SBP was reduced from 7.92±6.74 to 6.95±4.97 mmHg ( P<0.0001). Multiple regression analysis revealed an independent association between the change in the SD of c-SBP and the change in c-SBP ( P=0.0268) and, similarly, between the change in the SD of m-SBP and the change in m-SBP ( P=0.0258), after adjusting for age, sex, body mass index, and change in mean BP.


          This study indicated that 3 months of fimasartan treatment reduced day-to-day BP variability independent of BP reduction in patients with hypertension.

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          Most cited references 26

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          Limitations of the usual blood-pressure hypothesis and importance of variability, instability, and episodic hypertension.

           P M Rothwell (2010)
          Although hypertension is the most prevalent treatable vascular risk factor, how it causes end-organ damage and vascular events is poorly understood. Yet, a widespread belief exists that underlying usual blood pressure can alone account for all blood-pressure-related risk of vascular events and for the benefits of antihypertensive drugs, and this notion has come to underpin all major clinical guidelines on diagnosis and treatment of hypertension. Other potentially informative measures, such as variability in clinic blood pressure or maximum blood pressure reached, have been neglected, and effects of antihypertensive drugs on such measures are largely unknown. Clinical guidelines recommend that episodic hypertension is not treated, and the potential risks of residual variability in blood pressure in treated hypertensive patients have been ignored. This Review discusses shortcomings of the usual blood-pressure hypothesis, provides background to accompanying reports on the importance of blood-pressure variability in prediction of risk of vascular events and in accounting for benefits of antihypertensive drugs, and draws attention to clinical implications and directions for future research. Copyright 2010 Elsevier Ltd. All rights reserved.
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            Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: the CAMELOT study: a randomized controlled trial.

            The effect of antihypertensive drugs on cardiovascular events in patients with coronary artery disease (CAD) and normal blood pressure remains uncertain. To compare the effects of amlodipine or enalapril vs placebo on cardiovascular events in patients with CAD. Double-blind, randomized, multicenter, 24-month trial (enrollment April 1999-April 2002) comparing amlodipine or enalapril with placebo in 1991 patients with angiographically documented CAD (>20% stenosis by coronary angiography) and diastolic blood pressure <100 mm Hg. A substudy of 274 patients measured atherosclerosis progression by intravascular ultrasound (IVUS). Patients were randomized to receive amlodipine, 10 mg; enalapril, 20 mg; or placebo. IVUS was performed at baseline and study completion. The primary efficacy parameter was incidence of cardiovascular events for amlodipine vs placebo. Other outcomes included comparisons of amlodipine vs enalapril and enalapril vs placebo. Events included cardiovascular death, nonfatal myocardial infarction, resuscitated cardiac arrest, coronary revascularization, hospitalization for angina pectoris, hospitalization for congestive heart failure, fatal or nonfatal stroke or transient ischemic attack, and new diagnosis of peripheral vascular disease. The IVUS end point was change in percent atheroma volume. Baseline blood pressure averaged 129/78 mm Hg for all patients; it increased by 0.7/0.6 mm Hg in the placebo group and decreased by 4.8/2.5 mm Hg and 4.9/2.4 mm Hg in the amlodipine and enalapril groups, respectively (P<.001 for both vs placebo). Cardiovascular events occurred in 151 (23.1%) placebo-treated patients, in 110 (16.6%) amlodipine-treated patients (hazard ratio [HR], 0.69; 95% CI, 0.54-0.88 [P = .003]), and in 136 (20.2%) enalapril-treated patients (HR, 0.85; 95% CI, 0.67-1.07 [P = .16]. Primary end point comparison for enalapril vs amlodipine was not significant (HR, 0.81; 95% CI, 0.63-1.04 [P = .10]). The IVUS substudy showed a trend toward less progression of atherosclerosis in the amlodipine group vs placebo (P = .12), with significantly less progression in the subgroup with systolic blood pressures greater than the mean (P = .02). Compared with baseline, IVUS showed progression in the placebo group (P<.001), a trend toward progression in the enalapril group (P = .08), and no progression in the amlodipine group (P = .31). For the amlodipine group, correlation between blood pressure reduction and progression was r = 0.19, P = .07. Administration of amlodipine to patients with CAD and normal blood pressure resulted in reduced adverse cardiovascular events. Directionally similar, but smaller and nonsignificant, treatment effects were observed with enalapril. For amlodipine, IVUS showed evidence of slowing of atherosclerosis progression.
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              The relationship between visit-to-visit variability in systolic blood pressure and all-cause mortality in the general population: findings from NHANES III, 1988 to 1994.

              Recent data suggest that visit-to-visit variability of blood pressure is associated with stroke incidence. Correlates of increased visit-to-visit variability in blood pressure and the relationship between variability and all-cause mortality were examined using data on US adults ≥ 20 years of age from the Third National Health and Nutrition Examination Survey (n = 956). Three consecutive blood pressure readings were taken during 3 separate study visits from 1988 to 1994. Based on the mean of the second and third measurements from each visit, visit-to-visit blood pressure variability for each participant was defined using the standard deviation and coefficient of variation across visits. Mortality was assessed through December 31, 2006 (median follow-up = 14 years; n = 240 deaths). The mean of the standard deviation for systolic blood pressure across visits was 7.7 mm Hg. After multivariable adjustment, older age, female gender, history of myocardial infarction, higher mean systolic blood pressure and pulse pressure, and use of angiotensin converting enzyme inhibitors were associated with higher standard deviation in systolic blood pressure. The multivariable adjusted hazard ratios for all-cause mortality associated with a standard deviation of systolic blood pressure of 4.80 to 8.34 mm Hg and ≥ 8.35 mm Hg, versus <4.80 mm Hg, were 1.57 (95% CI, 1.07 to 2.18) and 1.50 (95% CI, 1.03 to 2.18), respectively. Results were similar when coefficient of variation for systolic blood pressure was evaluated. Visit-to-visit variability for diastolic blood pressure was not associated with mortality. In this population-based study of US adults, higher levels of short-term visit-to-visit variability in systolic blood pressure were associated with increased all-cause mortality.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                05 May 2016
                : 10
                : 1573-1580
                [1 ]Division of Cardiology, Department of Internal Medicine, Gachon University Gil Medical Center, Incheon, South Korea
                [2 ]Office of Biostatistics, Ajou University School of Medicine, Suwon, South Korea
                [3 ]Department of Preventive Medicine, Yonsei University College of Medicine, Seoul, South Korea
                [4 ]Division of Cardiology, Department of Internal Medicine, St Paul’s Hospital, Catholic University of Korea, Seoul, South Korea
                [5 ]Division of Cardiology, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, South Korea
                [6 ]Cardiology Division, Severance Cardiovascular Hospital and Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, South Korea
                [7 ]Division of Cardiology, Paik Hospital, Inje University College of Medicine, Busan, South Korea
                [8 ]Division of Cardiology, Jeju National University Hospital, Jeju, South Korea
                [9 ]Division of Cardiology, Wonju Severance Christian Hospital, Wonju Medical College, Yonsei University, Wonju, South Korea
                [10 ]Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, South Korea
                [11 ]Division of Medicine/Cardiology, Department of Internal Medicine, Cheil General Hospital, Dankook University College of Medicine, Seoul, South Korea
                Author notes
                Correspondence: Jeong Bae Park, Division of Medicine/Cardiology, Cheil General Hospital, Dankook University College of Medicine, 17, Seoae-ro 1-gil, Jung-gu, Seoul 100-380, South Korea, Tel +82 2 2000 7260, Fax +82 2 2000 7249, Email mdparkjb@ 123456gmail.com
                © 2016 Shin et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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