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      The Different Therapeutic Choices with ARBs. Which One to Give? When? Why?

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      Publication date (Electronic):
      Journal: American Journal of Cardiovascular Drugs
      Publisher: Springer International Publishing

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          Abstract

          The renin–angiotensin–aldosterone system plays an important role in the pathophysiology of hypertension and is closely related with cardio- and cerebrovascular events and chronic kidney diseases. Each angiotensin receptor blocker (ARB) is important in the treatment of hypertension, according to the results of recent years. This is a practical review of the available evidence on the different benefits of ARBs beyond their blood pressure-lowering effect, with an emphasis on the differences found between the particular compounds and the therapeutic implications of the findings, with specific reference to the co-morbidities.

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          15-year longitudinal study of blood pressure and dementia.

          I Skoog, B Lernfelt, S Landahl … (1996)
          Vascular causes of dementia may be more common than supposed. Vascular factors may also have a role in late-onset Alzheimer's disease, but the role of hypertension in the development of dementia is unclear. As part of the Longitudinal Population Study of 70-year-olds in Göteborg, Sweden, we analysed the relation between blood pressure and the development of dementia in the age intervals 70-75, 75-79, and 79-85 years in those non-demented at age 70 (n = 382). The sample was followed up for 15 years and examined repeatedly with a comprehensive investigation, including a psychiatric and physical examination. a Participants who developed dementia at age 79-85 had higher systolic blood pressure at age 70 (mean 178 vs 164 mm Hg, p = 0.034) and higher diastolic blood pressure at ages 70 (101 vs 92, p = 0.004) and 75 (97 vs 90, p = 0.022) than those who did not develop dementia. For subtypes of dementia, higher diastolic blood pressure was recorded at age 70 (101, p = 0.019) for those developing Alzheimer's disease and at age 75 (101, p = 0.015) for those developing vascular dementia than for those who did not develop dementia. Participants with white-matter lesions on computed tomography at age 85 had higher blood pressure at age 70 than those without such lesions. Blood pressure declined in the years before dementia onset and was then similar to or lower than that in non-demented individuals. Previously increased blood pressure may increase the risk for dementia by inducing small-vessel disease and white-matter lesions. To what extent the decline in blood pressure before dementia onset is a consequence or a cause of the brain disease remains to be elucidated.
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            Pathophysiology of progressive nephropathies.

            G. Remuzzi, T Bertani (1998)
            Article 0 comments Cited 182 times – based on 0 reviews     Review now
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              Telmisartan to prevent recurrent stroke and cardiovascular events.

              Ralph Sacco, Chuanzhen Lu, Robin Roberts … (2008)
              Prolonged lowering of blood pressure after a stroke reduces the risk of recurrent stroke. In addition, inhibition of the renin-angiotensin system in high-risk patients reduces the rate of subsequent cardiovascular events, including stroke. However, the effect of lowering of blood pressure with a renin-angiotensin system inhibitor soon after a stroke has not been clearly established. We evaluated the effects of therapy with an angiotensin-receptor blocker, telmisartan, initiated early after a stroke. In a multicenter trial involving 20,332 patients who recently had an ischemic stroke, we randomly assigned 10,146 to receive telmisartan (80 mg daily) and 10,186 to receive placebo. The primary outcome was recurrent stroke. Secondary outcomes were major cardiovascular events (death from cardiovascular causes, recurrent stroke, myocardial infarction, or new or worsening heart failure) and new-onset diabetes. The median interval from stroke to randomization was 15 days. During a mean follow-up of 2.5 years, the mean blood pressure was 3.8/2.0 mm Hg lower in the telmisartan group than in the placebo group. A total of 880 patients (8.7%) in the telmisartan group and 934 patients (9.2%) in the placebo group had a subsequent stroke (hazard ratio in the telmisartan group, 0.95; 95% confidence interval [CI], 0.86 to 1.04; P=0.23). Major cardiovascular events occurred in 1367 patients (13.5%) in the telmisartan group and 1463 patients (14.4%) in the placebo group (hazard ratio, 0.94; 95% CI, 0.87 to 1.01; P=0.11). New-onset diabetes occurred in 1.7% of the telmisartan group and 2.1% of the placebo group (hazard ratio, 0.82; 95% CI, 0.65 to 1.04; P=0.10). Therapy with telmisartan initiated soon after an ischemic stroke and continued for 2.5 years did not significantly lower the rate of recurrent stroke, major cardiovascular events, or diabetes. (ClinicalTrials.gov number, NCT00153062.) 2008 Massachusetts Medical Society
              Article 0 comments Cited 141 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Csaba András Dézsi: dcsa62@gmail.com
                Journal
                Journal ID (nlm-ta): Am J Cardiovasc Drugs
                Journal ID (iso-abbrev): Am J Cardiovasc Drugs
                Title: American Journal of Cardiovascular Drugs
                Publisher: Springer International Publishing (Cham )
                ISSN (Print): 1175-3277
                ISSN (Electronic): 1179-187X
                Publication date (Electronic): 3 March 2016
                Publication date PMC-release: 3 March 2016
                Publication date (Print): 2016
                Volume: 16
                Pages: 255-266
                Affiliations
                Department of Cardiology, Petz Aladár County Teaching Hospital, Gyor, Hungary
                Article
                Publisher ID: 165
                DOI: 10.1007/s40256-016-0165-4
                PMC ID: 4947116
                PubMed ID: 26940560
                SO-VID: 98552f06-c07e-46ba-a52d-f8451897ad18
                Copyright © © The Author(s) 2016
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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                Subject: Review Article
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                issue-copyright-statement © Springer International Publishing Switzerland 2016

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