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  • 1. Ahlgren, AR
    et al.
    Piitulainen, E
    Sandgren, T
    Länne, Toste
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Alfa1-antitrypsin deficiency and blood pressure regulation2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, p. S151-S151Conference paper (Other academic)
  • 2.
    Andersen, Kasper
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Ärnlöv, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Muscle Morphology And Risk Of Cardiovascular Disease2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, p. E353-E353Article in journal (Other academic)
  • 3.
    Arefalk, Gabriel
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Hergens, M. P.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Ärnlöv, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Ye, W.
    Nyrén, O.
    Lambe, M.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Smokeless Tobacco (Snus) And Risk Of Heart Failure In Two Swedish Cohorts2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, p. E48-E49Article in journal (Other academic)
  • 4. Arefalk, Gabriel
    et al.
    Hergens, Maria-Pia
    Ingelsson, Erik
    Ärnlöv, Johan
    Dalarna University, School of Education, Health and Social Studies, Medical Science.
    Michaëlsson, Karl
    Lind, Lars
    Ye, Weimin
    Nyrén, Olof
    Lambe, Mats
    Sundström, Johan
    Smokeless tobacco (snus) and risk of heart failure: results from two Swedish cohorts2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no suppl.A, p. E48-E49Article in journal (Refereed)
  • 5. Bang, Casper N.
    et al.
    Gerdts, Eva
    Aurigemma, Gerard P.
    Boman, Kurt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Dahlof, Bjoern
    Roman, Mary J.
    Kober, Lars
    Wachtell, Kristian
    Devereux, Richard B.
    Systolic left ventricular function according to left ventricular concentricity and dilatation in hypertensive patients: the Losartan Intervention For Endpoint reduction in hypertension study2013In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 31, no 10, p. 2060-2068Article in journal (Refereed)
    Abstract [en]

    Background:Left ventricular hypertrophy [LVH, high left ventricular mass (LVM)] is traditionally classified as concentric or eccentric based on left ventricular relative wall thickness. We evaluated left ventricular systolic function in a new four-group LVH classification based on left ventricular dilatation [high left ventricular end-diastolic volume (EDV) index and concentricity (LVM/EDV(2/3))] in hypertensive patients.Methods and results:Nine hundred thirty-nine participants in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy had measurable LVM at enrolment. Patients with LVH (LVM/body surface area 116g/m(2) in men and 96g/m(2) in women) were divided into four groups; eccentric nondilated' (normal LVM/EDV and EDV), eccentric dilated' (increased EDV, normal LVM/EDV), concentric nondilated' (increased LVM/EDV with normal EDV), and concentric dilated' (increased LVM/EDV and EDV) and compared to patients with normal LVM. At baseline, 12% had eccentric nondilated, 20% eccentric dilated, 29% concentric nondilated, and 14% concentric dilated LVH, with normal LVM in 25%. Compared with the concentric nondilated LVH group, those with concentric dilated LVH had significantly lower pulse pressure/stroke index and ejection fraction; higher LVM index, stroke volume, cardiac output, left ventricular midwall shortening, left atrial volume and isovolumic relaxation time; and more had segmental wall motion abnormalities (all P<0.05). Similar differences existed between patients with eccentric dilated and those with eccentric nondilated LVH (all P<0.05). Compared with patients with normal LVM, the eccentric nondilated had higher LV stroke volume, pulse pressure/stroke index, Cornell voltage product and SBP, and lower heart rate and fewer were African-American (all P<0.05).Conclusion:The new four-group classification of LVH identifies dilated subgroups with reduced left ventricular function among patients currently classified with eccentric or concentric LVH.

  • 6.
    Beijer, Kristina
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Organismal Biology, Environmental toxicology.
    Lampa, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Nilsson, Peter M.
    SUS Malmo, Dept Clin Sci, Malmo, Sweden..
    Elmstahl, Solve
    Lund Univ, Div Geriatr Med, Dept Hlth Sci, Malmo Univ Hosp, Malmo, Sweden..
    Pedersen, Nancy L.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Interaction between physical activity and television time on blood pressure level: cross-sectional data from 45000 individuals2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 5, p. 1041-1050Article in journal (Refereed)
    Abstract [en]

    Objectives:The aim was to investigate if there is an interaction between sitting time and leisure time physical activity on blood pressure and if there are age differences and sex differences in this respect.

    Methods:Linear regression analysis on cross-sectional data was performed in more than 45000 men and women from two Swedish cohort studies, EpiHealth (45-75 years) and LifeGene (18-45 years). Self-reported leisure time physical activity was given in five levels from low (level 1) to vigorous physical activity (level 5) and television time was used as a proxy measure of sitting time.

    Results:High physical activity was associated with lower DBP (P=0.001), but not SBP. Active middle-aged men had lower DBP (-1.1mmHg; 95% CI -1.7 to -0.4) compared with inactive participants. Prolonged television time was associated with higher SBP (P<0.001) and DBP (P=0.011) in both sexes and in most age groups. Watching 3h instead of 1h television per day was associated with higher SBP in middle-aged women (SBP: 1.1mmHg; 95% CI 0.7-1.4) and men (SBP: 1.2mmHg; 95% CI 0.8-1.6). Only in young men, a high physical activity (level 4 instead of level 1) could compensate for a prolonged television time (3h per day) in terms of DBP.

    Conclusion:Prolonged television time was associated with higher SBP and DBP in both sexes and at most ages, whereas an increased physical activity was mainly associated with a lower DBP. Only in young men, a high physical activity could compensate for prolonged television time regarding DBP.

  • 7. Bejan-Angoulvant, Theodora
    et al.
    Saadatian-Elahi, Mitra
    Wright, James M
    Schron, Eleanor B
    Lindholm, Lars H
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Fagard, Robert
    Staessen, Jan A
    Gueyffier, François
    Treatment of hypertension in patients 80 years and older: the lower the better? A meta-analysis of randomized controlled trials.2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no 7, p. 1366-1372Article in journal (Refereed)
    Abstract [en]

    Background: Results of randomized controlled trials are consistent in showing reduced rates of stroke, heart failure and cardiovascular events in very old patients treated with antihypertensive drugs. However, inconsistencies exist with regard to the effect of these drugs on total mortality.

    Methods: We performed a meta-analysis of available data on hypertensive patients 80 years and older by selecting total mortality as the main outcome. Secondary outcomes were coronary events, stroke, cardiovascular events, heart failure and cause-specific mortality. The common relative risk (RR) of active treatment versus placebo or no treatment was assessed using a random-effect model. Linear meta-regression was performed to explore the relationship between intensity of antihypertensive therapy and blood pressure (BP) reduction and the log-transformed value of total mortality odds ratios (ORs).

    Results: The overall RR for total mortality was 1.06 (95% confidence interval 0.89–1.25), with significant heterogeneity between hypertension in the very elderly trial (HYVET) and the other trials. This heterogeneity was not explained by differences in the follow-up duration between trials. The meta-regression suggested that a reduction in mortality was achieved in trials with the least BP reductions and the lowest intensity of therapy. Antihypertensive therapy significantly reduced (P < 0.001) the risk of stroke (35%), cardiovascular events (27%) and heart failure (50%). Cause-specific mortality was not different between treated and untreated patients.

    Conclusion: Treating hypertension in very old patients reduces stroke and heart failure with no effect on total mortality. The most reasonable strategy is the one associated with significant mortality reduction; thiazides as first-line drugs with a maximum of two drugs.

  • 8.
    Bjarnegård, Niclas
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences.
    Ahlgren, AR
    Sandgren, T
    Sonesson, B
    Länne, Toste
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Effects of age and sympathetic stimulation on the mechanical properties of the proximal brachial artery2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, p. S248-S249Conference paper (Other academic)
  • 9.
    Borghi, Claudio
    et al.
    University of Bologna, Italy.
    Rodriguez-Artalejo, Fernando
    Univ Autonoma Madrid IdiPaz, Spain ; Inst Salud Carlos III, Spain.
    De Backer, Guy
    Univ Ghent, Belgium.
    Dallongeville, Jean
    Univ Lille Nord France, France.
    Medina, Jesús
    AstraZeneca Farmaceut Spain, Spain.
    Guallar, Eliseo
    Johns Hopkins Bloomberg Sch Publ Hlth, USA ; Johns Hopkins Bloomberg Sch Publ Hlth, USA.
    Perk, Joep
    Linnaeus University, Faculty of Health and Life Sciences, Department of Health and Caring Sciences.
    Banegas, José R.
    Univ Autonoma Madrid IdiPaz, Spain ; Inst Salud Carlos III, Spain.
    Tubach, Florence
    Hop Bichat Claude Bernard, France ; ECEVE, France ; Univ Paris Diderot, France.
    Roy, Carine
    Hop Bichat Claude Bernard, France ; ECEVE, France ; Hop Bichat Claude Bernard, France.
    Halcox, Julian P.
    Swansea Univ, UK.
    The association between blood pressure and lipid levels in Europe: European study on cardiovascular risk prevention and management in usual daily practice2016In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 34, no 11, p. 2155-2163Article in journal (Refereed)
    Abstract [en]

    Objectives:Several studies have suggested a positive association between serum lipid levels and blood pressure (BP). This study investigated this association in a large population from 12 European countries.Methods:Data were taken from the European Study on Cardiovascular Risk Prevention and Management in Usual Daily Practice (ClinicalTrials.gov identifier: NCT00882336). Associations between BP and lipid levels in patients free from cardiovascular disease and with at least one major cardiovascular disease risk factor (N=7641) were assessed using linear regression analyses.Results:Overall, 72.8 and 64.8% of patients had hypertension and dyslipidaemia, respectively; 47.0% had both conditions. Regression coefficients (95% confidence interval) for the associations of LDL cholesterol, non-HDL cholesterol, total cholesterol and apolipoprotein B levels with SBP, adjusted for age, sex and BMI, were 0.93mmHg/mmol per l (0.54-1.31), 1.07mmHg/mmol per l (0.73-1.40), 1.02mmHg/mmol per l (0.69-1.35) and 4.94mmHg/g per l (3.43-6.46), respectively. The corresponding values (95% confidence interval) for the associations with DBP were 0.96mmHg/mmol per l (0.73-1.19), 0.95mmHg/mmol per l (0.75-1.15), 0.87mmHg/mmol per l (0.67-1.07) and 4.33mmHg/g per l (3.42-5.23), respectively. Most of these associations remained significant whether patients were treated with statins or not.Conclusion:Small but statistically significant associations between lipid levels and BP were observed in a large, multinational European population. Further research is warranted to assess the causality of this association and its implications on the management of patients with both hypertension and dyslipidaemia.

  • 10.
    Brunström, Mattias
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Response to 'SPRINTin context: meta-analysis of trials with baseline normotension and lowlevels of previous cardiovascular disease' Reply2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 7, p. 1603-1604Article in journal (Refereed)
  • 11.
    Brunström, Mattias
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    SPRINT in context: meta-analysis of trials with baseline normotension and low levels of previous cardiovascular disease2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 5, p. 979-986Article, review/survey (Refereed)
    Abstract [en]

    Objective: To estimate the effect of antihypertensive treatment in trials with baseline normotension and low levels of previous cardiovascular disease. To test if the results from SPRINT are compatible with those from other trials, and test the impact of SPRINT results on overall effect estimates. Methods: Systematic review and meta-analysis of randomized controlled trials with at least 1000 patient-years of follow-up, comparing antihypertensive treatment versus placebo, or different blood pressure goals against each other. Trials with at least 50% previous cardiovascular disease were excluded. Results: Sixteen trials, including 66816 participants, were included in the meta-analyses. Mean baseline SBP was 138mmHg, and mean difference between treatment arms was 5.5mmHg. Antihypertensive treatment was associated with a neutral effect on all-cause mortality [relative risk 0.98, 95% confidence interval (CI) 0.92-1.05] and major cardiovascular events (0.97, 0.91-1.03). Results from SPRINT differed significantly from those of other trials (P=0.012 for all-cause mortality; P=0.016 for major cardiovascular events), but overall effect estimates were similar when SPRINT was excluded (1.01, 0.95-1.06 for all-cause mortality; 0.98, 0.93-1.03 for major cardiovascular events). Treatment was associated with reduced risk of secondary outcomes stroke (0.84, 0.71-1.00) and heart failure (0.88, 0.78-0.98), although heterogeneity was high in the stroke analysis (I-2=54%). Conclusion: SPRINT results are not representative for trials with baseline normotension and low levels of previous cardiovascular disease. Antihypertensive treatment does not protect against death or major cardiovascular events in this setting.

  • 12.
    Brunström, Mattias
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Medicine.
    Standardization according to blood pressure lowering in meta-analyses of antihypertensive trials: comparison of three methodological approaches2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 1, p. 4-15Article, review/survey (Refereed)
    Abstract [en]

    OBJECTIVE: Assess how standardization of relative risks (RRs) and standard errors (SEs), according to blood pressure differences within trials, affects heterogeneity, overall effect estimates and study weights in meta-analyses of antihypertensive treatment.

    METHOD: Data from a previous systematic review were used. Three sets of analyses were performed, using both random-effects and fixed-effects model for meta-analyses. First, we used raw data from the included trials. Second, we standardized RRs as if SBP was reduced by 10 mmHg in all trials. Third, we standardized both RRs and SEs.

    RESULTS: When RRs were standardized according to blood pressure lowering, heterogeneity between trials increased (I = 36 vs. 93% for mortality). This conferred large differences in treatment effect estimates using random-effects and fixed-effects model (RR 0.79, 95% confidence interval 0.70-0.89, respectively, 0.97, 0.94-0.99). When SEs were standardized, confidence intervals for individual trials widened, resulting in lower power to detect heterogeneity across trials. Study weights were dissociated from number of events in trials (P < 0.0001, R = 0.99 before standardization vs. P = 0.063, R = 0.05 after standardization). This induced a secondary shift in weight from trials with lower baseline SBP to trials with higher baseline SBP, resulting in exaggerated overall effect estimates.

    CONCLUSION: Standardization of RRs exaggerates differences between trials and makes meta-analyses highly sensitive to choice of statistical method. Standardization of SEs masks heterogeneity and results in biased effect estimates.

  • 13.
    Brunström, Mattias
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Eliasson, Mats
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Nilsson, Peter M
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Blood pressure treatment levels and choice of antihypertensive agent in people with diabetes mellitus: an overview of systematic reviews2017In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 35, p. 435-462Article, review/survey (Refereed)
    Abstract [en]

    OBJECTIVE: Multiple systematic reviews address the effect of antihypertensive treatment in people with diabetes. Here, we summarize current systematic reviews concerning antihypertensive treatment effect at different blood pressure (BP) levels, and relative treatment effect of different antihypertensive agents.

    METHODS: We searched MEDLINE, BIOSIS, DARE and CDSR during years 2005-2016. Eligibility criteria, number of trials and participants, outcomes analysed, statistical methods used for data synthesis, and principal results were extracted for each review. Review quality was assessed using the assessment of multiple systematic reviews tool.

    RESULTS: We found four reviews concerning BP treatment level. These consistently showed that the effect of antihypertensive treatment on mortality, cardiovascular disease and coronary heart disease was attenuated at lower BP levels. If SBP was more than 140 mmHg, treatment reduced all-cause and cardiovascular mortality, cardiovascular disease, stroke, myocardial infarction and heart failure. If SBP was less than 140 mmHg, treatment increased the risk of cardiovascular death. We found eight reviews concerning choice of agent. We found no difference between angiotensin-converting enzyme inhibitors, angotensin receptor blockers, beta-blockers, calcium channel blockers and diuretics in preventing all-cause or cardiovascular mortality, combined cardiovascular disease, coronary heart disease and end-stage renal disease. Minor differences exist for stroke and heart failure. Data were limited on people with type 1 diabetes and very elderly patients with type 2 diabetes. None of the reviews concerning choice of agent included all relevant trials.

    CONCLUSION: The available evidence supports treatment in people with type 2 diabetes and SBP more than 140 mmHg, using any of the major antihypertensive drug classes.

  • 14.
    Burger, Dylan
    et al.
    University of Ottawa, Ottawa, Ontario, Canada.
    Veerabhadrappa, Praveen
    Temple University, Philadelphia, Pennsylvania, USA.
    Charchar, Fadi
    University of Ballarat, Ballarat, Victoria, Australia.
    Tomaszewski, Maciej
    University of Leicester, Leicester, UK.
    Harrap, Stephen
    University of Melbourne, Melbourne, Victoria, Australia.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Touyz, Rhian M.
    University of Ottawa, Ottawa, Ontario, Canada.
    Report of the first International Society of Hypertension (ISH) Trainee/New Investigator Symposium: A Global Hypertension Initiative2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 3, p. 631-632Article in journal (Refereed)
  • 15.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Is lower really better?: Issue of the J curve hypothesis in hypertension2016In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 34, p. e196-Article in journal (Refereed)
    Abstract [en]

    The J curve hypothesis propose that the relation between blood pressure and risk for cardiovascular events is non-linear. Instead of a decreased risk with lower blood pressure, the risk increases at lower blood pressures. This issue has been discussed for many years, and is still a hot topic. The debates have most often had its origin in the question about how far blood pressure should be lowered with antihypertensive drugs.One one hand, we know that many patients with hypertension is not treated to targets according to guidelines and that this contributes to the high risk for cardiovascular diseases in patients with hypertension. On the other hand, overtreatment could be one reason for the subobtimal effect of antihypertensive drugs on cardiovascular diseases.The issue about a J curve in the effect of antihypertensive drugs is complicated.The relation between blood pressure and cardiovascular risk is different for different cardiovascular outcomes. For example, the risk for intracerebral hemorrhage seem to increase steeper at higher blood pressure than for most other outcomes. On the other hand, the risk for abdominal aortic aneurysm increases only modestly with higher blood pressure. In addition, end stage renal disease and cognitive decline could have other relations between blood pressure and risk. Age, cardiovascular disease and diabetes have also been found to modify the relation between risk and outcome.Earlier this year, we published a meta-analysis of randomized controlled trials with antihypertensive drugs in patients with diabetes mellitus (ref). Included trials had to compare treatment with an antihypertensive drug against placebo, two antihypertensive agents against one or one blood pressure target against another target. The studies were stratified according to blood pressure at randomization (baseline blood pressure), mimicking the situation you as a clinician meet when you decide to recommend a patients additional antihypertensive therapy or not. We contacted authors to receive data from diabetic subgroups in large studies. Thus, we were able to include more studies than in previous systematic reviews in this field. All together, we included data from 49 randomized controlled trials, including 73 738 patients.The systematic review showed that the effect of antihypertensive drugs on cardiovascular outcomes is different at different blood pressure levels. For most outcomes, adding antihypertensive drugs were beneficial in patients with diabetes mellitus and high blood pressure. However, this benefit decreased with decreasing blood pressure. The risk for cardiovascular death increased when therapy was added in patents with diabetes and systolic blood pressure below 140 mmHg. The benefits of adding antihypertensive treatment at different blood pressure levels are summarized in the figure below.Thus, in patients with diabetes, the relations between treatment effect of antihypertensive drugs are different at different blood pressure levels. Treatment effects differ for different cardiovascular outcomes. These data question previous guidelines that recommend a systolic blood pressure target below 130 mmHg in patients with diabetes mellitus.In a very recent systematic review, we have reexamined the relation between randomization blood pressure and cardiovascular stratified for different baseline blood pressures. The meta-analyses include patients with and without diabetes, with and without previous cardiovascular disease etc. Altogether, 58 trials with 290 000 patients were included. The study shows that the effect of blood pressure lowering on cardiovascular outcomes is dependent on baseline systolic blood pressure but also differ between different subsets of patients. This study is under review and the results will be presented during the lecture.

  • 16.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Proteinuria early in the development of hypertension2014In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 32, no 12, p. 2351-2352Article in journal (Other academic)
  • 17.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    The challenge of preventing dementia by antihypertensive treatment2013In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 31, no 9, p. 1780-1781Article in journal (Other academic)
  • 18.
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    What do we know about the risks of stopping antihypertensive treatment?2014In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 32, no 7, p. 1400-1401Article in journal (Other academic)
  • 19.
    Carlström, Mattias
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Wentzel, Parri
    Skott, Ole
    Persson, A. Erik G.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Eriksson, Ulf J.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Angiogenesis inhibition causes hypertension and placental dysfunction in a rat model of preeclampsia2009In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 27, no 4, p. 829-837Article in journal (Refereed)
    Abstract [en]

    Background Preeclampsia is a serious pregnancy complication, accompanied by increased maternal and fetal morbidity. Different models have been used to study preeclampsia, but none of these display all the key features of the disease. Method We investigated the effects on maternal blood pressure and fetal outcome exerted by the angiogenesis inhibitor Suramin (1100 mg/kg i.p.) during early placentation. Blood pressure and heart rate were measured continuously with telemetry in Sprague - Dawley rats of four experimental groups: nonpregnant controls, Suramin-treated nonpregnant rats, pregnant controls and pregnant Suramin-treated rats. Blood samples were collected before pregnancy and at gestational day 20 for analysis of renin and sFIt-1. The fetal and placental morphology were evaluated after caesarian section on gestational day 20. Results The blood pressure of the pregnant Suramin-treated rats successively increased during pregnancy and differed by 17 mmHg at gestational day 20 compared with the pregnant control rats. In the pregnant Suramin-treated rats group, the renin levels increased (+122%) and the sFIt-1 levels decreased (-58%) during pregnancy. The pregnant Suramin-treated fetuses and placentae were smaller (2.8 g and 0.51 g) than the pregnant controls rats' fetuses and placentae (3.5g and 0.56g). Resorptions tended to be higher in the pregnant Suramin-treated rat litters compared with the pregnant control rat litters (P = 0.08). The area of the maternal blood vessels in the mesometrial triangle was smaller in the pregnant Suramin-treated rats group than in the pregnant control rats group. Conclusion The inhibition of uterine angiogenesis increases maternal blood pressure and compromises fetal and placental development. Placental hypoxia and subsequent activation of the renin-angiotensin system may play an important role for the hypertension. J Hypertens 27:829-837 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.

  • 20.
    Carlström, Mattias
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrativ Fysiologi.
    Wåhlin, Nils
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrativ Fysiologi.
    Sällström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrativ Fysiologi.
    Skott, Ole
    Brown, Russell
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrativ Fysiologi.
    Persson, A. Erik G.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrativ Fysiologi.
    Hydronephrosis causes salt-sensitive hypertension in rats2006In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 24, no 7, p. 1437-1443Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Hypertension is a common disease in the Western world and approximately 5% of all cases are secondary to kidney malfunction. It is not clear whether unilateral hydronephrosis due to partial obstruction affects blood pressure. AIM: The aim of this study was to determine whether hypertension develops and to investigate the effects of different salt diets on the blood pressure in hydronephrotic animals. METHODS: Unilateral partial ureteral obstruction was created in 3-week-old Sprague-Dawley rats. A telemetric device was implanted 4-6 weeks later and blood pressure was measured on normal, low- and high-salt diets. Plasma samples were collected on all diets for renin analysis. RESULTS: All hydronephrotic animals developed hypertension that correlated to the degree of hydronephrosis. The blood pressure increased slowly with time and was salt sensitive. In severe hydronephrosis, blood pressure increased from 118 ± 5 mmHg on low salt to 140 ± 6 mmHg on high salt intake, compared to control levels of 82 ± 2 and 84 ± 2 mmHg, respectively. Plasma renin concentration was increased in the hydronephrotic group of animals compared to controls on all diets, but the difference was only significant on a normal salt diet, 165 ± 15 versus 86 ± 12 μGU/ml respectively. In animals with severe hydronephrosis the plasma renin levels were lower, and the changes less, than in those with mild and moderate hydronephrosis. CONCLUSION: This study demonstrates the presence of a salt-sensitive hypertension in hydronephrosis. A systemic effect of the renin-angiotensin system alone cannot be responsible for the hypertension.

  • 21.
    Cars, T.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Neovius, M.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    TWENTY-YEAR TRENDS IN CARDIOVASCULAR RISK FACTORS AMONG SWEDISH MEN: IMPACT OF OVERWEIGHT AND OBESITY2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, p. E482-E483Article in journal (Other academic)
  • 22.
    Cars, Thomas
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Neovius, M.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    LONGITUDINAL ANTIHYPERTENSIVE DRUG USE TRENDS AND TREATMENT DURATIONS BETWEEN 1970 AND 20052010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, p. E325-E325Article in journal (Other academic)
  • 23.
    Castiglioni, Laura
    et al.
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Pignieri, Alice
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Fiasche, Melania
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Giudici, Marco
    KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Centres, Wallenberg Center for Protein Research. Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Crestani, Maurizio
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Mitro, Nico
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Abbate, Mauro
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Zoja, Carlamaria
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Rottoli, Daniela
    IRCCS Ist Ric Farmacol Mario Negri, Ctr Anna Maria Astori, Sci & Technol Pk Kilometro Rosso, Bergamo, Italy..
    Foray, Claudia
    IRCCS Ist Ric Farmacol Mario Negri, Dept Cardiovasc Res, Milan, Italy..
    Fiordaliso, Fabio
    IRCCS Ist Ric Farmacol Mario Negri, Dept Cardiovasc Res, Milan, Italy..
    Guerrini, Uliano
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy..
    Tremoli, Elena
    Ctr Cardiol Monzino, Milan, Italy..
    Sironi, Luigi
    Univ Milan, Dept Pharmacol & Biomol Sci, Via G Balzaretti 9, I-20133 Milan, Italy.;Ctr Cardiol Monzino, Milan, Italy..
    Gelosa, Paolo
    Ctr Cardiol Monzino, Milan, Italy..
    Fenofibrate attenuates cardiac and renal alterations in young salt-loaded spontaneously hypertensive stroke-prone rats through mitochondrial protection2018In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 36, no 5, p. 1129-1146Article in journal (Refereed)
    Abstract [en]

    Objectives:The simultaneous presence of cardiac and renal diseases is a pathological condition that leads to increased morbidity and mortality. Several lines of evidence have suggested that lipid dysmetabolism and mitochondrial dysfunction are pathways involved in the pathological processes affecting the heart and kidney. In the salt-loaded spontaneously hypertensive stroke-prone rat (SHRSP), a model of cardiac hypertrophy and nephropathy that shows mitochondrial alterations in the myocardium, we evaluated the cardiorenal effects of fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR) agonist that acts by modulating mitochondrial and peroxisomal fatty acid oxidation.Methods:Male SHRSPs aged 6-7 weeks were divided in three groups: standard diet (n=6), Japanese diet with vehicle (n=6), and Japanese diet with fenofibrate 150mg/kg/day (n=6) for 5 weeks. Cardiac and renal functions were assessed in vivo by MRI, ultrasonography, and biochemical assays. Mitochondria were investigated by transmission electron microscopy, succinate dehydrogenase (SDH) activity, and gene expression analysis.Results:Fenofibrate attenuated cardiac hypertrophy, as evidenced by histological and MRI analyses, and protected the kidneys, preventing morphological alterations, changes in arterial blood flow velocity, and increases in 24-h proteinuria. Cardiorenal inflammation, oxidative stress, and cellular senescence were also inhibited by fenofibrate. In salt-loaded SHRSPs, we observed severe morphological mitochondrial alterations, reduced SDH activity, and down-regulation of genes regulating mitochondrial fatty-acid oxidation (i.e. PPAR, SIRT3, and Acadm). These changes were counteracted by fenofibrate. In vitro, a direct protective effect of fenofibrate on mitochondrial membrane potential was observed in albumin-stimulated NRK-52E renal tubular epithelial cells.Conclusion:The results suggest that the cardiorenal protective effects of fenofibrate in young male salt-loaded SHRSPs are explained by its capacity to preserve mitochondrial function.

  • 24.
    Cederholm, Jan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Gudbjornsdottir, Soffia
    Eliasson, Björn
    Zethelius, Bjorn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Eeg-Olofsson, Katarina
    Nilsson, Peter M.
    Blood pressure and risk of cardiovascular diseases in type 2 diabetes: further findings from the Swedish National Diabetes Register (NDR-BP II)2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 10, p. 2020-2030Article in journal (Refereed)
    Abstract [en]

    Objectives: Estimate risks of coronary heart disease (CHD), stroke and cardiovascular disease (CVD) with updated mean systolic (SBP) and diastolic (DBP) blood pressure in an observational study of patients with type 2 diabetes. Methods: Thirty-five thousand and forty-one patients treated with antihypertensive drugs, and 18 512 untreated patients, aged 30-75 years, without previous heart failure, followed for 6 years until 2009. Results: In treated patients, nonlinear splines for 6-year risk of fatal/nonfatal CHD, stroke and CVD by BP as a continuous variable showed a progressive increase with higher SBP from 140 mmHg and higher, and with DBP from 80 mmHg, with a J-shaped risk curve at lowest SBP levels, but not obviously at lowest DBP levels. Analysing intervals of SBP with 130-134 mmHg as reference at Cox regression, adjusted hazard ratios (HR) for fatal/nonfatal CHD, stroke and CVD with at least 140 mmHg were 1.22 [95% confidence interval (CI): 1.08-1.39], 1,43 (1.18-1.72), 1.26 (1.13-1.41), all P<0.001. HR with 115-129 and 135-139 mmHg were nonsignificant, whereas increased with 100-114 mmHg, 1.96 (P<0.001), 1.75 (P=0.02), 2.08 (P < 0.001), respectively. With DBP 75-79 mmHg as reference, adjusted HR for fatal/nonfatal CHD, stroke and CVD with DBP 80-84 mmHg were 1.42 (1.26-1.59), 1.46 (1.24-1.72), 1.39 (1.26-1.53), all P< 0.001. Corresponding HR with DBP at least 85 mmHg were 1.70 (1.50-1.92), 2.35 (1.99-2.77), 1..87 (1.69-2.07), all P < 0.001. Corresponding HR with DBP 60-69 and 70-74 mmHg were nonsignificant. The picture was similar in 7059 patients with previous CVD and in untreated patients. Conclusion: BP around 130-135/75-79 mmHg showed lower risks of cardiovascular diseases in patients with type 2 diabetes.

  • 25.
    Cederholm, Jan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Clinical Epidemiology.
    Gudbjörnsdottir, Soffia
    Eliasson, Björn
    Zethelius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Eeg-Olofsson, Katarina
    Nilsson, Peter M.
    Systolic blood pressure and risk of cardiovascular diseases in type 2 diabetes: an observational study from the Swedish national diabetes register2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no 10, p. 2026-2035Article in journal (Refereed)
    Abstract [en]

    Objectives: To estimate risks of fatal/nonfatal coronary heart disease (CHD), stroke and cardiovascular disease (CVD) with SBP in an observational study of patients with type 2 diabetes.

    Methods: Twelve thousand, six hundred and seventy-seven patients aged 30–75 years, treated with antihypertensive drugs, without previous congestive heart failure, followed for 5 years.

    Results: Risk curves of CHD and stroke increased progressively with higher baseline or updated mean SBP in a Cox model, in all participants, and in two subgroups without (n = 10 304) or with (n = 2373) a history of CVD, with no J-shaped risk curves at low SBP levels. Hazard ratios for CHD and stroke per 10-mmHg increase in updated mean SBP in all participants, adjusting for clinical characteristics and traditional risk factors, were 1.08 (1.04–1.13) and 1.20 (1.13–1.27), P < 0.001. With updated mean SBP of 110–129 mmHg as reference, SBP of at least 140 mmHg showed risk increases of 37% for CHD, 86% for stroke and 44% for CVD (P = 0.001 to <0.001), whereas SBP of 130–139 mmHg showed nonsignificant risk increases for these outcomes. With baseline SBP of 110–129 mmHg, CHD and CVD risks increased with further SBP reduction, hazard ratios were 1.77 and 1.73 (P = 0.002), but decreased considerably for CHD, stroke and CVD with higher baseline SBP.

    Conclusion: Risks of CHD and stroke increased progressively with higher SBP, with no J-shaped curves, although risk increase was significant only for SBP of at least 140 mmHg, but not comparing 130–139 and 110–129 mmHg. Additionally, baseline SBP of 110–129 mmHg showed increased CHD and CVD risk with further SBP reduction during follow-up, whereas baseline SBP of at least 130 showed benefits.

  • 26.
    Cederholm, Jan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Zethelius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Eliasson, Bjorn
    Gudbjornsdottir, Soffia
    Nilsson, Peter M.
    Different methods to present the effect of blood pressure on cardiovascular diseases by Cox regression2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 1, p. 235-237Article in journal (Refereed)
  • 27. Chinali, Marcello
    et al.
    de Simone, Giovanni
    Wachtell, Kristian
    Gerdts, Eva
    Gardin, Julius M
    Boman, Kurt
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Nieminen, Markku S
    Papademetriou, Vasilios
    Dahlöf, Björn
    Devereux, Richard B
    Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study.2008In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 26, no 7, p. 1472-6Article in journal (Refereed)
    Abstract [en]

    In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload.

  • 28. Cicala, Silvana
    et al.
    de Simone, Giovanni
    Gerdts, Eva
    Dahlöf, Björn
    Lindholm, Lars H
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Kjeldsen, Sverre E
    Devereux, Richard B
    Are coronary revascularization and myocardial infarction a homogeneous combined endpoint in hypertension trials? The Losartan intervention for endpoint reduction in hypertension study2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no 6, p. 1134-1140Article in journal (Refereed)
    Abstract [en]

    Objective: Construction of prognostically relevant endpoints for clinical trials in hypertension has increasingly included coronary revascularization with myocardial infarction (MI) as manifestations of coronary artery disease. However, whether coronary revascularization and MI predict other cardiovascular events similarly is unknown.

     

    Methods: We examined risks of cardiovascular death, all-cause death, and stroke following MI or coronary revascularization in hypertensive patients with left ventricular hypertrophy (LVH) enrolled in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE). We studied 9113 patients after excluding those who died within 7 days after MI or underwent coronary revascularization within 24 h after MI.

     

    Results: In multivariate Cox regression adjusting for participating countries, time-varying systolic blood pressure, and Framingham risk score, hazard ratios for cardiovascular death, all-cause death, and stroke were, respectively, 4.5 (P < 0.0001), 2.9 (P < 0.0001), and 1.9 (P = 0.003) in 321 patients with MI as first event. In similar models, coronary revascularization as first event (n = 202) was not associated with increased risks of cardiovascular death, all-cause death, and stroke (P = 0.06–0.86).

     

    Conclusion: During follow-up of hypertensive patients with LVH, occurrence of MI but not coronary revascularization as first cardiovascular event significantly increased risk of subsequent cardiovascular death, all-cause death, and stroke. In view of differences in prognostic implications, when the goal is to have a prognostically relevant composite endpoint for trials in hypertensive patients, caution should be used in combining coronary revascularization with MI.

  • 29. Cicala, Silvana
    et al.
    de Simone, Giovanni
    Wachtell, Kristian
    Gerdts, Eva
    Boman, Kurt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Nieminen, Markku S
    Dahlöf, Björn
    Devereux, Richard B
    Clinical impact of 'in-treatment' wall motion abnormalities in hypertensive patients with left ventricular hypertrophy: the LIFE study2008In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 26, no 4, p. 806-812Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Left ventricular systolic wall motion abnormalities have prognostic value. Whether wall motion detected by serial echocardiographic examinations predicts prognosis in hypertensive patients with left ventricular hypertrophy (LVH) without clinically recognized atherosclerotic disease has, however, never been investigated. We examined whether 'in-treatment' wall motion abnormalities predicted outcome in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension echocardiographic substudy.

    METHODS: We studied 749 patients without coronary artery disease, myocardial infarction (MI), or stroke history. Echocardiographic segmental wall motion abnormalities at baseline and annual re-evaluations ('as time-varying covariate') were examined in relation to endpoints (cardiovascular mortality, MI, stroke, and hospitalized heart failure). Adjusted Cox regression was used to analyze the primary composite endpoint of cardiovascular death, MI, or stroke and, separately, for fatal and nonfatal MI and hospitalized heart failure.

    RESULTS: During a mean follow-up of 4.8 years, an event was recorded in 67 (9%) patients. In Cox models after adjusting for age, gender, treatment, blood pressure lowering, and serial change of left ventricular mass index, 'in-treatment' segmental wall motion abnormalities were associated with subsequent composite endpoint [hazard ratio = 2.1, 95% confidence interval (CI) 1.1-3.8; P = 0.019] and MI [hazard ratio = 3.7 (1.5-8.9); P = 0.004].

    CONCLUSION: In hypertensive patients with LVH and no history of cardiovascular disease, 'in-treatment' left ventricular wall motion abnormalities are associated with increased likelihood of subsequent cardiovascular events independent of age, gender, blood pressure lowering, treatment modality, and in-treatment left ventricular mass index.

  • 30. Edlinger, Michael
    et al.
    Strohmaier, Susanne
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Bjørge, Tone
    Manjer, Jonas
    Borena, Wegene T
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, Anders
    Tretli, Steinar
    Concin, Hans
    Nagel, Gabriele
    Selmer, Randi
    Johansen, Dorthe
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Ulmer, Hanno
    Blood pressure and other metabolic syndrome factors and risk of brain tumour in the large population-based Me-Can cohort study2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 2, p. 290-296Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES:: Brain tumour has few established determinants. We assessed to which extent risk of brain tumour was related to metabolic syndrome factors in adults. METHODS:: In the Me-Can project, 580 000 individuals from Sweden, Austria, and Norway were followed for a median of 10 years after baseline measurement. Data on brain tumours were obtained from national cancer registries. The factors of metabolic syndrome (BMI, SBP and DBP, and blood levels of glucose, cholesterol, and triglycerides), separately and combined, were analysed in quintiles and for transformed z-scores (mean transformed to 0 and standard deviation to 1). Cox proportional hazards multivariate regression models were used, with corrections for measurement error. RESULTS:: During follow-up, 1312 primary brain tumours were diagnosed, predominantly meningioma (n = 348) and high-grade glioma (n = 436). For meningioma, the hazard ratio was increased for z-scores of SBP [hazard ratio = 1.27 per unit standard deviation, 95% confidence interval (CI) 1.03-1.57], of DBP (hazard ratio = 1.29, 95% CI 1.04-1.58), and of the combined metabolic syndrome score (hazard ratio = 1.31, 95% CI 1.11-1.54). An increased risk of high-grade glioma was found for DBP (hazard ratio = 1.23, 95% CI 1.01-1.50) and triglycerides (hazard ratio = 1.35, 95% CI 1.05-1.72). For both meningioma and high-grade glioma, the risk was more than double in the fifth quintiles of DBP compared to the lowest quintile. For meningioma this risk was even larger for SBP. CONCLUSION:: Increased blood pressure was associated with risk of brain tumours, especially of meningiomas.

  • 31.
    Eiken, Ola
    et al.
    KTH, School of Technology and Health (STH), Environmental Physiology.
    Kölegård, Roger
    KTH, School of Technology and Health (STH), Environmental Physiology.
    Repeated exposures to moderately increased intravascular pressure increases stiffness in human arteries and arterioles2011In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 29, no 10, p. 1963-1971Article in journal (Refereed)
    Abstract [en]

    The aim was to investigate whether repeated exposures to moderate pressure elevations in the blood vessels of the arms (pressure training; PT) affect pressure distension in arteries/arterioles of healthy subjects (n=11). PT and vascular pressure-distension determinations were conducted with the subject seated in a pressure chamber with one arm slipped through a hole in the chamber door. Increased intravascular pressure was accomplished by increasing chamber pressure. Before PT, one arm was investigated (control arm) during stepwise increases in chamber pressure to 180 mmHg. Artery diameter and flow were measured in the brachial artery using ultrasonography/Doppler techniques. Thereafter, the contralateral arm underwent a PT regimen consisting of three 40 min sessions/ week during 5 weeks. Chamber pressure was increased during PT from 65 mmHg during the first week to 105 mmHg during the last week. After PT, pressure-distension relationships were examined in both the trained arm and the control arm. Prior to and following PT, endothelium-dependent and endothelium-independent dilatations of the brachial artery were studied. PT reduced (p<0.01) arterial pressure distension by 46 ± 18%. Likewise, the pressure-induced increase in arterial flow was less pronounced after (350 ± 249%) compared with before (685 ± 216 %) PT. The PT-induced reductions in arterial/arteriolar pressure distension were reversed 5 weeks post-PT. Neither endothelium-dependent nor endothelium-independent arterial dilatation were affected by PT. It thus appears that the in vivo wall stiffness in arteries and arterioles increases markedly in response to intermittent, moderate increments of transmural pressure during 5 weeks. The increases in arterial/arteriolar stiffness are reversible and do not reflect a reduced capacity to dilate the vessels. The findings are compatible with the notion that local load serves as “ a prime mover” in the development of vascular changes in hypertension.

  • 32.
    Emmelin, Maria
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Weinehall, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Stegmayr, Birgitta
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Dahlgren, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Wall, Stig
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Self-rated ill-health strengthens the effect of biomedical risk factors in predicting stroke especially for men: An incident case referent study2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, no 5, p. 887-896Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To examine how self-rated ill-health interacts with biomedical stroke risk factors in predicting stroke and to explore differences between men and women and educational groups. DESIGN: An incident case-referent study where the study subjects had participated in a prior health survey. SETTING: Nested within the Västerbotten Intervention Program (VIP) and the Northern Sweden MONICA cohorts. SUBJECTS: The 473 stroke cases had two referents per case, matched for age, sex and residence, from the same study cohorts. RESULTS: Self-rated ill-health independently increased the risk of stroke, specifically for men. The interaction effect between self-rated health and biomedical risk factor load was greater for men than for women. The attributable proportion due to interaction between having a risk factor load of 2+ and self-rated ill-health was 42% for men and 15% for women. Better-educated individuals with self-rated ill-health and two or more of the biomedical risk factors had a higher risk of stroke than the less educated. Calculations of the respective contribution to the stroke cases of self-rated health, hypertension and smoking showed that self-rated ill-health had a role in 20% of the cases and could alone explain more than one-third of the cases among those who rated their health as bad, more so for men than for women. CONCLUSIONS: The results underscore the importance of including both a gender and a social perspective in discussing the role of self-rated health as a predictor of disease outcome. Physicians must be more gender sensitive when discussing their patient's own evaluation of health in relation to biomedical risk factors.

  • 33.
    Eriksson, Jan W.
    et al.
    Lundberg Laboratory for Diabetes Research, Department of Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
    Jansson, Per-Anders
    Foley, Karen
    Lithell, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Insulin sensitivity following treatment with the alpha 1-blocker bunazosin retard and the beta 1-blocker atenolol in hypertensive non-insulin-dependent diabetes mellitus patients1996In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 14, no 12, p. 1469-1475Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE:

    To compare the effects of the alpha 1-blocker bunazosin retard and the beta 1-blocker atenolol (Uniloc) on insulin sensitivity and glucose and lipid homeostasis in patients with type-2 diabetes and hypertension.

    METHODS:

    Patients with controlled type-2 diabetes (non-insulin-dependent diabetes mellitus), treated by diet or oral sulphonylurea derivatives, and with mild-to-moderate hypertension were include in a randomized, parallel group, double-blind, multicentre study. After a single-blind placebo run-in period lasting 4-6 weeks, the patients were treated either with bunazosin retard or with atenolol for a further 16 weeks including an initial dose titration period to achieve blood pressure control. Treatment involved 3, 6 or 12 mg bunazosin retard tablets or 25, 50 or 100 mg atenolol tablets, administered orally once a day and prescribed according to blood pressure response. The euglycaemic hyper-insulinaemic clamp technique was used to assess insulin sensitivity both after the placebo period and after the active treatment. A total of 95 patients was enrolled in the study (placebo phase). Forty-eight patients were withdrawn from the placebo phase, mainly due to their blood pressures being outside the required range (seated diastolic blood pressure 90-114 mmHg) and 47 patients were allocated randomly to active treatment. Of these, 23 were administered bunazosin retard and 24 atenolol. All evaluations were on an intention-to-treat basis.

    RESULTS:

    Insulin sensitivity assessed as glucose utilization during the clamp was significantly higher following bunazosin retard compared with following atenolol administration (3.52 +/- 0.27 versus 2.86 +/- 0.19 units of metabolic clearance rate of glucose index, P < 0.05). The insulin level attained during clamps (infusion rate 56 mU/m2 per min) was higher (P < 0.05) following atenolol (117 +/- 5 mU/l) than it was following bunazosin retard administration (102 +/- 5) or placebo (108 +/- 3), possibly due to an impaired insulin clearance. Compared with placebo, atenolol treatment resulted in significantly increased glucosylated haemoglobin whereas bunazosin retard had no significant effect. The two drugs did not show any consistent differences in lipid profile or fibrinogen and plasminogen activator inhibitor 1 levels. During the study seven serious adverse events were reported and one was reported shortly after completion of the study. All except one were classified as not related to the study drug and five of them occurred during placebo treatment. The non-serious side effects were in general considered to be either unrelated to the test drugs or expected effects of the two respective drug classes. Both bunazosin retard and atenolol displayed acceptable safety profiles.

    CONCLUSION:

    Bunazosin retard treatment in hypertensive non-insulin-dependent diabetes mellitus patients appears to be associated with a slightly higher insulin sensitivity than is atenolol.

  • 34. Fagard, R H
    et al.
    Grassi, G
    Hall, J
    Harrap, S
    Lindholm, Lars H
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Schiffrin, E
    Heagerty, T
    International Society of Hypertension Low and Middle Income Countries Committee Review of the Goals of the Committee and of 5 years of ISH activities in Low and Middle Income Countries2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no 3, p. 635-636Article in journal (Refereed)
  • 35. Fan, Hong-Qi
    et al.
    Li, Yan
    Thijs, Lutgarde
    Hansen, Tine W.
    Boggia, Jose
    Kikuya, Masahiro
    Björklund-Bodegård, Kristina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Richart, Tom
    Ohkubo, Takayoshi
    Jeppesen, Jorgen
    Torp-Pedersen, Christian
    Dolan, Eamon
    Kuznetsova, Tatiana
    Stolarz-Skrzypek, Katarzyna
    Tikhonoff, Valerie
    Malyutina, Sofia
    Casiglia, Edoardo
    Nikitin, Yuri
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Sandoya, Edgardo
    Kawecka-Jaszcz, Kalina
    Imai, Yutaka
    Ibsen, Hans
    O'Brien, Eoin
    Wang, Jiguang
    Staessen, Jan A.
    Prognostic value of isolated nocturnal hypertension on ambulatory measurement in 8711 individuals from 10 populations2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no 10, p. 2036-2045Article in journal (Refereed)
    Abstract [en]

    Background: We and other investigators previously reported that isolated nocturnal hypertension on ambulatory measurement (INH) clustered with cardiovascular risk factors and was associated with intermediate target organ damage. We investigated whether INH might also predict hard cardiovascular endpoints.

    Methods and results: We monitored blood pressure (BP) throughout the day and followed health outcomes in 8711 individuals randomly recruited from 10 populations (mean age 54.8 years, 47.0% women). Of these, 577 untreated individuals had INH (daytime BP <135/85 mmHg and night-time BP >=120/70 mmHg) and 994 untreated individuals had isolated daytime hypertension on ambulatory measurement (IDH; daytime BP >=135/85 mmHg and night-time BP <120/70 mmHg). During follow-up (median 10.7 years), 1284 deaths (501 cardiovascular) occurred and 1109 participants experienced a fatal or nonfatal cardiovascular event. In multivariable-adjusted analyses, compared with normotension (n = 3837), INH was associated with a higher risk of total mortality (hazard ratio 1.29, P = 0.045) and all cardiovascular events (hazard ratio 1.38, P = 0.037). IDH was associated with increases in all cardiovascular events (hazard ratio 1.46, P = 0.0019) and cardiac endpoints (hazard ratio 1.53, P = 0.0061). Of 577 patients with INH, 457 were normotensive (<140/90 mmHg) on office BP measurement. Hazard ratios associated with INH with additional adjustment for office BP were 1.31 (P = 0.039) and 1.38 (P = 0.044) for total mortality and all cardiovascular events, respectively. After exclusion of patients with office hypertension, these hazard ratios were 1.17 (P = 0.31) and 1.48 (P = 0.034).

    Conclusion: INH predicts cardiovascular outcome in patients who are normotensive on office or on ambulatory daytime BP measurement.

  • 36.
    Fredrikson, Mats
    et al.
    Uppsala universitet.
    Tuomisto, Martti
    University of Tampere.
    Sundin, Örjan
    Classical conditioning of vascular responses in mild hypertensives and normotensives1990In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, no 8, p. 1105-1109Article in journal (Refereed)
  • 37. Gelosa, P
    et al.
    Fandriks, L
    de Gasparo, M
    Pigneri, A
    Hallberg, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Medicinal Chemistry, Organic Pharmaceutical Chemistry.
    Banfi, C
    Castiglioni, L
    Guerrini, U
    Turolo, L
    Tremoli, E
    Sironi, L
    Stimulation of AT2-receptor provides end-organ protection in stroke-prone rats: (Meeting Abstract)2009In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 27, no Suppl. 4, p. S14-S14Article in journal (Refereed)
  • 38. Gelosa, Paolo
    et al.
    Pignieri, Alice
    Fandriks, Lars
    de Gasparo, Marc
    Hallberg, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Medicinal Chemistry, Organic Pharmaceutical Chemistry.
    Banfi, Cristina
    Castiglioni, Laura
    Turolo, Lucia
    Guerrini, Uliano
    Tremoli, Elena
    Sironi, Luigi
    Stimulation of AT2 receptor exerts beneficial effects in stroke-prone rats: focus on renal damage2009In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 27, no 12, p. 2444-2451Article in journal (Refereed)
    Abstract [en]

    Background and aim Angiotensin II acts through two major receptors: AT1-R and AT2-R. It is known that the stimulation of AT1-R mediates vasoconstriction, cell proliferation and fibrosis, aldosterone release and inflammatory response but, although the stimulation of AT2-R is thought to promote vasodilation and anti-inflammatory effects, its real in-vivo functions are still unclear. The aim of this study was to investigate the effects of specific and selective AT2-R stimulation on the pathological events occurring in spontaneously hypertensive stroke-prone rats (SHRSPs). Methods and results SHRSPs who were fed a high-salt diet underwent long-term treatment with vehicle or compound 21 (C21), a nonpeptide selective AT2-R agonist, at doses of 0.75, 5 and 10 mg/kg per day. The vehicle-treated rats developed brain abnormalities detectable by magnetic resonance imaging after 42.5 +/- 7.5 days, and died 43 +/- 9.5 days after the start of the dietary treatment. The highest C21 dose delayed the occurrence of brain damage (P<0.001 vs. vehicle-treated SHRSPs) and prolonged survival (P<0.001) without affecting blood pressure. These beneficial effects of C21 were abolished by the administration of PD123319, an AT2-R antagonist. C21 treatment preserved renal structure by preventing inflammatory cell infiltration, collagen accumulation, and the neo-expression of vimentin; it also prevented the increased plasma renin activity and accumulation of urinary acute-phase proteins observed in the vehicle-treated rats. Conclusion Specific and selective AT2-R stimulation has beneficial effects on the pathological events occurring in SHRSPs. These data indicate a new avenue for the pharmacological treatment of diseases in which modulation of the renin-angiotensin system is required.

  • 39.
    Granroth, Sofie
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Syvänen, Ann-Christine
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular Medicine.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Kurland, L.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Genetic variation in the ddah-1 gene in relation to adma levels and endothelial function2010In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 28, no Suppl. A, p. E124-E125Article in journal (Other academic)
    Abstract [en]

    Background:

    Asymmetric dimethylarginine (ADMA), an endogenous methylated amino acid, has been identified as a competitive inhibitor of nitric oxide synthase (NOS). Elevated ADMA levels have been demonstrated in cardiovascular disorders and many studies have reported an inverse correlation between ADMA and endothelial function. The majority of ADMA is metabolized by dimethylarginine dimethylaminohydrolases (DDAH-1 and DDAH-2). Our aim was to study the genetic variation in the DDAH-1 gene in relation to ADMA levels and endothelial function.

    Methods:

    A total of 959 individuals, aged 70, from the community based Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study were included. Plasma concentrations of ADMA were measured by high performance liquid chromatography. Endothelial function was evaluated with both the invasive forearm technique (measuring endothelial dependent vasodilation in resistance arteries) and with brachial artery ultrasound (measuring flow mediated dilation in a conduit artery). Forty common single nucleotide polymorphisms (SNPs) in the DDAH-1 gene were analyzed.

    Results:

    There were significant associations between DDAH-1 genotype and ADMA levels in 20 of the 40 selected SNPs. However, no associations were seen between DDAH-1 genotype and endothelial function.

    Conclusion:

    These results indicate that genetic variation in the DDAH-1 gene has an impact on ADMA concentration in plasma. However, it does not seem to have a major influence on endothelial function.

  • 40. Gueyffier, Francois
    et al.
    Marchant, Ivanny
    Carlberg, Bo
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Modeling the impact of cardiovascular prevention strategies: toward better information for public health decisions2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 1, p. 51-52Article in journal (Refereed)
  • 41. Hallberg, P
    et al.
    Karlsson, J
    Kurland, L
    Lind, L
    Kahan, T
    Malmqvist, K
    Ohman, KP
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine.
    Nyström, Fredrik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Melhus, H
    The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial2002In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 10, p. 2089-2093Article in journal (Refereed)
  • 42. Hallberg, P
    et al.
    Lind, L
    Michaelsson, K
    Karlsson, J
    Kurland, L
    Kahan, T
    Malmqvist, K
    Öhman, KP
    Nyström, Fredrik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MC - Medicincentrum, EMT-endo.
    Melhus, H
    B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: Results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, no 3, p. 621-624Article in journal (Refereed)
    Abstract [en]

    Objective: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy. Design and methods: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the ▀1 -adrenoceptor antagonist atenolol. Results: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 ▒ 4.6 versus -21.6 ▒ 2.2 g/m2, P = 0.03). Conclusions: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment. ⌐ 2003 Lippincott Williams & Wilkins.

  • 43.
    Hallberg, Pär
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Karlsson, Julia
    Kurland, Lisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Lind, Lars
    Kahan, Thomas
    Malmqvist, Karin
    Öhman, K. Peter
    Nyström, Fredrik
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial2002In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, no 10, p. 2089-2093Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan. Single nucleotide polymorphisms in the CYP2C9 gene result in the expression of three important variants, CYP2C9*1(wild-type), CYP2C9*2 and CYP2C9*3, the last two exhibiting reduced catalytic activity compared with the wild-type. The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan. However, its influence on clinical response to treatment with the AT(1) receptor antagonist, irbesartan, has not been investigated. OBJECTIVE: To determine whether the CYP2C9genotype influences the blood pressure-decreasing response to antihypertensive treatment with irbesartan. DESIGN AND METHODS: One hundred and two patients with essential hypertension and left ventricular hypertrophy were allocated randomly to groups to receive double-blind treatment with either irbesartan (n = 49) or the beta(1)-adrenergic receptor blocker, atenolol ( n= 53). Blood pressure was measured before and after 12 weeks of treatment. genotyping was performed using solid-phase minisequencing. RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036). A similar trend was seen for systolic blood pressure. In contrast, no relation was seen between the CYP2C9 genotype and blood pressure response to atenolol, a drug not metabolized via CYP2C9. CONCLUSIONS: The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension.

  • 44.
    Hallberg, Pär
    et al.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Karlsson, Julia
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Kurland, Lisa
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Lind, Lars
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden; AstraZeneca Research & Development, Mölndal, Sweden.
    Kahan, Thomas
    Division of Internal Medicine, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
    Malmqvist, Karin
    Division of Internal Medicine, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
    Öhman, K. Peter
    AstraZeneca Research & Development, Mölndal, Sweden; Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Nyström, Fredrik
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden; Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping, Sweden.
    Melhus, Håkan
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial2002In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, no 10, p. 2089-2093Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan. Single nucleotide polymorphisms in the CYP2C9 gene result in the expression of three important variants, CYP2C9*1(wild-type), CYP2C9*2 and CYP2C9*3, the last two exhibiting reduced catalytic activity compared with the wild-type. The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan. However, its influence on clinical response to treatment with the AT(1) receptor antagonist, irbesartan, has not been investigated.

    OBJECTIVE: To determine whether the CYP2C9genotype influences the blood pressure-decreasing response to antihypertensive treatment with irbesartan.

    DESIGN AND METHODS: One hundred and two patients with essential hypertension and left ventricular hypertrophy were allocated randomly to groups to receive double-blind treatment with either irbesartan (n = 49) or the beta(1)-adrenergic receptor blocker, atenolol ( n= 53). Blood pressure was measured before and after 12 weeks of treatment. genotyping was performed using solid-phase minisequencing.

    RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036). A similar trend was seen for systolic blood pressure. In contrast, no relation was seen between the CYP2C9 genotype and blood pressure response to atenolol, a drug not metabolized via CYP2C9.

    CONCLUSIONS: The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension.

  • 45.
    Hallberg, Pär
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Karlsson, Julia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Kurland, Lisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Kahan, Thomas
    Malmqvist, Karin
    Öhman, K. Peter
    Nyström, Fredrik
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, no 3, p. 621-4Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy. DESIGN AND METHODS: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol. RESULTS: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 +/- 4.6 versus -21.6 +/- 2.2 g/m2, P = 0.03). CONCLUSIONS: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.

  • 46. Hallberg, Pär
    et al.
    Lind, Lars
    Michaëlsson, Karl
    Karlsson, Julia
    Kurland, Lisa
    Kahan, Thomas
    Malmqvist, Karin
    Öhman, K. Peter
    Nyström, Fredrik
    Melhus, Håkan
    B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial2003In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 21, no 3, p. 621-624Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy.

    DESIGN AND METHODS: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol.

    RESULTS: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 +/- 4.6 versus -21.6 +/- 2.2 g/m2, P = 0.03).

    CONCLUSIONS: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.

  • 47. Hansen, Tine W.
    et al.
    Kikuya, Masahiro
    Thijs, Lutgarde
    Björklund-Bodegård, Kristina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Kuznetsova, Tatiana
    Ohkubo, Takayoshi
    Richart, Tom
    Torp-Pedersen, Christian
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Jeppesen, Jørgen
    Ibsen, Hans
    Imai, Yutaka
    Staessen, Jan A.
    Prognostic superiority of daytime ambulatory over conventional blood pressure in four populations: a meta-analysis of 7,030 individuals2007In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 25, no 8, p. 1554-1564Article in journal (Refereed)
    Abstract [en]

    Objective To investigate the multivariate-adjusted predictive value of systolic and diastolic blood pressures on conventional (CBP) and daytime (10-20h) ambulatory (ABP) measurement. Methods We randomly recruited 7030 subjects (mean age 56.2 years; 44.8% women) from populations in Belgium, Denmark, Japan and Sweden. We constructed the International Database on Ambulatory blood pressure and Cardiovascular Outcomes. Results During follow-up (median = 9.5 years), 932 subjects died. Neither CBP nor ABP predicted total mortality, of which 60.9% was due to noncardiovascular causes. The incidence of fatal combined with nonfatal cardiovascular events amounted to 863 (228 deaths, 326 strokes and 309 cardiac events). In multivariate-adjusted continuous analyses, both CBP and ABP predicted cardiovascular, cerebrovascular, cardiac and coronary events. However, in fully-adjusted models, including both CBP and ABP, CBP lost its predictive value (P>0.052), whereas systolic and diastolic ABP retained their prognostic significance (P< 0.007) with the exception of diastolic ABP as predictor of cardiac and coronary events (P>0.21). In adjusted categorical analyses, normotension was the referent group (CBP<140/90 mmHg and ABP<135/ 85 mmHg). Adjusted hazard ratios for all cardiovascular events were 1.22 [95% confidence interval (Cl) = 0.96-1.53; P=0.09] for white-coat hypertension (≥140/90 and <135/85 mmHg); 1.62 (95% Cl = 1.35-1.96; P< 0.0001) for masked hypertension (<140/90 and ≥ 135/85 mmHg); and 1.80 (95% Cl = 1.59-2.03; P<0.0001) for sustained hypertension (≥140/90 and ≥135/85 mmHg). Conclusions ABP is superior to CBP in predicting cardiovascular events, but not total and noncardiovascular mortality. Cardiovascular risk gradually increases from normotension over white-coat and masked hypertension to sustained hypertension.

  • 48.
    Hedblad, B
    et al.
    Lund Univ, Malmö, Sweden .
    Melander, H
    Med Prod Agcy, Uppsala, Sweden .
    de Faire, U
    Karolinska Inst, Stockholm, Sweden .
    Lindholm, Lars H
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Family Medicine.
    Kahan, T
    Karolinska Inst, Stockholm, Sweden .
    Beta blockers reduce left ventricular mass less than other antihypertensive drugs: a systematic review and meta analysis2009In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 27, no Suppl. 4, p. s319-s319Article in journal (Refereed)
  • 49.
    Herlitz, Johan
    et al.
    [external].
    Brandrup-Wognsen, H
    Haglid, M
    Hartford, M
    Emanuelsson, H
    Karlson, BW
    Karlsson, T
    Hjalmarson, Å
    Mortality and morbidity during a period of 2 years after coronary artery bypass surgery in patients with and without a history of hypertension1996In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 14, no 3, p. 309-314Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To describe mortality and morbidity during a period of 2 years after coronary artery bypass grafting (CABG) in relation to a history of hypertension. PATIENTS: All patients in western Sweden in whom CABG was undertaken between June 1988 and June 1991 and in whom simultaneous valve surgery was not performed were included in the study. DESIGN: A prospective 2-year follow-up study. RESULTS: Patients with a history of hypertension (n = 777) differed from patients without such a history (n = 1348) in that the proportion of women was higher, they were older and more frequently had a history of congestive heart failure, diabetes mellitus, renal dysfunction, cerebro-vascular disease, intermittent claudication and obesity, and the number of smokers and patients with previous CABG was lower. They were also more likely to develop post-operative cerebrovascular complications and signs of myocardia damage. Patients with hypertension tended to have increased mortality during the first 30 days after CABG and the late mortality (between day 30 and 2 years) was significantly higher than in non-hypertensive participants. Whereas the development of myocardial infarction was similar in both groups, the hypertensive study participants more frequently developed stroke during 2 years of follow-up. In a multivariate analysis including age, sex, history of different cardiovascular diseases, smoking, ejection fraction, and the occurrence of three-vessel disease, hypertension did not emerge as an independent predictor of death in the early or late phase or during a total of 2 years of follow-up. CONCLUSION: Among CABG patients, those with a history of hypertension have a different pattern of risk factors. They have a higher mean age, include a higher proportion of women and have a higher prevalence of congestive heart failure, diabetes mellitus, renal dysfunction, cerebro-vascular disease, intermittent claudication, and obesity. They also have an increased frequency of immediate post-operative complications and an increased 2-year mortality, even if a history of hypertension was not an independent predictor of death during 2 years of follow-up.

  • 50.
    Herlitz, Johan
    et al.
    [external].
    Karlson, BW
    Richter, A
    Wiklund, O
    Jablonskiene, D
    Hjalmarson, Å
    Prognosis in hypertensives with acute myocardial infarction1992In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 10, no 10, p. 1265-1271Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: A previous history of hypertension is overrepresented among patients with ischaemic heart disease. The present study aims at describing the influence of a previous history of hypertension upon the prognosis among patients hospitalized due to acute myocardial infarction. DESIGN: Patients were followed for 1 year. Mortality and morbidity are described during hospitalization and after discharge from hospital. SETTING: Sahlgrenska Hospital, serving half of the area of Gothenburg in Sweden. PATIENTS: All patients admitted to Sahlgrenska Hospital during 21 months due to acute myocardial infarction regardless of age and whether they were admitted to the coronary care unit. RESULTS: Among all patients with confirmed acute myocardial infarction (n = 917) a previous history of hypertension was reported in 324 patients. Hypertensives more frequently had a previous history of acute myocardial infarction, angina pectoris, congestive heart failure and diabetes mellitus. Their mortality during hospitalization was similar to that in normotensives. However, the total mortality during 1 year of follow-up was 35% in hypertensives and 25% for normotensives (P < 0.01), and a previous history of hypertension was an independent risk indicator for death after discharge from hospital. Place and mode of death appeared similar in normotensives and hypertensives. Reinfarction was twice as common in hypertensives as in normotensives, and a previous history of hypertension was an independent risk indicator for reinfarction. CONCLUSIONS: Among patients with acute myocardial infarction a previous history of hypertension indicates a poor prognosis, one-third of patients dying and one-quarter developing reinfarction during the first year after onset of acute myocardial infarction.

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