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  • 1. Bakris, George L
    et al.
    Lindholm, Lars H
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Black, Henry R
    Krum, Henry
    Linas, Stuart
    Linseman, Jennifer V
    Arterburn, Sarah
    Sager, Philip
    Weber, Michael
    Divergent results using clinic and ambulatory blood pressures report of a darusentan-resistant hypertension trial2010Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 56, nr 5, s. 824-830Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with resistant hypertension are at increased risk for cardiovascular events. The addition of new treatments to existing therapies will help achieve blood pressure (BP) goals in more resistant hypertension patients. In the current trial, 849 patients with resistant hypertension receiving ≥3 antihypertensive drugs, including a diuretic, at optimized doses were randomized to the selective endothelin A receptor antagonist darusentan, placebo, or the central α-2 agonist guanfacine. The coprimary end points of the study were changes from baseline to week 14 in trough, sitting systolic BP, and diastolic BP measured in the clinic. Decreases from baseline to week 14 in systolic BP for darusentan (−15±14 mm Hg) were greater than for guanfacine (−12±13 mm Hg; P<0.05) but not greater than placebo (−14±14 mm Hg). Darusentan, however, reduced mean 24-hour systolic BP (−9±12 mm Hg) more than placebo (−2±12 mm Hg) or guanfacine (−4±12 mm Hg) after 14 weeks of treatment (P<0.001 for each comparison). The most frequent adverse event associated with darusentan was fluid retention/edema at 28% versus 12% in each of the other groups. More patients withdrew because of adverse events on darusentan as compared with placebo or guanfacine. We conclude that darusentan provided greater reduction in systolic BP in resistant hypertension patients as assessed by ambulatory BP monitoring, in spite of not meeting its coprimary end points. The results of this trial highlight the importance of ambulatory BP monitoring in the design of hypertension clinical studies.

  • 2.
    Brunström, Mattias
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Kjeldsen, Sverre E.
    Department of Cardiology, University of Oslo, Ullevaal Hospital, Norway.
    Kreutz, Reinhold
    Department of Clinical Pharmacology and Toxicology, Charité Medical University, Berlin, Germany.
    Gjesdal, Knut
    Department of Cardiology, University of Oslo, Ullevaal Hospital, Norway.
    Narkiewicz, Krzysztof
    Department of Hypertension and Diabetology, Medical University of Gdansk, Poland.
    Burnier, Michel
    Service of Nephrology and Hypertension, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
    Oparil, Suzanne
    Vascular Biology and Hypertension Program, Department of Medicine, University of Alabama, Birmingham, United States.
    Mancia, Giuseppe
    University of Milano-Bicocca, Milan, Italy.
    Missing verification of source data in hypertension research: The HYGIA PROJECT in perspective2021Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 78, nr 2, s. 555-558Artikel i tidskrift (Refereegranskat)
  • 3.
    Brunström, Mattias
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Thomopoulos, Costas
    Department of Cardiology, Helena Venizelou Hospital, Athens, United States.
    Carlberg, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Kreutz, Reinhold
    Charité - Universitätsmedizin Berlin, Institute of Clinical Pharmacology and Toxicology, Germany (R.K.), Charitéplatz 1, Berlin, Germany.
    Mancia, Giuseppe
    University of Milano-Bicocca, Milan, United States.
    Methodological Aspects of Meta-Analyses Assessing the Effect of Blood Pressure-Lowering Treatment on Clinical Outcomes2022Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 79, nr 3, s. 491-504Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Systematic reviews and meta-analyses are often considered the highest level of evidence, with high impact on clinical practice guidelines. The methodological literature on systematic reviews and meta-analyses is extensive and covers most aspects relevant to the design and interpretation of meta-analysis findings in general. Analyzing the effect of blood pressure-lowering on clinical outcomes poses several challenges over and above what is covered in the general literature, including how to combine placebo-controlled trials, target-trials, and comparative studies depending on the research question, how to handle the potential interaction between baseline blood pressure level, common comorbidities, and the estimated treatment effect, and how to consider different magnitudes of blood pressure reduction across trials. This review aims to address the most important methodological considerations, to guide the general reader of systematic reviews and meta-analyses within our field, and to help inform the design of future studies. Furthermore, we highlight issues where published meta-analyses have applied different analytical strategies and discuss pros and cons with different strategies.

  • 4. Carlsson, Axel C.
    et al.
    Ruge, Toralph
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Sundstrom, Johan
    Ingelsson, Erik
    Larsson, Anders
    Lind, Lars
    Arnlov, Johan
    Association Between Circulating Endostatin, Hypertension Duration, and Hypertensive Target-Organ Damage2013Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 62, nr 6, s. 1146-1151Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Our aim is to study associations between circulating endostatin, hypertension duration, and hypertensive target-organ damage. Long-term hypertension induces cardiovascular and renal remodeling. Circulating endostatin, a biologically active derivate of collagen XVIII, has been suggested to be a relevant marker for extracellular matrix turnover and remodeling in various diseases. However, the role of endostatin in hypertension and hypertensive target-organ damage is unclear. Serum endostatin was measured in 2 independent community-based cohorts: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS; women 51%; n=812; mean age, 75 years) and the Uppsala Longitudinal Study of Adult Men (ULSAM; n=785; mean age, 77.6 years). Retrospective data on blood pressure measurements and antihypertensive medication (PIVUS >5 years, ULSAM >27 years), and cross-sectional data on echocardiographic left ventricular mass, endothelial function (endothelium-dependent vasodilation assessed by the invasive forearm model), and urinary albumin/creatinine ratio were available. In PIVUS, participants with 5 years of history of hypertension portrayed 0.42 SD (95% confidence interval, 0.23-0.61; P<0.001) higher serum endostatin, compared with that of normotensives. This association was replicated in ULSAM, in which participants with 27 years hypertension duration had the highest endostatin (0.57 SD higher; 95% confidence interval, 0.35-0.80; P<0.001). In addition, higher endostatin was associated with higher left ventricular mass, worsened endothelial function, and higher urinary albumin/creatinine ratio (P<0.03 for all) in participants with prevalent hypertension. Circulating endostatin is associated with the duration of hypertension, and vascular, myocardial, and renal indices of hypertensive target-organ damage. Further studies are warranted to assess the prognostic role of endostatin in individuals with hypertension.

  • 5. Devereux, Richard B.
    et al.
    Bang, Casper N.
    Roman, Mary J.
    Palmieri, Vittorio
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Gerdts, Eva
    Nieminen, Markku S.
    Papademetriou, Vasilios
    Wachtell, Kristian
    Hille, Darcy A.
    Dahlof, Bjorn
    Left Ventricular Wall Stress-Mass-Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients LIFE Study2015Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 66, nr 5, s. 945-953Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study, 4.8 years' losartan- versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke. However, there was no difference in myocardial infarction (MI), possibly related to greater reduction in myocardial oxygen demand by atenolol-based treatment. Myocardial oxygen demand was assessed indirectly by the left ventricular massxwall stressxheart rate (triple product) in 905 LIFE participants. The triple product was included as time-varying covariate in Cox models assessing predictors of the LIFE primary composite end point (cardiovascular death, MI, or stroke), its individual components, and all-cause mortality. At baseline, the triple product in both treatment groups was, compared with normal adults, elevated in 70% of patients. During randomized treatment, the triple product was reduced more by atenolol, with prevalences of elevated triple product of 39% versus 51% on losartan (both P0.001). In Cox regression analyses adjusting for age, smoking, diabetes mellitus, and prior stroke, MI, and heart failure, 1 SD lower triple product was associated with 23% (95% confidence interval 13%-32%) fewer composite end points, 31% (18%-41%) less cardiovascular mortality, 30% (15%-41%) lower MI, and 22% (11%-33%) lower all-cause mortality (all P0.001), without association with stroke (P=0.34). Although losartan-based therapy reduced ventricular mass more, greater heart rate reduction with atenolol resulted in larger reduction of the triple product. Lower triple product during antihypertensive treatment was strongly, independently associated with lower rates of the LIFE primary composite end point, cardiovascular death, and MI, but not stroke.

  • 6. Donat-Vargas, Carolina
    et al.
    Åkesson, Agneta
    Tornevi, Andreas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Wennberg, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Sommar, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Kiviranta, Hannu
    Rantakokko, Panu
    Bergdahl, Ingvar A.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Persistent Organochlorine Pollutants in Plasma, Blood Pressure, and Hypertension in a Longitudinal Study2018Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 71, nr 6, s. 1258-1268Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Persistent organochlorine pollutants (POPs) have shown to be involved in the atherosclerotic process and to cause endothelial cell dysfunction. To assess longitudinally whether plasma concentrations of different POPs were associated with blood pressure and risk of hypertension in middle-aged women and men. Study subjects were 850 participants in the VIP (Västerbotten Intervention Programme) with 2 blood samples and blood pressure measurements, 10 years apart, during 1990 to 2003 (baseline) and during 2000 to 2013 (follow-up). Dioxin-like and nondioxin-like polychlorinated biphenyls (DL-PCBs, NDL-PCBs) and p,p'-dichlorodiphenyldichloroethylene (DDE) were measured. Associations were assessed using generalized estimating equations. At baseline sampling 49% and at follow-up 64% had hypertension. DL-PCBs and DDE, but not NDL-PCBs or hexachlorobenzene, were associated with hypertension. Only the association for DL-PCBs remained statistically significant after lipid-standardization and adjustment for body mass index and total serum lipids. The multivariable-adjusted odds ratio of hypertension based on repeated measurements were 1.52 (95% confidence interval, 1.08-2.13) for DL-PCBs (third versus first tertile of lipid-standardized POPs). In stratified adjusted analyses, odds ratio for those born after 1950 increased to 3.99 (95% confidence interval, 2.15-7.43), whereas no association was observed among those born earlier. Based on repeated measurements, the accumulated exposure to DL-PCBs and DDE, although less clear for the latter, may disrupt the normal blood pressure levels and increase the odds of hypertension. Moreover, individuals experiencing early-life POP exposure may be at elevated risk of vascular POP effects.

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  • 7.
    Eriksson, Jan W
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Jansson, Per-Anders
    Carlberg, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Hägg, Anders
    Kurland, Lisa
    Svensson, Maria K
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Ahlström, Håkan
    Ström, Conny
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Diagnostisk radiologi.
    Lönn, Lars
    Ojbrandt, Kristina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Johansson, Lars
    Lind, Lars
    Hydrochlorothiazide, but not Candesartan, aggravates insulin resistance and causes visceral and hepatic fat accumulation. The mechanisms for the diabetes preventing effect of Candesartan (MEDICA) Study.2008Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 52, nr 6, s. 1030-1037Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Treatment with angiotensin II receptor blockers is associated with lower risk for the development of type 2 diabetes mellitus compared with thiazide diuretics. The Mechanisms for the Diabetes Preventing Effect of Candesartan Study addressed insulin action and secretion and body fat distribution after treatment with candesartan, hydrochlorothiazide, and placebo. Twenty-six nondiabetic, abdominally obese, hypertensive patients were included in a multicenter 3-way crossover trial, and 22 completers (by predefined criteria; 10 men and 12 women) were included in the analyses. They underwent 12-week treatment periods with candesartan (C; 16 to 32 mg), hydrochlorothiazide (H; 25 to 50 mg), and placebo (P), respectively, and the treatment order was randomly assigned and double blinded. Intravenous glucose tolerance tests and euglycemic hyperinsulinemic (56 mU/m(2) per minute) clamps were performed. Intrahepatic and intramyocellular and extramyocellular lipid content and subcutaneous and visceral abdominal adipose tissue were measured using proton magnetic resonance spectroscopy and MRI. Insulin sensitivity (M-value) was reduced following H versus C and P (6.07+/-2.05, 6.63+/-2.04, and 6.90+/-2.10 mg/kg of body weight per minute, mean+/-SD; P<0.05) following H than both P and C. The subcutaneous to visceral abdominal adipose tissue ratio was reduced following H versus C and P (P<0.01). Glycosylated hemoglobin, alanine aminotransferase, aspartate aminotransferase, and high-sensitivity C-reactive protein levels were higher (P<0.05) after H, but not C, versus P. There were no changes in body fat, intramyocellular lipid, extramyocellular lipid, or first-phase insulin secretion. Blood pressure was reduced similarly by C and H versus P. In conclusion, visceral fat redistribution, liver fat accumulation, low-grade inflammation, and aggravated insulin resistance were demonstrated after hydrochlorothiazide but not candesartan treatment. These findings can partly explain the diabetogenic potential of thiazides.

  • 8. Gerdts, Eva
    et al.
    Okin, Peter M
    de Simone, Giovanni
    Cramariuc, Dana
    Wachtell, Kristian
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Devereux, Richard B
    Gender differences in left ventricular structure and function during antihypertensive treatment: the Losartan intervention for endpoint reduction in hypertension study2008Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 51, nr 4, s. 1109-1114Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In hypertensive patients with left ventricular hypertrophy, antihypertensive treatment induces changes in left ventricular structure and function. However, less is known about gender differences in this response. Baseline and annual echocardiograms until the end of study or a primary end point occurred were assessed in 863 hypertensive patients with electrocardiographic left ventricular hypertrophy aged 55 to 80 years (mean: 66 years) during 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Echocardiography substudy. Left ventricular hypertrophy was diagnosed as left ventricular mass divided by height(2.7) >or=46.7 g/m(2.7) and 49.2 g/m(2.7) in women and men, respectively, and systolic function as ejection fraction and stress-corrected midwall fractional shortening. Women included more patients with obesity, isolated systolic hypertension, and mitral regurgitation (all P<0.01). Ejection fraction, stress-corrected midwall shortening, and prevalence of left ventricular hypertrophy were higher in women at baseline and at the end of study (all P<0.01). In particular, more women had residual eccentric hypertrophy (47% versus 32%; P<0.01) in spite of similar in-treatment reduction in mean blood pressure. In logistic regression, left ventricular hypertrophy at study end was more common in women (odds ratio: 1.61; 95% CI: 1.16 to 2.26; P<0.01) independent of other significant covariates. In linear regression analyses, female gender also predicted 2% higher mean in-treatment ejection fraction and 2% higher mean stress-corrected midwall shortening (both beta=0.07; P<0.01). Hypertensive women in this study retained higher left ventricular ejection fraction and stress-corrected midwall shortening in spite of less hypertrophy regression during long-term antihypertensive treatment.

  • 9. Langrish, Jeremy
    et al.
    Lundbäck, Magnus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mills, Nicholas
    Johnston, Neil
    Webb, David
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Newby, David E
    Contribution of endothelin-1 to the vascular effects of diesel exhaust inhalation in humans2009Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 54, nr 4, s. 910-915Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Diesel exhaust inhalation impairs vascular function, and, althoughthe underlying mechanism remains unclear, endothelin (ET) 1and NO are potential mediators. The aim of this study was toidentify whether diesel exhaust inhalation affects the vascularactions of ET-1 in humans. In a randomized, double-blind crossoverstudy, 13 healthy male volunteers were exposed to either filteredair or dilute diesel exhaust (331±13 µg/m3). Plasmaconcentrations of ET-1 and big-ET-1 were determined at baselineand throughout the 24-hour study period. Bilateral forearm bloodflow was measured 2 hours after the exposure during infusionof either ET-1 (5 pmol/min) or the ETA receptor antagonist,BQ-123 (10 nmol/min) alone and in combination with the ETB receptorantagonist, BQ-788 (1 nmol/min). Diesel exhaust exposure hadno effect on plasma ET-1 and big-ET-1 concentrations (P>0.05for both) or 24-hour mean blood pressure or heart rate (P>0.05for all). ET-1 infusion increased plasma ET-1 concentrationsby 58% (P<0.01) but caused vasoconstriction only after dieselexhaust exposure (–17% versus 2% after air; P<0.001).In contrast, diesel exhaust exposure reduced vasodilatationto isolated BQ-123 infusion (20% versus 59% after air; P<0.001)but had no effect on vasodilatation to combined BQ-123 and BQ-788administration (P>0.05). Diesel exhaust inhalation increasesvascular sensitivity to ET-1 and reduces vasodilatation to ETAreceptor antagonism despite unchanged plasma ET-1 concentrations.Given the tonic interaction between the ET and NO systems, weconclude that diesel exhaust inhalation alters vascular reactivityto ET-1 probably through its effects on NO bioavailability.

  • 10.
    Mancia, Giuseppe
    et al.
    University Milano-Bicocca, Milan, Italy.
    Brunström, Mattias
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Burnier, Michel
    Faculty of Biology and Medicine, University of Lausanne, Switzerland.
    Grassi, Guido
    Clinica Medica, University Milano-Bicocca, Milan, Italy.
    Januszewicz, Andrzej
    Department of Hypertension, National Institute of Cardiology, Warsaw, Poland.
    Kjeldsen, Sverre E.
    Institute for Clinical Medicine, University of Oslo, Norway; Departments of Cardiology and Nephrology, Ullevaal Hospital, Oslo, Norway.
    Muiesan, Maria Lorenza
    UOC 2 Medicina, ASST Spedali Civili di Brescia, Department of Clinical and Experimental Sciences, University of Brescia, Italy.
    Thomopoulos, Costas
    Department of Cardiology, General Hospital of Athens Laiko, Greece.
    Tsioufis, Konstantinos
    First Department of Cardiology, Medical School, University of Athens, Hippokration Hospital, Greece.
    Kreutz, Reinhold
    Charite-Universitaetsmedizin Berlin, Institute of Clinical Pharmacology and Toxicology, Germany.
    Rationale for the inclusion of β-blockers among major antihypertensive drugs in the 2023 European society of hypertension guidelines2024Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 81, nr 5, s. 1021-1030Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    We address the reasons why, unlike other guidelines, in the 2023 guidelines of the European Society of Hypertension β-blockers (BBs) have been regarded as major drugs for the treatment of hypertension, at the same level as diuretics, calcium channel blockers, and blockers of the renin-angiotensin system. We argue that BBs, (1) reduce blood pressure (the main factor responsible for treatment-related protection) not less than other drugs, (2) reduce pooled cardiovascular outcomes and mortality in placebo-controlled trials, in which there has also been a sizeable reduction of all major cause-specific cardiovascular outcomes, (3) have been associated with a lower global cardiovascular protection in 2 but not in several other comparison trials, in which the protective effect of BBs versus the other major drugs has been similar or even greater, with a slightly smaller or no difference of global benefit in large trial meta-analyses and a similar protective effect when comparisons extend to BBs in combination versus other drug combinations. We mention the large number of cardiac and other comorbidities for which BBs are elective drugs, and we express criticism against the exclusion of BBs because of their lower protective effect against stroke in comparison trials, because, for still uncertain reasons, differences in protection against cause-specific events (stroke, heart failure, and coronary disease) have been reported for other major drugs. These partial data cannot replace global benefits as the main deciding factor for drug choice, also because in the general hypertensive population whether and which type of event might occur is unknown.

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  • 11. Parikh, Nisha I.
    et al.
    Norberg, Margareta
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Ingelsson, Erik
    Cnattingius, Sven
    Vasan, Ramachandran S.
    Domellöf, Magnus
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Jansson, Jan Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Edstedt Bonamy, Anna-Karin
    Association of Pregnancy Complications and Characteristics With Future Risk of Elevated Blood Pressure: The Västerbotten Intervention Program2017Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 69, nr 3, s. 475-483Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pregnancy characteristics are associated with risk of cardiovascular diseases, but their independent associations with hypertension or blood pressure (BP) levels remain uncertain. We linked the Swedish Medical Birth Register with Västerbotten Intervention Program data (Northern Sweden). Using linear and logistic regression, we related pregnancy factors in any prior pregnancy with BP and hypertension at 40 years of age in 15 896 parous women free of prepregnancy hypertension. Pregnancy factors included parity, age at first delivery, preeclampsia, gestational diabetes mellitus, placental abruption, shortest gestational age small for gestational age baby (<third percentile for birth weight) or stillbirth. We defined hypertension as systolic BP ≥140 mm Hg and diastolic BP ≥90 mm Hg or antihypertensive use. Multivariable models were adjusted for all pregnancy factors and potential lifestyle and sociodemographic confounders. At 40 years of age, 1535 women (9.6%) had hypertension. In multivariable models, lower parity, younger age at first birth, preeclampsia, small for gestational age, and placental abruption were independently associated with higher systolic and diastolic BP levels at 40 years of age. Younger age at first birth, preeclampsia, gestational age <32 versus ≥37 weeks, and small for gestational age were independently associated with hypertension. Our findings raise the possibility that earlier and more frequent BP screening may be desirable in women with these pregnancy characteristics.

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  • 12.
    Rieck, Åshild E.
    et al.
    Institute of Medicine, University of Bergen, Bergen, Norway.
    Cramariuc, Dana
    Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin. Skellefteå Hospital, Skellefteå, Sweden.
    Gohlke-Bärwolf, Christa
    Herz-Zentrum Bad Krozingen, Bad Krozingen, Germany.
    Staal, Eva M.
    Department of Cardiology, Stavanger University Hospital, Stavanger, Norway.
    Lønnebakken, Mai Tone
    Institute of Medicine, University of Bergen, Bergen, Norway; Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
    Rossebø, Anne B.
    Division of Cardiology, Aker University Hospital, Oslo, Norway.
    Gerdts, Eva
    Institute of Medicine, University of Bergen, 5021 Bergen, Norway; Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
    Hypertension in aortic stenosis implications for left ventricular structure and cardiovascular events2012Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 60, nr 1, s. 90-97Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The impact of hypertension on left ventricular structure and outcome during progression of aortic valve stenosis has not been reported from a large prospective study. Data from 1616 patients with asymptomatic aortic stenosis randomized to placebo-controlled treatment with combined simvastatin and ezetimibe in the Simvastatin Ezetimibe in Aortic Stenosis Study were used. The primary study end point included combined cardiovascular death, aortic valve events, and ischemic cardiovascular events. Hypertension was defined as history of hypertension or elevated baseline blood pressure. Left ventricular hypertrophy was defined as left ventricular mass/height2 7 >46.7 g/m2.7 in women and >49.2 g/m2.7 in men and concentric geometry as relative wall thickness >043. Baseline peak aortic jet velocity and aortic stenosis progression rate did not differ between hypertensive (n= 1340) and normotensive (n=276) patients. During 4.3 years of follow-up, the prevalence of concentric left ventricular hypertrophy increased 3 times in both groups. Hypertension predicted 51% higher incidence of abnormal LV geometry at final study visit independent of other confounders (P<0.01). In time-varying Cox regression, hypertension did not predict increased rate of the primary study end point. However, hypertension was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold increased mortality (both P<0.01), independent of aortic stenosis severity, abnormal left ventricular geometry, in-treatment systolic blood pressure, and randomized study treatment. No impact on aortic valve replacement was found. In conclusion, among patients with initial asymptomatic mild-to-moderate aortic stenosis, hypertension was associated with more abnormal left ventricular structure and increased cardiovascular morbidity and mortality. 

  • 13.
    Stocks, Tanja
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Van Hemelrijck, Mieke
    Manjer, Jonas
    Bjørge, Tone
    Ulmer, Hanno
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning. Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning.
    Lindkvist, Björn
    Selmer, Randi
    Nagel, Gabriele
    Tretli, Steinar
    Concin, Hans
    Engeland, Anders
    Jonsson, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Stattin, Pär
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Blood pressure and risk of cancer incidence and mortality in the metabolic syndrome and cancer project2012Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 59, nr 4, s. 802-810Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Observational studies have shown inconsistent results for the association between blood pressure and cancer risk. We investigated the association in 7 cohorts from Norway, Austria, and Sweden. In total, 577799 adults with a mean age of 44 years were followed for, on average, 12 years. Incident cancers were 22184 in men and 14744 in women, and cancer deaths were 8724 and 4525, respectively. Cox regression was used to calculate hazard ratios of cancer per 10-mmHg increments of midblood pressure, which corresponded with 0.7 SDs and, for example, an increment of systolic/diastolic blood pressure of 130/80 to 142/88 mmHg. All of the models used age as the time scale and were adjusted for possible confounders, including body mass index and smoking status. In men, midblood pressure was positively related to total incident cancer (hazard ratio per 10 mmHg increment: 1.07 [95% CI: 1.04-1.09]) and to cancer of the oropharynx, colon, rectum, lung, bladder, kidney, malignant melanoma, and nonmelanoma skin cancer. In women, midblood pressure was not related to total incident cancer but was positively related to cancer of the liver, pancreas, cervix, uterine corpus, and malignant melanoma. A positive association was also found for cancer mortality, with HRs per 10-mmHg increment of 1.12 (95% CI: 1.08-1.15) for men and 1.06 (95% CI: 1.02-1.11) for women. These results suggest a small increased cancer risk overall in men with elevated blood pressure level and a higher risk for cancer death in men and women.

  • 14. Veerabhadrappa, Praveen
    et al.
    Burger, Dylan
    Charchar, Fadi
    Tomaszewski, Maciej
    Carlberg, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Harrap, Stephen
    Touyz, Rhian M
    Council for high blood pressure research/InterAmerican society of hypertension/International society of hypertension: first new investigators symposium at the high blood pressure research 2011 scientific sessions2012Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 59, nr 2, s. 382-383Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    For the very first time, the International Society of Hypertension (ISH) sponsored the ISH New Investigators Symposium on September 21, 2011, in Orlando, FL, entitled, “A Global Hypertension Initiative: Trainee/New Investigator Session” as part of the High Blood Pressure Research 2011 Scientific Sessions. This symposium was cosponsored by ISH, the InterAmerican Society of Hypertension, the American Heart Association's Council for High Blood Pressure Research and the Council on the Kidney in Cardiovascular Disease, and was organized entirely by the newly formed ISH New Investigators Committee (NIC; Figure 1) and young/new investigators (students, postdoctoral fellows, and early career scientists) in hypertension research.1 The symposium consisted of a half-day event with both oral and poster presentations of highly rated abstracts highlighting the most recent advances in hypertension research by young researchers. The scientific program was abstract based with >100 abstracts reviewed by new investigators as assigned by NIC. Top-scoring abstracts received an invitation for either oral or poster presentation based on their scientific merit. The program provided an opportunity for learning, networking, and socializing among budding scientists from around the world. More than 50 new investigators across 5 continents presented their research at the session, making it a truly “global” hypertension initiative, which was targeted toward young researchers.

  • 15.
    Vinnars, Marie-Therese
    et al.
    Department of Laboratory Medicine, Division of Pathology, and Department of Obstetrics and Gynecology, CLINTEC, Karolinska Institutet, Stockholm, Sweden.
    Wijnaendts, Liliane C.D.
    Westgren, Magnus
    Bolte, Annemieke C.
    Papadogiannakis, Nikos
    Nasiell, Josefine
    Severe Preeclampsia With and Without HELLP Differ With Regard to Placental Pathology2008Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 51, nr 5, s. 1295-1299Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The aim of the present study was to evaluate the histopathology in placentas from patients with severe preeclampsia with and without hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. An additional aim was to compare the prevalence of infants born small for gestational age in the 2 groups. The study is retrospective and includes 178 women who have been diagnosed at the Karolinska University Hospital Huddinge or at the Free University Medical Center between 2000 and 2005 with severe preeclampsia. A total of 96 women had severe preeclampsia without signs of HELLP (preeclampsia group), whereas 82 fulfilled the criteria for having HELLP syndrome (HELLP group). Infarction (P=0.014), intervillous thrombosis (P<0.001), and abruption (P=0.002) were more common in the preeclampsia group than in the HELLP group. There was no statistically significant difference in the frequency of accelerated villous maturation (P=0.61), decidual arteriopathy (P=0.27), or chorioamnionitis (P=0.61). Furthermore, there was a higher mean placental weight, adjusted for gestational age, in the Swedish HELLP material than in the preeclampsia group (P<0.001). Finally, mothers in the preeclampsia group gave birth significantly more often to small for gestational age babies than mothers suffering from HELLP syndrome (P<0.001). The histopathologic profile and the range of placental lesions were partly different in the preeclampsia and HELLP patients. Considering the central role that placenta seems to have in preeclampsia, the present result might suggest that different underlying pathogenetic mechanisms and courses can be in play in patients with preeclampsia and HELLP syndrome.

  • 16. Vishram-Nielsen, Julie K. K.
    et al.
    Laurent, Stephane
    Nilsson, Peter M.
    Linneberg, Allan
    Sehested, Thomas S. G.
    Greve, Sara V.
    Pareek, Manan
    Palmieri, Luigi
    Giampaoli, Simona
    Donfrancesco, Chiara
    Kee, Frank
    Mancia, Giuseppe
    Cesana, Giancarlo
    Veronesi, Giovanni
    Kuulasmaa, Kari
    Salomaa, Veikko
    Kontto, Jukka
    Palosaari, Tarja
    Sans, Susana
    Ferrieres, Jean
    Dallongeville, Jean
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Moitry, Marie
    Drygas, Wojciech
    Tamosiunas, Abdonas
    Peters, Annette
    Brenner, Hermann
    Njolstad, Inger
    Olsen, Michael H.
    Does Estimated Pulse Wave Velocity Add Prognostic Information?: MORGAM Prospective Cohort Project2020Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 75, nr 6, s. 1420-1428Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Reference Values for Arterial Stiffness Collaboration has derived an equation using age and mean blood pressure to estimated pulse wave velocity (ePWV), which predicted cardiovascular events independently of Systematic COoronary Risk Evaluation (SCORE) and Framingham Risk Score. The study aim was to investigate the independent association between ePWV and clinical outcomes in 107 599 apparently healthy subjects (53% men) aged 19 to 97 years from the MORGAM Project who were included between 1982 and 2002 in 38 cohorts from 11 countries. Using multiple Cox-regression analyses, the predictive value of ePWV was calculated adjusting for country of inclusion and either SCORE, Framingham Risk Score, or traditional cardiovascular risk factors (age, sex, smoking, systolic blood pressure, body mass index [BMI], total and high-density lipoprotein cholesterol). Cardiovascular mortality consisted of fatal stroke, fatal myocardial infarction, or coronary death, and the composite cardiovascular end point consisted of stroke, myocardial infarction, or coronary death. Model discrimination was assessed using Harrell's C-statistic. Adjusting for country and logSCORE or Framingham Risk Score, ePWV was associated with all-cause mortality (hazard ratio, 1.23 [95% CI 1.20-1.25] per m/s or 1.32 [1.29-1.34]), cardiovascular mortality (1.26 [1.21-1.32] or 1.35 [1.31-1.40]), and composite cardiovascular end point (1.19 [1.16-1.22] or 1.23 [1.20-1.25]; all P<0.001). However, after adjusting for traditional cardiovascular risk factors, ePWV was only associated with all-cause mortality (1.15 [1.08-1.22], P<0.001) and not with cardiovascular mortality (0.97 [0.91-1.03]) nor composite cardiovascular end point (1.10 [0.97-1.26]). The areas under the last 3 receiver operator characteristic curves remained unchanged when adding ePWV. Elevated ePWV was associated with subsequent mortality and cardiovascular morbidity independently of systematic coronary risk evaluation and Framingham Risk Score but not independently of traditional cardiovascular risk factors.

  • 17.
    Vishram-Nielsen, Julie K.K.
    et al.
    Center for Clinical Research and Prevention, Bispebjerg and Frederiksberg Hospital, The Capital Region of Denmark, Copenhagen, Frederiksberg, Denmark; Department of Cardiology, Rigshospitalet, University of Copenhagen, Denmark.
    Kristensen, Anna M. Dyrvig
    Department of Cardiology, North Zealand Hospital, Hillerød, Denmark.
    Pareek, Manan
    Department of Cardiology, North Zealand Hospital, Hillerød, Denmark; Department of Internal Medicine, Yale New Haven Hospital, Yale University School of Medicine, CT, New Haven, United States.
    Laurent, Stephane
    Department of Clinical Pharmacology and INSERM U 970, Team 7, Paris CV Research Center (PARCC), Hôpital Européen Georges Pompidou, France.
    Nilsson, Peter M.
    Department for Clinical Sciences Medicine, University Hospital, Malmö, Sweden.
    Linneberg, Allan
    Center for Clinical Research and Prevention, Bispebjerg and Frederiksberg Hospital, The Capital Region of Denmark, Copenhagen, Frederiksberg, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
    Greve, Sara V.
    Cardiovascular and Metabolic Preventive Clinic, Department of Endocrinology, Odense University Hospital, Denmark.
    Palmieri, Luigi
    Department of Cardiovascular, Endocrine-metabolic Diseases and Aging, Istituto Superiore di Sanità (ISS), Rome, Italy.
    Giampaoli, Simona
    Department of Cardiovascular, Endocrine-metabolic Diseases and Aging, Istituto Superiore di Sanità (ISS), Rome, Italy.
    Donfrancesco, Chiara
    Department of Cardiovascular, Endocrine-metabolic Diseases and Aging, Istituto Superiore di Sanità (ISS), Rome, Italy.
    Kee, Frank
    Centre for Public Health, The Queeńs University of Belfast, United Kingdom.
    Mancia, Giuseppe
    University of Milano-Bicocca and Policlinico di Monza, Italy.
    Cesana, Giancarlo
    Research Centre on Public Health, University of Milano Bicocca, Villa Serena, Monza, Italy.
    Veronesi, Giovanni
    Research Centre in Epidemiology and Preventive Medicine (EPIMED), Department of Medicine and Surgery, University of Insubria, Italy.
    Grassi, Guido
    Clinica Medica, Department of Medicine and Surgery, University of Milano Bicocca, Villa Serena, Monza, Italy.
    Kuulasmaa, Kari
    Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
    Salomaa, Veikko
    Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
    Palosaari, Tarja
    Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
    Sans, Susana
    Catalan Department of Health, Barcelona, Spain.
    Ferrieres, Jean
    Department of Cardiology, Toulouse University School of Medicine, Rangueil Hospital, France.
    Dallongeville, Jean
    Institut Pasteur de Lille, France.
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Moitry, Marie
    Department of Epidemiology and Public Health, University of Strasbourg and University Hospital of Strasbourg, France.
    Drygas, Wojciech
    Department of Epidemiology, CVD Prevention and Health Promotion, National Institute of Cardiology, Warsaw, Poland.
    Tamosiunas, Abdonas
    Lithuanian University of Health Sciences, Institute of Cardiology, Kaunas, Lithuania.
    Peters, Annette
    German Research Center for Environmental Health, Institute of Epidemiology II, Neuherberg, Germany.
    Brenner, Hermann
    German Cancer Research Center, Heidelberg, Germany; Network Aging Research, University of Heidelberg, Germany.
    Grimsgaard, Sameline
    Department of Community Medicine, UiT the Arctic University of Norway, Tromsø, Norway.
    Savallampi, Matti
    Finnish Institute for Health and Welfare (THL), Helsinki, Finland.
    Olsen, Michael H.
    Department of Internal Medicine, Holbaek Hospital, Denmark; Centre of Individualized Medicine in Arterial Diseases (CIMA), Department of Regional Health Research, University of Southern Denmark, Denmark.
    Predictive importance of blood pressure characteristics with increasing age in healthy men and women: The MORGAM Project2021Ingår i: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 77, nr 4, s. 1076-1085Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    It remains unclear which blood pressure (BP) characteristics best predict cardiovascular risk in different age groups and between sexes. We leveraged data from the MORGAM (MONICA [Monitoring of Trends and Determinants in Cardiovascular Disease], Risk, Genetics, Archiving and Monograph) Project to investigate determinants of BP characteristics and their prognostic importance, in younger and older (</≥50 years) men and women. The study population comprised 107 599 individuals (53% men) aged 19 to 97 years without established cardiovascular disease, not on antihypertensive treatment, recruited between 1982 and 2008 in 38 cohorts. Covariates of BP characteristics were explored using multivariable linear regression. Prognostic importance was examined using multivariable Cox proportional-hazards regression, area under the receiver operating characteristic curve, and net reclassification improvement. The primary end point was a composite cardiovascular end point (CEP), defined as fatal or nonfatal stroke, death from coronary heart disease or nonfatal myocardial infarction. The positive association between age and systolic BP was more pronounced among individuals ≥50 years while the same was true for diastolic BP in those <50 years (P interaction <0.001). Higher systolic BP and mean BP were significantly associated with cardiovascular end point, irrespective of age group (P<0.001), but diastolic BP only demonstrated an independent relationship in the younger group (P<0.001). Brachial pulse pressure was associated with cardiovascular end point in the older age group (P<0.001). In subjects <50 years, diastolic BP significantly improved area under the receiver operating characteristic curve compared with Systematic Coronary Risk Evaluation variables (including systolic BP) alone (0.842 versus 0.840, P=0.03), enhanced continuous net reclassification improvement (0.150 [95% CI, 0.087-0.215]) and improved the prognostic value of the European Society of Cardiology/European Society of Hypertension hypertension definition (categorical net reclassification improvement=0.0255, P=0.005). In conclusion, diastolic BP may provide additional prognostic utility beyond systolic BP, in predicting composite cardiovascular events among younger individuals.

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