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  • 1.
    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.

  • 2. 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.

  • 3.
    Khalili, Payam
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Nilsson, Peter M.
    Department of Medicine, University Hospital, S-205 02 Malmö.
    Nilsson, Jan-Åke
    Department of Medicine, University Hospital, S-205 02 Malmö.
    Berglund, Göran
    Department of Medicine, University Hospital, S-205 02 Malmö.
    Smoking as a modifier of the systolic blood pressure-induced risk of cardiovascular events and mortality: a population-based prospective study of middle-aged men2002In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, no 9, p. 1759-1764Article in journal (Refereed)
    Abstract [en]

    Objective To examine to what degree smoking habits modulate the relationship between systolic blood pressure (SBP) and risk for cardiovascular morbidity (first event) and mortality in middle-aged men. Design and methods In all, 22 444 middle-aged men were recruited from a population-based screening study (mean attendance rate 71%). Risk factor intervention was offered to about 20% of participants. Subjects were followed in local and national registers for cardiovascular morbidity and mortality during more than 17 years of follow-up. Lifestyle variables were investigated at baseline, including smoking habits. Event rates were calculated in relation to quintiles (Q1-Q5) of baseline SBP in untreated subjects, subdivided into categories of smoking habits, but also for 915 previously known, treated hypertensive (tHT) patients at baseline. Results We found an increasing incidence of first cardiovascular event (CE) with increasing SBP levels, ranging from 63.5 CE/10 000 person-years (Q1) to 62.3, 70.5,82.3 and 115.1 CE/10 000 person-years (Q2-Q5). The corresponding figure in tHTs; was 153 CE/10 000 person-years. If further subdivided into smokers/ex-smokers/non-smokers, the relative risks (RR) of smokers were 1.9 [95% confidence interval (Cl): 1.5-2.4], 2.1 (1.8-2.5), 2.3 (1.8-2.9), 1.8 (1.5-2.1), and 1.7 (1.5-2.0) compared to present non-smokers, in relation to SBP (Q1-Q5). In tHTs; the RR was 1.4 (1.1-1.8). Cardiovascular mortality rates differed in relation to SBP and smoking habits, from 40.3 (present non-smokers) and 70.7 (smokers) deaths/10 000 person-years in Q1, to 54.2 and 134.0 deaths/10 000 person-years in Q5. In tHTs the corresponding figures were 81.6 and 149.4 deaths/10 000 person-years, respectively. No difference in risk was found for never-smokers compared to ex-smokers in relation to SBP. The risk in moderate/heavy smokers (> 10 cigarettes/day) compared to other smokers (less than or equal to 10 cigarettes/day) was significantly (P < 0.005) increased only in Q5. Conclusion Increasing systolic blood pressure levels in middle-aged men is associated with an increasing risk of future cardiovascular events and mortality, an association modified by smoking habits. Patients with treated hypertension in the 1970-1980s were also at an increased risk in spite of healthcare efforts. This calls for a more comprehensive multiple risk factor approach for the management and reduction of cardiovascular risk in these patients. (C) 2002 Lippincott Williams Wilkins.

  • 4.
    Khalili, Payam
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Cardiology and Acute Internal Medicine, Central Hospital, Karlstad, Sweden .
    Sundström, Johan
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden .
    Franklin, Stanley S.
    Department of Medicine, Medical Sciences, University of California, Irvine, USA.
    Jendle, Johan
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Cardiology and Acute Internal Medicine, Central Hospital, Karlstad, Sweden.
    Lundin, Fredrik
    Statistical Unit, Värmland County Council, Karlstad, Sweden.
    Jungner, Ingmar
    Department of Medicine, Clinical Epidemiological Unit, Karolinska Institute, Stockholm, Sweden .
    Nilsson, Peter M.
    Faculty of Health and Medicine, Örebro University, Örebro, Sweden; Department of Clinical Sciences, Lund University, University Hospital, Malmö, Sweden.
    Combined effects of brachial pulse pressure and sialic acid for risk of cardiovascular events during 40 years of follow-up in 37 843 individuals2012In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 30, no 9, p. 1718-1724Article in journal (Refereed)
    Abstract [en]

    Objective: Pulse pressure (PP) is a risk marker for cardiovascular disease (CVD) in individuals 50 years and older. Inflammation is suggested to influence atherosclerosis, but could also increase PP. We aimed to examine the combined effects of PP and the inflammatory marker sialic acid, and their independent roles on CVD risk.

    Methods: From a population-based study in Sweden between 1962 and 1965, 18 429 men and 19 414 women at the age of 50 or older were selected and followed for first CVD event until 2005. We investigated the biological interactions between sialic acid and PP. The associations of PP and sialic acid with risk of CVD were calculated by using Cox proportional hazards model. Adjustments were made for conventional risk factors, mean arterial pressure (MAP) and socioeconomic status.

    Results: The mean age was 59.5 (SD 6.5) years and the number of incident CVD events in men and women were 3641 and 3227, respectively. No biological interaction was seen between PP and sialic acid. In men, the adjusted hazard ratio for PP was 0.92 [95% confidence interval (CI) 0.88-0.96, P < 0.0001) for 1 SD of PP, and 1.09 (95% CI 1.05-1.13, P < 0.0001) for 1 SD of sialic acid. In women, the corresponding figures were 1.02 (95% CI 0.97-1.07, P = 0.48) and 1.09 (95% CI 1.05-1.13, P < 0.0001).

    Conclusions: Sialic acid but not PP was an independent risk factor for CVD. The risk induced by PP is highly affected by MAP. This suggests that both estimated arterial stiffness and inflammation contribute through different pathways to risk of CVD.

  • 5.
    Kurland, Lisa
    et al.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Melhus, Håkan
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Karlsson, Julia
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Kahan, Thomas
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.
    Malmqvist, Karin
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.
    Öhman, K. Peter
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Nyström, Fredrik
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Hägg, Anders
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Lind, Lars
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Angiotensin converting enzyme gene polymorphism predicts blood pressure response to angiotensin II receptor type 1 antagonist treatment in hypertensive patients2001In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 19, no 10, p. 1783-1787Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment; more specifically, in response to treatment with irbesartan or atenolol.

    DESIGN AND METHODS: Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the beta1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction.

    RESULTS: The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18 +/- 11 SD versus -7 +/- 10 mmHg, P = 0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P = 0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment.

    CONCLUSIONS: ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment.

  • 6.
    Kurland, Lisa
    et al.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Melhus, Håkan
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Karlsson, Julia
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, 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, Peter
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Nyström, Fredrik
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Hägg, Anders
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Lind, Lars
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial2002In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, no 4, p. 657-663Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Our aim was to determine if gene polymorphisms in the renin-angiotensin-aldosterone system (RAAS) were related to the degree of change in left ventricular hypertrophy (LVH) during antihypertensive treatment.

    METHODS AND RESULTS: Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months. The angiotensinogen T174M and M235T, the angiotensin-converting enzyme I/D, the AT1-receptor A1166C and the aldosterone synthase (CYP11B2) -344 C/T polymorphisms were analysed and related to the change in left ventricular mass (LVM). Patients with the angiotensinogen 174 TM genotype treated with irbesartan responded with the greatest reduction in LVM (-23 +/- 31SD g/m2 for TM and +0.5 +/- 18 g/m2 for TT, P = 0.005), independent of blood pressure reduction. Both the angiotensinogen 235 T-allele (P = 0.02) and the AT1-receptor 1166 AC genotype responded with the greatest reduction in LVM when treated with irbesartan (-0.1 +/- 19 g/m2 for AA and -18 +/- 30 g/m2 for AC, P = 0.02), independent of blood pressure reduction. These polymorphisms were not associated with the change in LVM during treatment with atenolol.

    DISCUSSION: The angiotensinogen T174M and M235T and the AT1-receptor A1166C polymorphisms were related to the change in LVH during antihypertensive treatment with an AT1-receptor antagonist; of these angiotensinogen T174M was the most powerful. This highlights the role of the RAAS for left ventricular hypertrophy and the potential of pharmacogenetics as a tool for guidance of antihypertensive therapy.

  • 7.
    Liljedahl, Ulrika
    et al.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Kahan, Thomas
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.
    Malmqvist, Karin
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.
    Melhus, Håkan
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Syvänen, Ann-Christine
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Lind, Lars
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden; Astra Zeneca R&D, Mölndal, Sweden.
    Kurland, Lisa
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Single nucleotide polymorphisms predict the change in left ventricular mass in response to antihypertensive treatment2004In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 22, no 12, p. 2321-2328Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Our aim was to determine whether the change in left ventricular (LV) mass in response to antihypertensive treatment could be predicted by multivariate analysis of single nucleotide polymorphisms (SNPs) in candidate genes reflecting pathways likely to be involved in blood pressure control.

    METHODS: Patients with mild to moderate primary hypertension and LV hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta1 adrenoreceptor blocker atenolol (n = 49). A microarray-based minisequencing system was used for genotyping 74 SNPs in 25 genes. These genotypes were related to the change in LV mass index by echocardiography, after 12 weeks treatment as monotherapy, using stepwise multiple regression analysis.

    RESULTS: The blood pressure reductions were similar and significant in both treatment groups. Two SNPs in two separate genes (the angiotensinogen T1198C polymorphism, corresponding to the M235T variant and the apolipoprotein B G10108A polymorphism) for those treated with irbesartan, and the adrenoreceptor alpha2A A1817G for those treated with atenolol, significantly predicted the change in LV mass. The predictive power of these SNPs was independent of the degree of blood pressure reduction.

    CONCLUSION: SNPs in the angiotensinogen, apolipoprotein B, and the alpha2 adrenoreceptor gene predicted the change in LV mass during antihypertensive therapy. These results illustrate the potential of using microarray-based technology for SNP genotyping in predicting individual drug responses.

  • 8.
    Lind, Ylva Sjöberg
    et al.
    Dept Emergency Med, Linköping University Hospital, Linköping, Sweden.
    Lind, Lars
    Dept Med, Uppsala University, Uppsala, Sweden.
    Salihovic, Samira
    Örebro University, School of Science and Technology.
    van Bavel, Bert
    Örebro University, School of Science and Technology.
    Lind, P. Monica
    Uppsala University, Uppsala, Sweden.
    Persistent organic pollutants and abnormal geometry of the left ventricle in the elderly2013In: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 31, no 8, p. 1547-1553Article in journal (Refereed)
    Abstract [en]

    Background:Established risk factors for left ventricular hypertrophy (LVH) are hypertension, diabetes, and obesity. However, as these risk factors explain only part of the variation in left ventricular mass, we investigated whether persistent organic pollutants (POPs) might also play a role in LVH, because exposure to polychlorinated biphenyl 126 induced cardiac growth in rats.

    Methods:In the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS), left ventricular mass index (LVMI), relative wall thickness (RWT), and geometric groups of LVH, were determined by echocardiography and 21 POPs were measured by high-resolution chromatography coupled to high-resolution mass spectrometry (HRGC/HRMS) in 1016 individuals aged 70 years. All individuals with a history of myocardial infarction were excluded from analysis (n=72).

    Results:Several of the POPs were related to abnormal left ventricular geometry before adjustment for established risk factors, but lost in significance following adjustment. However, the pesticide hexachlorobenzene (HCB) levels were significantly related to RWT, and concentric left ventricular remodeling, also following adjustment for sex, blood pressure, antihypertensive treatment, diabetes, and BMI (P<0.0001).

    Conclusion:In this cross-sectional study, circulating levels of HCB were related to increased wall thickness of the left ventricle and concentric left ventricular remodeling, independently of LVH risk factors, suggesting a role of this environmental contaminant in abnormal growth of the left ventricle.

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