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  • 1.
    Andersson, Tommy
    et al.
    Örebro University, School of Medical Sciences.
    Magnuson, Anders
    School of Medical Sciences, Örebro University, Örebro, Sweden.
    Bryngelsson, Ing-Liss
    Department of Occupational and Environmental Medicine, School of Medical Sciences, Örebro University, Örebro, Sweden.
    Frøbert, Ole
    Örebro University, School of Medical Sciences. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Henriksson, Karin M.
    Department of Medical Science, Uppsala University, Uppsala and AstraZeneca R&D, Mölndal, Sweden.
    Edvardsson, Nils
    Sahlgrenska Academy at Sahlgrenska University Hospital, Göteborg, Sweden.
    Poçi, Dritan
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Cardiology, Örebro University Hospital, Örebro, Sweden.
    Patients without comorbidities at the time of diagnosis of atrial fibrillation: causes of death during long-term follow-up compared to matched controls2017In: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 40, no 11, p. 1076-1082Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Little is known about the long-term, cause-specific mortality risk in patients without comorbidities at the time of diagnosis of atrial fibrillation (AF).

    METHODS: From a nation-wide registry of patients hospitalized with incident AF between 1995 and 2008 we identified 9 519 patients with a first diagnosed AF and no comorbidities at the time of AF diagnosis. They were matched with 12 468 controls. The follow-up continued until December 2008. Causes of death were classified according to the ICD-10 codes.

    RESULTS: During follow-up, 11.1% of patients with AF and 8.3% of controls died. Cardiovascular diseases were the most common causes of death and the only diagnoses which showed significantly higher relative risk in patients with AF than controls (HR 2.0, 95% CI 1.8-2.3), and the relative risk was significantly higher in women than in men. Stroke was a more common cause among patients with AF, 13.1% versus 9.7% (HR 2.7, 95% CI 1.8-4.0), while cerebral hemorrhage was more common among controls, 4.7% versus 10.2% (HR 0.9, 95% CI 0.6-1.5). The time from AF diagnosis to death was 6.0 ± 3.1 years.

    CONCLUSIONS: In patients with incident AF and no known comorbidities at the time of AF diagnosis, only cardiovascular diseases were more often causes of death as compared to controls. Women carried a significantly higher relative risk than men.

  • 2.
    Hallberg, P.
    et al.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Karlsson, J.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Lind, L.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Michaëlsson, K.
    Department of Surgical Sciences, Uppsala University, Uppsala.
    Kurland, Lisa
    Department of Medical Sciences, Uppsala University, Uppsala.
    Kahan, T.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm.
    Malmqvist, K.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm.
    Öhman, K. P.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm; Department of Medicine and Care, Faculty of Health Sciences, Linköping.
    Nyström, F.
    Department of Medicine and Care, Faculty of Health Sciences, Linköping; Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping, Sweden.
    Liljedahl, U.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Syvänen, A. C.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Melhus, H.
    Department of Medical Sciences, Uppsala University, Uppsala.
    Gender-specific association between preproendothelin-1 genotype and reduction of systolic blood pressure during antihypertensive treatment–results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)2004In: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 27, no 5, p. 287-90Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies suggest that endothelin-1 contributes to the pathogenesis of hypertension. A G5665T gene polymorphism of preproendothelin-1 has been shown to be associated with higher blood pressure in overweight patients. No study has yet determined the effect of this polymorphism on the change in blood pressure during antihypertensive treatment.

    HYPOTHESIS: This study aimed to determine this effect in hypertensive patients with left ventricular (LV) hypertrophy during antihypertensive treatment with either irbesartan or atenolol.

    METHODS: We determined the preproendothelin-1 genotype using minisequencing in 102 patients with essential hypertension and LV hypertrophy verified by echocardiography, randomized in a double-blind fashion to treatment with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol.

    RESULTS: The change in systolic blood pressure (SBP) after 12 weeks of treatment was related to the preproendothelin-1 genotype in men; after adjustment for potential covariates (age, blood pressure, and LV mass index at study entry, dose of irbesartan/atenolol, and type of treatment), those carrying the T-allele responded on average with a more than two-fold greater reduction than those with the G/G genotype (-21.9 mmHg 13.9] vs. -8.9 [2.3], p = 0.007). No significant differences in blood pressure change between G/G and carriers of the T-allele were seen among women.

    CONCLUSIONS: Our finding suggests a gender-specific relationship between the G5665T preproendothelin-1 polymorphism and change in SBP in response to antihypertensive treatment with irbesartan or atenolol, suggesting the endothelin pathway to be a common mechanism included in the hypertensive action of the drugs.

  • 3.
    Hallberg, Pär
    et al.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Lind, Lars
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden; AstraZeneca Research & Development, Mölndal, Sweden.
    Billberger, Katarina
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Michaelsson, Karl
    Department of Surgical 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.
    Kahan, Thomas
    Division of Internal Medicine, Karolinska Institute, 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.
    Liljedahl, Ulrika
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Syvänen, Ann-Christine
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Melhus, Håkan
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Transforming growth factor beta1 genotype and change in left ventricular mass during antihypertensive treatment–results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)2004In: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 27, no 3, p. 169-173Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor beta1 (TGF-beta1); AT1-receptor antagonists reverse these changes. The TGF-beta1 G + 915C polymorphism is associated with interindividual variation in TGF-beta1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment.

    HYPOTHESIS: We aimed to determine whether the TGF-beta1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1-receptor antagonists or a beta1-adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group.

    METHODS: We determined the association between the TGF-beta1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol.

    RESULTS: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-beta1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI -44.7 g/m2 vs. -22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group.

    CONCLUSIONS: The TGF-beta1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1-receptor antagonist irbesartan.

  • 4.
    Hörer, Tal
    et al.
    Örebro University, School of Health and Medical Sciences.
    Vidlund, Mårten
    Lindell, Peter
    Jansson, Kjell
    A rare case of pacemaker electrode perforation of the heart with intra-abdominal migration2010In: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 33, no 8, p. E20-E20Article in journal (Refereed)
  • 5.
    Karlsson, J.
    et al.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Lind, L.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden; AstraZeneca Research and Development, Mölndal, Sweden.
    Hallberg, P.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Michaëlsson, K.
    Department of Surgical Sciences, Uppsala University, Uppsala.
    Kurland, Lisa
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Kahan, T.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.
    Malmqvist, K.
    Division of Internal Medicine, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
    Öhman, K. P.
    AstraZeneca Research and Development, Mölndal, Sweden; Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden.
    Nyström, F.
    Department of Medicine and Care, Faculty of Health Sciences, Linköping, Sweden; Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping, Sweden.
    Melhus, H.
    Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
    Beta1-adrenergic receptor gene polymorphisms and response to beta1-adrenergic receptor blockade in patients with essential hypertension2004In: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 27, no 6, p. 347-350Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies suggest that the Ser49Gly and Arg389Gly polymorphisms in the beta1-adrenergic receptor might be of functional importance for the cardiovascular system. Both have been associated with altered receptor activity in vitro, and with hypertension and cardiac failure in vivo.

    HYPOTHESIS: The aim of this study was to test whether these polymorphisms were associated with the change in heart rate or blood pressure in patients with essential hypertension and left ventricular (LV) hypertrophy treated with the beta1-adrenergic receptor blocker atenolol.

    METHODS: Blood pressure and heart rate were measured in 101 hypertensive patients with echocardiographically verified LV hypertrophy, randomized in a double-blind study to treatment with either the beta1-adrenergic receptor blocker atenolol or the angiotensin II type I receptor antagonist irbesartan. Changes in blood pressure and heart rate were evaluated after 12 weeks. Beta1-adrenergic receptor genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism.

    RESULTS: We found no significant associations between the changes in the measured variables and either of the two polymorphisms. However, carriers of the 49Gly allele showed a tendency toward a greater reduction in heart rate compared with patients with the Ser/Ser49 genotype (p = 0.06).

    CONCLUSIONS: The Ser49Gly and Arg389Gly beta1-adrenergic receptor polymorphisms do not seem to exert a major effect on the changes in heart rate and blood pressure during 12 weeks of treatment with atenolol in patients with essential hypertension and LV hypertrophy.

1 - 5 of 5
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  • ieee
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  • nn-NO
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