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  • 1.
    Helmersson-Karlqvist, Johanna
    et al.
    Department of Medical Sciences/Clinical Chemistry, Uppsala University, Uppsala SE-751 85, Sweden.
    Ärnlöv, Johan
    Dalarna University, School of Education, Health and Social Studies, Medical Science. Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden.
    Larsson, Anders
    Department of Medical Sciences/Clinical Chemistry, Uppsala University, Uppsala SE-751 85, Sweden.
    Basu, Samar
    Department of Public Health and Caring Sciences/Oxidative Stress and Inflammation, Uppsala University, Uppsala, Sweden, Centre of Excellence-Inflammation, Uppsala University Hospital, Uppsala, Sweden, Laboratory of Biochemistry, Molecular Biology, and Nutrition, University d'Auvergne, Clermont-Ferrand, France.
    Prostaglandin F2α formation is associated with mortality in a Swedish community-based cohort of older males2015In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 36, no 4, p. 238-243Article in journal (Refereed)
    Abstract [en]

    AIMS: An increasing number of clinical studies highlight the importance of the inflammatory mediator prostaglandin F2α (PGF2α). Prostaglandin F2α activity has been suggested to play pivotal roles in the development of cardiovascular diseases and cancer. However, whether systemic PGF2α concentrations may signal mortality is unknown. The aim was to evaluate in vivo PGF2α formation, by measuring urinary 15-keto-dihydro-PGF2α, and mortality risk in a community setting.

    METHODS AND RESULTS: Urinary 15-keto-dihydro-PGF2α was measured in a Swedish population of 670 men (aged 77-78 years) and the participants were followed up for a median of 9.7 years (383 died, among them 156 of cardiovascular causes and 102 of cancer). In Cox regression models, urinary 15-keto-dihydro-PGF2α was significantly associated with cardiovascular mortality [multivariate hazard ratio (HR) for 1 SD increase of urinary 15-keto-dihydro-PGF2α: 1.18; 95% CI:1.04-1.34; P = 0.01) independent of established cardiovascular risk factors including C-reactive protein. Urinary 15-keto-dihydro-PGF2α was also independently associated with total mortality (multivariate HR for 1 SD increase of urinary 15-keto-dihydro-PGF2α: 1.11; 95% CI: 1.01-1.21; P = 0.03). The combination of 15-keto-dihydro-PGF2α concentrations above the median and high serum high-sensitive C-reactive protein (>3 mg/L) was independently associated with a two-fold increased risk of cancer and total mortality (P = 0.02 and P < 0.001, respectively).

    CONCLUSION: This is the first study to show that the inflammatory mediator PGF2α was independently associated with mortality and specifically cardiovascular mortality 10 years later. The results are in line with the emerging evidence of the importance of the inflammatory mediator PGF2α in fatal cardiovascular disease.

  • 2.
    Strömsöe, Anneli
    et al.
    Dalarna University, School of Education, Health and Social Studies, Medical Science. Sahlgrenska University Hospital, Gothenburg.
    Svensson, Leif
    South Hospital, Stockholm.
    Axelsson, Åsa B.
    Sahlgrenska Academy at Gothenburg University, Gothenburg.
    Claesson, Andreas
    Prehospen University College of Borås, Borås; Kungälv Ambulance Service, Kungälv.
    Göransson, Katarina E.
    Karolinska University Hospital, Stockholm; Karolinska Institutet, Stockholm.
    Nordberg, Per
    Section of Cardiology, Södersjukhuset, Stockholm.
    Herlitz, Johan
    Sahlgrenska University Hospital, Gothenburg; Prehospen University College of Borås.
    Improved outcome in Sweden after out-of-hospital cardiac arrest and possible association with improvements in every link in the chain of survival2015In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 36, no 14, p. 863-871Article in journal (Refereed)
    Abstract [en]

    Aims: To describe out-of-hospital cardiac arrest (OHCA) in Sweden from a long-term perspective in terms of changes in outcome and circumstances at resuscitation.

    Methods and results: All cases of OHCA (n = 59 926) reported to the Swedish Cardiac Arrest Register from 1992 to 2011 were included. The number of cases reported (n/100 000 person-years) increased from 27 (1992) to 52 (2011). Crew-witnessed cases, cardiopulmonary resuscitation prior to the arrival of the emergency medical service (EMS), and EMS response time increased (P < 0.0001). There was a decrease in the delay from collapse to calling for the EMS in all patients and from collapse to defibrillation among patients found in ventricular fibrillation (P< 0.0001). The proportion of patients found in ventricular fibrillation decreased from 35 to 25% (P < 0.0001). Thirty-day survival increased from 4.8 (1992) to 10.7% (2011) (P < 0.0001), particularly among patients found in a shockable rhythm and patients with return of spontaneous circulation (ROSC) at hospital admission. Among patients hospitalized with ROSC in 2008–2011, 41% underwent therapeutic hypothermia and 28% underwent percutaneous coronary intervention. Among 30-day survivors in 2008–2011, 94% had a cerebral performance category score of 1 or 2 at discharge from hospital and the results were even better if patients were found in a shockable rhythm.

    Conclusion: From a long-term perspective, 30-day survival after OHCA in Sweden more than doubled. The increase in survival was most marked among patients found in a shockable rhythm and those hospitalized with ROSC. There were improvements in all four links in the chain of survival, which might explain the improved outcome.

  • 3. Sundström, J
    et al.
    Ingelsson, E
    Berglund, L
    Zethelius, B
    Lind, L
    Venge, P
    Ärnlöv, Johan
    Dalarna University, School of Education, Health and Social Studies, Medical Science.
    Cardiac troponin-I and risk of heart failure: a community-based cohort study2009In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 30, no 7, p. 773-781Article in journal (Refereed)
    Abstract [en]

    We examined if circulating levels of cardiac troponin-I (cTnI) predict subsequent heart failure in the community. 

    Using Cox proportional hazards models, we examined the risk of a first hospitalization for heart failure during a maximum of 11.4 years in a community-based sample of 1089 70-year-old men without heart failure, valvular disease, or electrocardiographic left ventricular hypertrophy. Adjusting for smoking, systolic blood pressure, antihypertensive medication use, diabetes, body mass index, serum cholesterol, and myocardial infarction before baseline or during follow-up, 0.01 mu g/L higher cTnI conferred a hazard ratio (HR) of 1.26 (95% confidence interval 1.15-1.38) for subsequent heart failure. Persons with cTnI >= 0.03 mu g/L had an HR of 5.25 (2.00-13.77) compared with persons with cTnI < 0.01 mu g/L. Adjusting additionally for serum NTproBNP attenuated the estimates somewhat [HR 1.22 (1.11-1.34) per 0.01 mu g/L of cTnI]. Excluding persons with myocardial infarction before baseline and censoring at time of myocardial infarction during follow-up, 0.01 mu g/L higher cTnI was associated with a multivariable-adjusted HR of 1.31 (1.16-1.47) for heart failure. 

    In a community-based sample, a direct measure of cardiomyocyte damage, cTnI, indicated a substantially increased risk of heart failure, accounting for other risk factors. Studies investigating the clinical utility of measuring cTnI in asymptomatic individuals are warranted.

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