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  • 1. Bergström, Göran
    et al.
    Persson, Margaretha
    Adiels, Martin
    Björnson, Elias
    Bonander, Carl
    Ahlström, Håkan
    Alfredsson, Joakim
    Angerås, Oskar
    Berglund, Göran
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Brandberg, John
    Börjesson, Mats
    Cederlund, Kerstin
    de Faire, Ulf
    Duvernoy, Olov
    Ekblom, Örjan
    Engström, Gunnar
    Engvall, Jan E.
    Fagman, Erika
    Eriksson, Mats
    Erlinge, David
    Fagerberg, Björn
    Flinck, Agneta
    Gonçalves, Isabel
    Hagström, Emil
    Hjelmgren, Ola
    Lind, Lars
    Lindberg, Eva
    Lindqvist, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Klinisk fysiologi.
    Ljungberg, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Magnusson, Martin
    Mannila, Maria
    Markstad, Hanna
    Mohammad, Moman A.
    Nystrom, Fredrik H.
    Ostenfeld, Ellen
    Persson, Anders
    Rosengren, Annika
    Sandström, Anette
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Själander, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Sköld, Magnus C.
    Sundström, Johan
    Swahn, Eva
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Torén, Kjell
    Östgren, Carl Johan
    Jernberg, Tomas
    Prevalence of Subclinical Coronary Artery Atherosclerosis in the General Population2021Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 144, nr 12, s. 916-929Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Early detection of coronary atherosclerosis using coronary computed tomography angiography (CCTA), in addition to coronary artery calcification (CAC) scoring, may help inform prevention strategies. We used CCTA to determine the prevalence, severity, and characteristics of coronary atherosclerosis and its association with CAC scores in a general population.

    Methods: We recruited 30 154 randomly invited individuals age 50 to 64 years to SCAPIS (the Swedish Cardiopulmonary Bioimage Study). The study includes individuals without known coronary heart disease (ie, no previous myocardial infarctions or cardiac procedures) and with high-quality results from CCTA and CAC imaging performed using dedicated dual-source CT scanners. Noncontrast images were scored for CAC. CCTA images were visually read and scored for coronary atherosclerosis per segment (defined as no atherosclerosis, 1% to 49% stenosis, or ≥50% stenosis). External validity of prevalence estimates was evaluated using inverse probability for participation weighting and Swedish register data.

    Results: In total, 25 182 individuals without known coronary heart disease were included (50.6% women). Any CCTA-detected atherosclerosis was found in 42.1%; any significant stenosis (≥50%) in 5.2%; left main, proximal left anterior descending artery, or 3-vessel disease in 1.9%; and any noncalcified plaques in 8.3% of this population. Onset of atherosclerosis was delayed on average by 10 years in women. Atherosclerosis was more prevalent in older individuals and predominantly found in the proximal left anterior descending artery. Prevalence of CCTA-detected atherosclerosis increased with increasing CAC scores. Among those with a CAC score >400, all had atherosclerosis and 45.7% had significant stenosis. In those with 0 CAC, 5.5% had atherosclerosis and 0.4% had significant stenosis. In participants with 0 CAC and intermediate 10-year risk of atherosclerotic cardiovascular disease according to the pooled cohort equation, 9.2% had CCTA-verified atherosclerosis. Prevalence estimates had excellent external validity and changed marginally when adjusted to the age-matched Swedish background population.

    Conclusions: Using CCTA in a large, random sample of the general population without established disease, we showed that silent coronary atherosclerosis is common in this population. High CAC scores convey a significant probability of substantial stenosis, and 0 CAC does not exclude atherosclerosis, particularly in those at higher baseline risk.

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  • 2.
    Brunstrom, Mattias
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Carlberg, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Lindholm, Lars H.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Perspective from Sweden on the global impact of the 2017 american college of cardiology/american heart association hypertension guidelines: a "sprint" beyond evidence in the United States2018Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 137, nr 9, s. 886-888Artikel i tidskrift (Övrigt vetenskapligt)
  • 3.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi. Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Hammargren, Edvin
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Whitaker, Heather
    Eliasson, Mats
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Holmgren, Lars
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Klingstrom, Jonas
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Increased Risk of Acute Myocardial Infarction and Stroke During Hemorrhagic Fever With Renal Syndrome A Self-Controlled Case Series Study2014Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 129, nr 12, s. 1295-1302Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background We recently observed that cardiovascular causes of death are common in patients with hemorrhagic fever with renal syndrome (HFRS), which is caused by hantaviruses. However, it is not known whether HFRS is a risk factor for the acute cardiovascular events of acute myocardial infarction (AMI) and stroke. Methods and Results Personal identification numbers from the Swedish HFRS patient database (1997-2012; n=6643) were cross-linked with the National Patient Register from 1987 to 2011. Using the self-controlled case series method, we calculated the incidence rate ratio of AMI/stroke in the 21 days after HFRS against 2 different control periods either excluding (analysis 1) or including (analysis 2) fatal AMI/stroke events. The incidence rate ratios for analyses 1 and 2 for all AMI events were 5.53 (95% confidence interval [CI], 2.6-11.8) and 6.02 (95% CI, 2.95-12.3) and for first AMI events were 3.53 (95% CI, 1.25-9.96) and 4.64 (95% CI, 1.83-11.77). The incidence rate ratios for analyses 1 and 2 for all stroke events were 12.93 (95% CI, 5.62-29.74) and 15.16 (95% CI, 7.21-31.87) and for first stroke events were 14.54 (95% CI, 5.87-36.04) and 17.09 (95% CI, 7.49-38.96). The majority of stroke events occurred in the first week after HFRS. Seasonal effects were not observed, and apart from 1 study, neither sex nor age interacted with the associations observed in this study. Conclusions There is a significantly increased risk for AMI and stroke in the immediate time period after HFRS. Therefore, HFRS patients should be carefully monitored during the acute phase of disease to ensure early recognition of symptoms of impending AMI or stroke.

  • 4. Di Castelnuovo, Augusto Filippo
    et al.
    Costanzo, Simona
    Bonaccio, Marialaura
    McElduff, Patrick
    Linneberg, Allan
    Salomaa, Veikko
    Mannisto, Satu
    Moitry, Marie
    Ferrieres, Jean
    Dallongeville, Jean
    Thorand, Barbara
    Brenner, Hermann
    Ferrario, Marco
    Tamosiunas, Abdonas
    Njolstad, Inger
    Drygas, Wojciech
    Nikitin, Yuri
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Kee, Frank
    Zeller, Tanja
    Kuulasmaa, Kari
    Blankenberg, Stefan
    Donati, Maria Benedetta
    de Gaetano, Giovanni
    Iacoviello, Licia
    Association of Alcohol Intake with Cardiovascular and Total Mortality2019Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 139Artikel i tidskrift (Övrigt vetenskapligt)
  • 5. Diller, Gerhard-Paul
    et al.
    Dimopoulos, Konstantinos
    Okonko, Darlington
    Li, Wei
    Babu-Narayan, Sonya V
    Broberg, Craig S
    Johansson, Bengt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Bouzas, Beatriz
    Mullen, Michael J
    Poole-Wilson, Philip A
    Francis, Darrel P
    Gatzoulis, Michael A
    Exercise intolerance in adult congenital heart disease: comparative severity, correlates, and prognostic implication.2005Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 112, nr 6, s. 828-35Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Although some patients with adult congenital heart disease (ACHD) report limitations in exercise capacity, we hypothesized that depressed exercise capacity may be more widespread than superficially evident during clinical consultation and could be a means of assessing risk.

    METHODS AND RESULTS: Cardiopulmonary exercise testing was performed in 335 consecutive ACHD patients (age, 33+/-13 years), 40 non-congenital heart failure patients (age, 58+/-15 years), and 11 young (age, 29+/-5 years) and 12 older (age, 59+/-9 years) healthy subjects. Peak oxygen consumption (peak VO2) was reduced in ACHD patients compared with healthy subjects of similar age (21.7+/-8.5 versus 45.1+/-8.6; P<0.001). No significant difference in peak VO2 was found between ACHD and heart failure patients of corresponding NYHA class (P=NS for each NYHA class). Within ACHD subgroups, peak VO2 gradually declined from aortic coarctation (28.7+/-10.4) to Eisenmenger (11.5+/-3.6) patients (P<0.001). Multivariable correlates of peak VO2 were peak heart rate (r=0.33), forced expiratory volume (r=0.33), pulmonary hypertension (r=-0.26), gender (r=-0.23), and body mass index (r=-0.19). After a median follow-up of 10 months, 62 patients (18.5%) were hospitalized or had died. On multivariable Cox analysis, peak VO2 predicted hospitalization or death (hazard ratio, 0.937; P=0.01) and was related to the frequency and duration of hospitalization (P=0.01 for each).

    CONCLUSIONS: Exercise capacity is depressed in ACHD patients (even in allegedly asymptomatic patients) on a par with chronic heart failure subjects. Lack of heart rate response to exercise, pulmonary arterial hypertension, and impaired pulmonary function are important correlates of exercise capacity, as is underlying cardiac anatomy. Poor exercise capacity identifies ACHD patients at risk for hospitalization or death.

  • 6.
    Fröbert, Ole
    et al.
    Faculty of Health, Department of Cardiology, Sweden (O.F., Örebro University.
    Götberg, Matthias
    Department of Cardiology, Clinical Sciences, Lund University, Skane University Hospital, D.E.
    Erlinge, David
    Department of Cardiology, Clinical Sciences, Lund University, Skane University Hospital, D.E.
    Akhtar, Zubair
    International Centre for Diarrhoeal Disease Research, Bangladesh.
    Christiansen, Evald H.
    Department of Cardiology, Aarhus University Hospital.
    MacIntyre, Chandini R.
    Kirby Institute, UNSW Medicine, University of New South Wales, Sydney, Canada.
    Oldroyd, Keith G.
    British Heart Foundation Glasgow Cardiovascular Research Centre, Institute of Cardiovascular and Medical Sciences, University of Glasgow, United Kingdom, and West of Scotland Heart and Lung Centre, Golden Jubilee National Hospital, Clydebank, Glasgow, United Kingdom (K.G.O.).
    Motovska, Zuzana
    Cardiocenter, Third Faculty of Medicine, Charles University, University Hospital Kralovske Vinohrady, Czech Republic (Z.M.), Prague, United States.
    Erglis, Andrejs
    Pauls Stradins Clinical University Hospital, University of Latvia.
    Moer, Rasmus
    Oslo, Norway.
    Hlinomaz, Ota
    International clinical research center, St. Anne University Hospital and Masaryk University, Czech Republic (O.H.), Brno.
    Jakobsen, Lars
    Department of Cardiology, Aarhus University Hospital.
    Engstrøm, Thomas
    Rigshospitalet, University of Copenhagen.
    Jensen, Lisette O.
    Department of Cardiology, Odense University Hospital, C.O.F.).
    Fallesen, Christian O.
    Department of Cardiology, Odense University Hospital, C.O.F.).
    Jensen, Svend E.
    Department of Cardiology, Aalborg University Hospital, Department of Clinical Medicine, Aalborg University.
    Angerås, Oskar
    Sahlgrenska University Hospital and Institute of Medicine, Department of molecular and clinical medicine, Gothenburg University.
    Calais, Fredrik
    Faculty of Health, Department of Cardiology, Sweden (O.F., Örebro University.
    Kåregren, Amra
    Västmanlands sjukhus Västerås, Sweden (A.K.).
    Lauermann, Jörg
    Department of Cardiology, Region Jönköping County, Department of Health, Medicine and Caring, Linköping University.
    Mokhtari, Arash
    Department of Cardiology, Clinical Sciences, Lund University, Skane University Hospital, D.E.
    Nilsson, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Persson, Jonas
    Division of Cardiovascular Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
    Stalby, Per
    Department of Cardiology, Karlstad Central Hospital.
    Islam, Abu K M M
    National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Dhaka, Bangladesh.
    Rahman, Afzalur
    National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Dhaka, Bangladesh.
    Malik, Fazila
    National Heart Foundation Hospital and Research Institute, Dhaka, Bangladesh.
    Choudhury, Sohel
    National Heart Foundation Hospital and Research Institute, Dhaka, Bangladesh.
    Collier, Timothy
    Department of Medical Statistics, London School of Hygiene and Tropical Medicine, United Kingdom (T.C..
    Pocock, Stuart J.
    Department of Medical Statistics, London School of Hygiene and Tropical Medicine, United Kingdom (T.C..
    Pernow, John
    Cardiology Unit, Department of Medicine Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Influenza Vaccination After Myocardial Infarction: A Randomized, Double-Blind, Placebo-Controlled, Multicenter Trial2021Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 144, nr 18, s. 1476-1484Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Observational and small, randomized studies suggest that influenza vaccine may reduce future cardiovascular events in patients with cardiovascular disease.

    METHODS: We conducted an investigator-initiated, randomized, double-blind trial to compare inactivated influenza vaccine with saline placebo administered shortly after myocardial infarction (MI; 99.7% of patients) or high-risk stable coronary heart disease (0.3%). The primary end point was the composite of all-cause death, MI, or stent thrombosis at 12 months. A hierarchical testing strategy was used for the key secondary end points: all-cause death, cardiovascular death, MI, and stent thrombosis.

    RESULTS: Because of the COVID-19 pandemic, the data safety and monitoring board recommended to halt the trial before attaining the prespecified sample size. Between October 1, 2016, and March 1, 2020, 2571 participants were randomized at 30 centers across 8 countries. Participants assigned to influenza vaccine totaled 1290 and individuals assigned to placebo equaled 1281; of these, 2532 received the study treatment (1272 influenza vaccine and 1260 placebo) and were included in the modified intention to treat analysis. Over the 12-month follow-up, the primary outcome occurred in 67 participants (5.3%) assigned influenza vaccine and 91 participants (7.2%) assigned placebo (hazard ratio, 0.72 [95% CI, 0.52-0.99]; P=0.040). Rates of all-cause death were 2.9% and 4.9% (hazard ratio, 0.59 [95% CI, 0.39-0.89]; P=0.010), rates of cardiovascular death were 2.7% and 4.5%, (hazard ratio, 0.59 [95% CI, 0.39-0.90]; P=0.014), and rates of MI were 2.0% and 2.4% (hazard ratio, 0.86 [95% CI, 0.50-1.46]; P=0.57) in the influenza vaccine and placebo groups, respectively.

    CONCLUSIONS: Influenza vaccination early after an MI or in high-risk coronary heart disease resulted in a lower risk of a composite of all-cause death, MI, or stent thrombosis, and a lower risk of all-cause death and cardiovascular death, as well, at 12 months compared with placebo.

    Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02831608.

  • 7. Gaziano, Liam
    et al.
    Sun, Luanluan
    Arnold, Matthew
    Bell, Steven
    Cho, Kelly
    Kaptoge, Stephen K.
    Song, Rebecca J.
    Burgess, Stephen
    Posner, Daniel C.
    Mosconi, Katja
    Robinson-Cohen, Cassianne
    Mason, Amy M.
    Bolton, Thomas R.
    Tao, Ran
    Allara, Elias
    Schubert, Petra
    Chen, Lingyan
    Staley, James R.
    Staplin, Natalie
    Altay, Servet
    Amiano, Pilar
    Arndt, Volker
    Ärnlöv, Johan
    Barr, Elizabeth L. M.
    Björkelund, Cecilia
    Boer, Jolanda M. A.
    Brenner, Hermann
    Casiglia, Edoardo
    Chiodini, Paolo
    Cooper, Jackie A.
    Coresh, Josef
    Cushman, Mary
    Dankner, Rachel
    Davidson, Karina W.
    de Jongh, Renate T.
    Donfrancesco, Chiara
    Engström, Gunnar
    Freisling, Heinz
    de la Cámara, Agustín Gómez
    Gudnason, Vilmundur
    Hankey, Graeme J.
    Hansson, Per-Olof
    Heath, Alicia K.
    Hoorn, Ewout J.
    Imano, Hironori
    Jassal, Simerjot K.
    Kaaks, Rudolf
    Katzke, Verena
    Kauhanen, Jussi
    Kiechl, Stefan
    Koenig, Wolfgang
    Kronmal, Richard A.
    Kyrø, Cecilie
    Lawlor, Deborah A.
    Ljungberg, Börje
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    MacDonald, Conor
    Masala, Giovanna
    Meisinger, Christa
    Melander, Olle
    Moreno Iribas, Conchi
    Ninomiya, Toshiharu
    Nitsch, Dorothea
    Nordestgaard, Børge G.
    Onland-Moret, Charlotte
    Palmieri, Luigi
    Petrova, Dafina
    Garcia, Jose Ramón Quirós
    Rosengren, Annika
    Sacerdote, Carlotta
    Sakurai, Masaru
    Santiuste, Carmen
    Schulze, Matthias B.
    Sieri, Sabina
    Sundström, Johan
    Tikhonoff, Valérie
    Tjønneland, Anne
    Tong, Tammy
    Tumino, Rosario
    Tzoulaki, Ioanna
    van der Schouw, Yvonne T.
    Monique Verschuren, W. M.
    Völzke, Henry
    Wallace, Robert B.
    Wannamethee, S. Goya
    Weiderpass, Elisabete
    Willeit, Peter
    Woodward, Mark
    Yamagishi, Kazumasa
    Zamora-Ros, Raul
    Akwo, Elvis A.
    Pyarajan, Saiju
    Gagnon, David R.
    Tsao, Philip S.
    Muralidhar, Sumitra
    Edwards, Todd L.
    Damrauer, Scott M.
    Joseph, Jacob
    Pennells, Lisa
    Wilson, Peter W. F.
    Harrison, Seamus
    Gaziano, Thomas A.
    Inouye, Michael
    Baigent, Colin
    Casas, Juan P.
    Langenberg, Claudia
    Wareham, Nick
    Riboli, Elio
    Gaziano, J. Michael
    Danesh, John
    Hung, Adriana M.
    Butterworth, Adam S.
    Wood, Angela M.
    Di Angelantonio, Emanuele
    Mild-to-moderate kidney dysfunction and cardiovascular disease: Observational and mendelian randomization analyses2022Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 146, nr 20, s. 1507-1517Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: End-stage renal disease is associated with a high risk of cardiovascular events. It is unknown, however, whether mild-to-moderate kidney dysfunction is causally related to coronary heart disease (CHD) and stroke.

    METHODS: Observational analyses were conducted using individual-level data from 4 population data sources (Emerging Risk Factors Collaboration, EPIC-CVD [European Prospective Investigation into Cancer and Nutrition-Cardiovascular Disease Study], Million Veteran Program, and UK Biobank), comprising 648 135 participants with no history of cardiovascular disease or diabetes at baseline, yielding 42 858 and 15 693 incident CHD and stroke events, respectively, during 6.8 million person-years of follow-up. Using a genetic risk score of 218 variants for estimated glomerular filtration rate (eGFR), we conducted Mendelian randomization analyses involving 413 718 participants (25 917 CHD and 8622 strokes) in EPIC-CVD, Million Veteran Program, and UK Biobank.

    RESULTS: There were U-shaped observational associations of creatinine-based eGFR with CHD and stroke, with higher risk in participants with eGFR values <60 or >105 mL·min-1·1.73 m-2, compared with those with eGFR between 60 and 105 mL·min-1·1.73 m-2. Mendelian randomization analyses for CHD showed an association among participants with eGFR <60 mL·min-1·1.73 m-2, with a 14% (95% CI, 3%-27%) higher CHD risk per 5 mL·min-1·1.73 m-2 lower genetically predicted eGFR, but not for those with eGFR >105 mL·min-1·1.73 m-2. Results were not materially different after adjustment for factors associated with the eGFR genetic risk score, such as lipoprotein(a), triglycerides, hemoglobin A1c, and blood pressure. Mendelian randomization results for stroke were nonsignificant but broadly similar to those for CHD.

    CONCLUSIONS: In people without manifest cardiovascular disease or diabetes, mild-to-moderate kidney dysfunction is causally related to risk of CHD, highlighting the potential value of preventive approaches that preserve and modulate kidney function.

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  • 8. Greve, Anders M.
    et al.
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Gohlke-Baerwolf, Christa
    Kesaniemi, Y. Antero
    Nienaber, Christoph
    Ray, Simon
    Egstrup, Kenneth
    Rossebo, Anne B.
    Devereux, Richard B.
    Kober, Lars
    Willenheimer, Ronnie
    Wachtell, Kristian
    Clinical implications of electrocardiographic left ventricular strain and hypertrophy in asymptomatic patients with aortic stenosis the simvastatin and ezetimibe in aortic stenosis study2012Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 125, nr 2, s. 346-353Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background-The prognostic impact of ECG left ventricular strain and left ventricular hypertrophy (LVH) in asymptomatic aortic stenosis is not well described.

    Methods and Results-Data were obtained in asymptomatic patients randomized to simvastatin/ezetimibe combination versus placebo in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Primary end point was the first of myocardial infarction, nonhemorrhagic stroke, heart failure, aortic valve replacement, or cardiovascular death. The predictive value of ECG left ventricular strain (defined as T-wave inversion in leads V(4) through V(6)) and LVH, assessed by Sokolow-Lyon voltage criteria (R(V5-6) +/- S(V1) >= 35 mV) and Cornell voltage-duration criteria {[RaVL + S(V3) + (6 mV in women)] x QRS duration >= 2440 mV.ms}, was evaluated by adjustment for other prognostic covariates. A total of 1533 patients were followed for 4.3 +/- 0.8 years (6592 patient-years of follow-up), and 627 cardiovascular events occurred. ECG strain was present in 340 patients (23.6%), with LVH by Sokolow-Lyon voltage in 260 (17.1%) and by Cornell voltage-duration product in 220 (14.6%). In multivariable analyses, ECG left ventricular strain was associated with 3.1-fold higher risk of in-study myocardial infarction (95% confidence interval, 1.4-6.8; P = 0.004). Similarly, ECG LVH by both criteria predicted, compared with no ECG LVH, 5.8-fold higher risk of heart failure (95% confidence interval, 2.0 -16.8), 2.0-fold higher risk of aortic valve replacement (95% confidence interval, 1.3-3.1; both P = 0.001), and 2.5-fold higher risk of a combined end point of myocardial infarction, heart failure, or cardiovascular death (95% confidence interval, 1.3-4.9; P = 0.008).

    Conclusions-ECG left ventricular strain and LVH were independently predictive of poor prognosis in patients with asymptomatic aortic stenosis.

  • 9. Hvidtfeldt, Ulla A
    et al.
    Tolstrup, Janne S
    Jakobsen, Marianne U
    Heitmann, Berit L
    Grønbaek, Morten
    O'Reilly, Eilis
    Bälter, Katarina
    Goldbourt, Uri
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Knekt, Paul
    Liu, Simin
    Pereira, Mark
    Pietinen, Pirjo
    Spiegelman, Donna
    Stevens, June
    Virtamo, Jarmo
    Willett, Walter C
    Rimm, Eric B
    Ascherio, Alberto
    Alcohol intake and risk of coronary heart disease in younger, middle-aged, and older adults2010Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 121, nr 14, s. 1589-1597Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Light to moderate alcohol consumption is associated with a reduced risk of coronary heart disease. This protective effect of alcohol, however, may be confined to middle-aged or older individuals. Coronary heart disease incidence is low in men <40 years of age and in women <50 years of age; for this reason, study cohorts rarely have the power to investigate the effects of alcohol on coronary heart disease risk in younger adults. This study examined whether the beneficial effect of alcohol on coronary heart disease depends on age. METHODS AND RESULTS: In this pooled analysis of 8 prospective studies from North America and Europe including 192,067 women and 74,919 men free of cardiovascular diseases, diabetes, and cancers at baseline, average daily alcohol intake was assessed at baseline with a food frequency or diet history questionnaire. An inverse association between alcohol and risk of coronary heart disease was observed in all age groups; hazard ratios among moderately drinking men (5.0 to 29.9 g/d) 39 to 50, 50 to 59, and >or=60 years of age were 0.58 (95% confidence interval [CI], 0.36 to 0.93), 0.72 (95% CI, 0.60 to 0.86), and 0.85 (95% CI, 0.75 to 0.97) compared with abstainers. However, the analyses indicated a smaller incidence rate difference between abstainers and moderate consumers in younger adults (incidence rate difference, 45 per 100,000; 90% CI, 8 to 84) than in middle-aged (incidence rate difference, 64 per 100,000; 90% CI, 24 to 102) and older (incidence rate difference, 89 per 100,000; 90% CI, 44 to 140) adults. Similar results were observed in women. CONCLUSIONS: Alcohol is also associated with a decreased risk of coronary heart disease in younger adults; however, the absolute risk was small compared with middle-aged and older adults.

  • 10. Jander, Nikolaus
    et al.
    Minners, Jan
    Holme, Ingar
    Gerdts, Eva
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Brudi, Philippe
    Chambers, John B.
    Egstrup, Kenneth
    Kesaniemi, Y. Antero
    Malbecq, William
    Nienaber, Christoph A.
    Ray, Simon
    Rossebo, Anne
    Pedersen, Terje R.
    Skjaerpe, Terje
    Willenheimer, Ronnie
    Wachtell, Kristian
    Neumann, Franz-Josef
    Gohlke-Baerwolf, Christa
    Outcome of Patients With Low-Gradient "Severe" Aortic Stenosis and Preserved Ejection Fraction2011Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 123, nr 8, s. 887-895Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background-Retrospective studies have suggested that patients with a low transvalvular gradient in the presence of an aortic valve area <1.0 cm(2) and normal ejection fraction may represent a subgroup with an advanced stage of aortic valve disease, reduced stroke volume, and poor prognosis requiring early surgery. We therefore evaluated the outcome of patients with low-gradient "severe" stenosis (defined as aortic valve area < 1.0 cm(2) and mean gradient <= 40 mm Hg) in the prospective Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study.

    Methods and Results-Outcome in patients with low-gradient "severe" aortic stenosis was compared with outcome in patients with moderate stenosis (aortic valve area 1.0 to 1.5 cm(2); mean gradient 25 to 40 mm Hg). The primary end point of aortic valve events included death from cardiovascular causes, aortic valve replacement, and heart failure due to aortic stenosis. Secondary end points were major cardiovascular events and cardiovascular death. In 1525 asymptomatic patients (mean age, 67 +/- 10 years; ejection fraction, >= 55%), baseline echocardiography revealed low-gradient severe stenosis in 435 patients (29%) and moderate stenosis in 184 (12%). Left ventricular mass was lower in patients with low-gradient severe stenosis than in those with moderate stenosis (182 +/- 64 versus 212 +/- 68 g; P < 0.01). During 46 months of follow-up, aortic valve events occurred in 48.5% versus 44.6%, respectively (P=0.37; major cardiovascular events, 50.9% versus 48.5%, P=0.58; cardiovascular death, 7.8% versus 4.9%, P=0.19). Low-gradient severe stenosis patients with reduced stroke volume index (<= 35 mL/m(2); n=223) had aortic valve events comparable to those in patients with normal stroke volume index (46.2% versus 50.9%; P=0.53).

    Conclusions-Patients with low-gradient "severe" aortic stenosis and normal ejection fraction have an outcome similar to that in patients with moderate stenosis.

  • 11. Jander, Nikolaus
    et al.
    Minners, Jan
    Neumann, Franz-Josef
    Gohlke-Baerwolf, Christa
    Holme, Ingar
    Gerdts, Eva
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Brudi, Philippe
    Chambers, John B.
    Egstrup, Kenneth
    Kesaniemi, Y. Antero
    Malbecq, William
    Nienaber, Christoph A.
    Ray, Simon
    Rossebo, Anne
    Pedersen, Terje R.
    Skjaerpe, Terje
    Willenheimer, Ronnie
    Wachtell, Kristian
    Response to Letters Regarding Article, "Outcome of Patients With Low-Gradient "Severe" Aortic Stenosis and Preserved Ejection Fraction"2011Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 124, nr 13, s. E362-E363Artikel i tidskrift (Refereegranskat)
  • 12. Jernberg, Tomas
    et al.
    Lindahl, Bertil
    Alfredsson, Joakim
    Berglund, Ellinor
    Bergström, Olle
    Engström, Anders
    Erlinge, David
    Herlitz, Johan
    Jumatate, Raluca
    Kellerth, Thomas
    Lauermann, Jörg
    Lindmark, Krister
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Lingman, Markus
    Ljung, Lina
    Nilsson, Carina
    Omerovic, Elmir
    Pernow, John
    Ravn-Fischer, Annica
    Sparv, David
    Yndigegn, Troels
    Östlund, Ollie
    James, Stefan K.
    Hofmann, Robin
    Long-Term Effects of Oxygen Therapy on Death or Hospitalization for Heart Failure in Patients With Suspected Acute Myocardial Infarction2018Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 138, nr 24, s. 2754-2762Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: In the DETO2X-AMI trial (Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction), we compared supplemental oxygen with ambient air in normoxemic patients presenting with suspected myocardial infarction and found no significant survival benefit at 1 year. However, important secondary end points were not yet available. We now report the prespecified secondary end points cardiovascular death and the composite of all-cause death and hospitalization for heart failure.

    Methods: In this pragmatic, registry-based randomized clinical trial, we used a nationwide quality registry for coronary care for trial procedures and evaluated end points through the Swedish population registry (mortality), the Swedish inpatient registry (heart failure), and cause of death registry (cardiovascular death). Patients with suspected acute myocardial infarction and oxygen saturation of ≥90% were randomly assigned to receive either supplemental oxygen at 6 L/min for 6 to 12 hours delivered by open face mask or ambient air.

    Results: A total of 6629 patients were enrolled. Acute heart failure treatment, left ventricular systolic function assessed by echocardiography, and infarct size measured by high-sensitive cardiac troponin T were similar in the 2 groups during the hospitalization period. All-cause death or hospitalization for heart failure within 1 year after randomization occurred in 8.0% of patients assigned to oxygen and in 7.9% of patients assigned to ambient air (hazard ratio, 0.99; 95% CI, 0.84–1.18; P=0.92). During long-term follow-up (median [range], 2.1 [1.0–3.7] years), the composite end point occurred in 11.2% of patients assigned to oxygen and in 10.8% of patients assigned to ambient air (hazard ratio, 1.02; 95% CI, 0.88–1.17; P=0.84), and cardiovascular death occurred in 5.2% of patients assigned to oxygen and in 4.8% assigned to ambient air (hazard ratio, 1.07; 95% CI, 0.87–1.33; P=0.52). The results were consistent across all predefined subgroups.

    Conclusions: Routine use of supplemental oxygen in normoxemic patients with suspected myocardial infarction was not found to reduce the composite of all-cause mortality and hospitalization for heart failure, or cardiovascular death within 1 year or during long-term follow-up.

    Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01787110.

  • 13. Key, Timothy J.
    et al.
    Appleby, Paul N.
    Bradbury, Kathryn E.
    Sweeting, Michael
    Wood, Angela
    Johansson, Ingegerd
    Umeå universitet, Medicinska fakulteten, Institutionen för odontologi.
    Kühn, Tilman
    Steur, Marinka
    Weiderpass, Elisabete
    Wennberg, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Würtz, Anne Mette Lund
    Agudo, Antonio
    Andersson, Jonas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Arriola, Larraitz
    Boeing, Heiner
    Boer, Jolanda M. A.
    Bonnet, Fabrice
    Boutron-Ruault, Marie-Christine
    Cross, Amanda J.
    Ericson, Ulrika
    Fagherazzi, Guy
    Ferrari, Pietro
    Gunter, Marc
    Huerta, José María
    Katzke, Verena
    Khaw, Kay-Tee
    Krogh, Vittorio
    La Vecchia, Carlo
    Matullo, Giuseppe
    Moreno-Iribas, Conchi
    Naska, Androniki
    Nilsson, Lena Maria
    Umeå universitet, Arktiskt centrum vid Umeå universitet (Arcum).
    Olsen, Anja
    Overvad, Kim
    Palli, Domenico
    Panico, Salvatore
    Molina-Portillo, Elena
    Quirós, J. Ramón
    Skeie, Guri
    Sluijs, Ivonne
    Sonestedt, Emily
    Stepien, Magdalena
    Tjønneland, Anne
    Trichopoulou, Antonia
    Tumino, Rosario
    Tzoulaki, Ioanna
    van der Schouw, Yvonne T.
    Verschuren, W. M. Monique
    Di Angelantonio, Emanuele
    Langenberg, Claudia
    Forouhi, Nita
    Wareham, Nick
    Butterworth, Adam
    Riboli, Elio
    Danesh, John
    Consumption of Meat, Fish, Dairy Products, Eggs and Risk of Ischemic Heart Disease: A Prospective Study of 7198 Incident Cases Among 409,885 Participants in the Pan-European EPIC Cohort2019Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 139, nr 25, s. 2835-2845Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: There is uncertainty about the relevance of animal foods to the etiology of ischemic heart disease (IHD). We examined meat, fish, dairy products and eggs and risk for IHD in the pan-European EPIC cohort.

    METHODS: A prospective study of 409,885 men and women in nine European countries. Diet was assessed using validated questionnaires, calibrated using 24-hour recalls. Lipids and blood pressure were measured in a subsample. During 12.6 years mean follow up, 7198 participants had a myocardial infarction or died from IHD. The relationships of animal foods with risk were examined using Cox regression with adjustment for other animal foods and relevant covariates.

    RESULTS: The hazard ratio (HR) for IHD was 1.19 (95% CI 1.06-1.33) for a 100 g/d increment in intake of red and processed meat, and this remained significant after excluding the first 4 years of follow-up (HR 1.25 [1.09-1.42]). Risk was inversely associated with intakes of yogurt (HR 0.93 [0.89-0.98] per 100 g/d increment), cheese (HR 0.92 [0.86-0.98] per 30 g/d increment) and eggs (HR 0.93 [0.88-0.99] per 20 g/d increment); the associations with yogurt and eggs were attenuated and non-significant after excluding the first 4 years of follow-up. Risk was not significantly associated with intakes of poultry, fish or milk. In analyses modelling dietary substitutions, replacement of 100 kcal/d from red and processed meat with 100 kcal/d from fatty fish, yogurt, cheese or eggs was associated with approximately 20% lower risk of IHD. Consumption of red and processed meat was positively associated with serum non-HDL cholesterol concentration and systolic blood pressure, and consumption of cheese was inversely associated with serum non-HDL cholesterol.

    CONCLUSIONS: Risk for IHD was positively associated with consumption of red and processed meat, and inversely associated with consumption of yogurt, cheese and eggs, although the associations with yogurt and eggs may be influenced by reverse causation bias. It is not clear whether the associations with red and processed meat and cheese reflect causality, but they were consistent with the associations of these foods with plasma non-HDL cholesterol, and for red and processed meat with systolic blood pressure, which could mediate such effects.

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  • 14. Lahrouchi, Najim
    et al.
    Tadros, Rafik
    Crotti, Lia
    Mizusawa, Yuka
    Postema, Pieter G.
    Beekman, Leander
    Walsh, Roddy
    Hasegawa, Kanae
    Barc, Julien
    Ernsting, Marko
    Turkowski, Kari L.
    Mazzanti, Andrea
    Beckmann, Britt M.
    Shimamoto, Keiko
    Diamant, Ulla-Britt
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik. European Reference Network for Rare, Low Prevalence, and Complex Diseases of the Heart - ERN GUARD-Heart.
    Wijeyeratne, Yanushi D.
    Kucho, Yu
    Robyns, Tomas
    Ishikawa, Taisuke
    Arbelo, Elena
    Christiansen, Michael
    Winbo, Annika
    Jabbari, Reza
    Lubitz, Steven A.
    Steinfurt, Johannes
    Rudic, Boris
    Loeys, Bart
    Shoemaker, M. Ben
    Weeke, Peter E.
    Pfeiffer, Ryan
    Davies, Brianna
    Andorin, Antoine
    Hofman, Nynke
    Dagradi, Federica
    Pedrazzini, Matteo
    Tester, David J.
    Bos, J. Martijn
    Sarquella-Brugada, Georgia
    Campuzano, Oscar
    Platonov, Pyotr G.
    Stallmeyer, Birgit
    Zumhagen, Sven
    Nannenberg, Eline A.
    Veldink, Jan H.
    van den Berg, Leonard H.
    Al-Chalabi, Ammar
    Shaw, Christopher E.
    Shaw, Pamela J.
    Morrison, Karen E.
    Andersen, Peter M.
    Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Klinisk neurovetenskap. Department of Neurology, Ulm University, Germany (P.M.A.).
    Mueller-Nurasyid, Martina
    Cusi, Daniele
    Barlassina, Cristina
    Galan, Pilar
    Lathrop, Mark
    Munter, Markus
    Werge, Thomas
    Ribases, Marta
    Aung, Tin
    Khor, Chiea C.
    Ozaki, Mineo
    Lichtner, Peter
    Meitinger, Thomas
    van Tintelen, J. Peter
    Hoedemaekers, Yvonne
    Denjoy, Isabelle
    Leenhardt, Antoine
    Napolitano, Carlo
    Shimizu, Wataru
    Schott, Jean-Jacques
    Gourraud, Jean-Baptiste
    Makiyama, Takeru
    Ohno, Seiko
    Itoh, Hideki
    Krahn, Andrew D.
    Antzelevitch, Charles
    Roden, Dan M.
    Saenen, Johan
    Borggrefe, Martin
    Odening, Katja E.
    Ellinor, Patrick T.
    Tfelt-Hansen, Jacob
    Skinner, Jonathan R.
    van den Berg, Maarten P.
    Olesen, Morten Salling
    Brugada, Josep
    Brugada, Ramon
    Makita, Naomasa
    Breckpot, Jeroen
    Yoshinaga, Masao
    Behr, Elijah R.
    Rydberg, Annika
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik. European Reference Network for Rare, Low Prevalence, and Complex Diseases of the Heart - ERN GUARD-Heart.
    Aiba, Takeshi
    Kaeaeb, Stefan
    Priori, Silvia G.
    Guicheney, Pascale
    Tan, Hanno L.
    Newton-Cheh, Christopher
    Ackerman, Michael J.
    Schwartz, Peter J.
    Schulze-Bahr, Eric
    Probst, Vincent
    Horie, Minoru
    Wilde, Arthur A.
    Tanck, Michael W. T.
    Bezzina, Connie R.
    Transethnic Genome-Wide Association Study Provides Insights in the Genetic Architecture and Heritability of Long QT Syndrome2020Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 142, nr 4, s. 324-338Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Long QT syndrome (LQTS) is a rare genetic disorder and a major preventable cause of sudden cardiac death in the young. A causal rare genetic variant with large effect size is identified in up to 80% of probands (genotype positive) and cascade family screening shows incomplete penetrance of genetic variants. Furthermore, a proportion of cases meeting diagnostic criteria for LQTS remain genetically elusive despite genetic testing of established genes (genotype negative). These observations raise the possibility that common genetic variants with small effect size contribute to the clinical picture of LQTS. This study aimed to characterize and quantify the contribution of common genetic variation to LQTS disease susceptibility. Methods: We conducted genome-wide association studies followed by transethnic meta-analysis in 1656 unrelated patients with LQTS of European or Japanese ancestry and 9890 controls to identify susceptibility single nucleotide polymorphisms. We estimated the common variant heritability of LQTS and tested the genetic correlation between LQTS susceptibility and other cardiac traits. Furthermore, we tested the aggregate effect of the 68 single nucleotide polymorphisms previously associated with the QT-interval in the general population using a polygenic risk score. Results: Genome-wide association analysis identified 3 loci associated with LQTS at genome-wide statistical significance (P<5x10(-8)) nearNOS1AP,KCNQ1, andKLF12, and 1 missense variant inKCNE1(p.Asp85Asn) at the suggestive threshold (P<10(-6)). Heritability analyses showed that approximate to 15% of variance in overall LQTS susceptibility was attributable to common genetic variation (h2SNP0.148; standard error 0.019). LQTS susceptibility showed a strong genome-wide genetic correlation with the QT-interval in the general population (r(g)=0.40;P=3.2x10(-3)). The polygenic risk score comprising common variants previously associated with the QT-interval in the general population was greater in LQTS cases compared with controls (P<10-13), and it is notable that, among patients with LQTS, this polygenic risk score was greater in patients who were genotype negative compared with those who were genotype positive (P<0.005). Conclusions: This work establishes an important role for common genetic variation in susceptibility to LQTS. We demonstrate overlap between genetic control of the QT-interval in the general population and genetic factors contributing to LQTS susceptibility. Using polygenic risk score analyses aggregating common genetic variants that modulate the QT-interval in the general population, we provide evidence for a polygenic architecture in genotype negative LQTS.

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  • 15.
    Ljungberg, Johan
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Janiec, Mikael
    Bergdahl, Ingvar
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning.
    Holmgren, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Hultdin, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Johansson, Bengt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Näslund, Ulf
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Siegbahn, Agneta
    Fall, Tove
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Proteomic Biomarkers for Incident Aortic Stenosis Requiring Valvular Replacement2018Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 138, nr 6Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Aortic valve stenosis (AS) is the most common indication for cardiac valve surgery; untreated AS is linked to high mortality. The etiological background of AS is unknown. Previous human studies were typically based on case-control studies. Biomarkers identified in prospective studies could lead to novel mechanistic insights. Methods: Within a large population survey with blood samples obtained at baseline, 334 patients were identified who later underwent surgery for AS (median age [interquartile range], 59.9 [10.4] years at survey and 68.3 [12.7] at surgery; 48% female). For each case, 2 matched referents were allocated. Plasma was analyzed with the multiplex proximity extension assay for screening of 92 cardiovascular candidate proteins. Conditional logistic regression models were used to assess associations between each protein and AS, with correction for multiple testing. A separate set of 106 additional cases with 212 matched referents was used in a validation study. Results: Six proteins (growth differentiation factor 15, galectin-4, von Willebrand factor, interleukin 17 receptor A, transferrin receptor protein 1, and proprotein convertase subtilisin/kexin type 9) were associated with case status in the discovery cohort; odds ratios ranged from 1.25 to 1.37 per SD increase in the protein signal. Adjusting the multivariable models for classical cardiovascular risk factors at baseline yielded similar results. Subanalyses of case-referent triplets (n=133) who showed no visible coronary artery disease at the time of surgery in the index person supported associations between AS and growth differentiation factor 15 (odds ratio, 1.40; 95% confidence interval, 1.10-1.78) and galectin-4 (odds ratio, 1.27; 95% confidence interval, 1.02-1.59), but these associations were attenuated after excluding individuals who donated blood samples within 5 years before surgery. In triplets (n=201), which included index individuals with concurrent coronary artery disease at the time of surgery, all 6 proteins were robustly associated with case status in all sensitivity analyses. In the validation study, the association of all but 1 (interleukin 17 receptor A) of these proteins were replicated in patients with AS with concurrent coronary artery disease but not in patients with AS without coronary artery disease. Conclusions: We provide evidence that 5 proteins were altered years before AS surgery and that the associations seem to be driven by concurrent atherosclerotic disease.

  • 16. Lucking, Andrew J
    et al.
    Lundbäck, Magnus
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Barath, Stefan L
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mills, Nicholas L
    Sidhu, Manjit K
    Langrish, Jeremy P
    Boon, Nicholas A
    Pourazar, Jamshid
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Badimon, Juan J
    Gerlofs-Nijland, Miriam E
    Cassee, Flemming R
    Boman, Christoffer
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik, Energiteknik och termisk processkemi.
    Donaldson, Kenneth
    Sandstrom, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Newby, David E
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Particle traps prevent adverse vascular and prothrombotic effects of diesel engine exhaust inhalation in men2011Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 123, nr 16, s. 1721-1728Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: In controlled human exposure studies, diesel engine exhaust inhalation impairs vascular function and enhances thrombus formation. The aim of the present study was to establish whether an exhaust particle trap could prevent these adverse cardiovascular effects in men.

    METHODS AND RESULTS: Nineteen healthy volunteers (mean age, 25±3 years) were exposed to filtered air and diesel exhaust in the presence or absence of a particle trap for 1 hour in a randomized, double-blind, 3-way crossover trial. Bilateral forearm blood flow and plasma fibrinolytic factors were assessed with venous occlusion plethysmography and blood sampling during intra-arterial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil. Ex vivo thrombus formation was determined with the use of the Badimon chamber. Compared with filtered air, diesel exhaust inhalation was associated with reduced vasodilatation and increased ex vivo thrombus formation under both low- and high-shear conditions. The particle trap markedly reduced diesel exhaust particulate number (from 150 000 to 300 000/cm(3) to 30 to 300/cm(3); P<0.001) and mass (320±10 to 7.2±2.0 μg/m(3); P<0.001), and was associated with increased vasodilatation, reduced thrombus formation, and an increase in tissue-type plasminogen activator release.

    CONCLUSIONS: Exhaust particle traps are a highly efficient method of reducing particle emissions from diesel engines. With a range of surrogate measures, the use of a particle trap prevents several adverse cardiovascular effects of exhaust inhalation in men. Given these beneficial effects on biomarkers of cardiovascular health, the widespread use of particle traps on diesel-powered vehicles may have substantial public health benefits and reduce the burden of cardiovascular disease.

  • 17. Magnussen, Christina
    et al.
    Niiranen, Teemu J.
    Ojeda, Francisco M.
    Gianfagna, Francesco
    Blankenberg, Stefan
    Njølstad, Inger
    Vartiainen, Erkki
    Sans, Susana
    Pasterkamp, Gerard
    Hughes, Maria
    Costanzo, Simona
    Donati, Maria Benedetta
    Jousilahti, Pekka
    Linneberg, Allan
    Palosaari, Tarja
    de Gaetano, Giovanni
    Bobak, Martin
    den Ruijter, Hester M.
    Mathiesen, Ellisiv
    Jørgensen, Torben
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Kuulasmaa, Kari
    Zeller, Tanja
    Iacoviello, Licia
    Salomaa, Veikko
    Schnabel, Renate B.
    Sex Differences and Similarities in Atrial Fibrillation Epidemiology, Risk Factors, and Mortality in Community Cohorts Results From the BiomarCaRE Consortium (Biomarker for Cardiovascular Risk Assessment in Europe)2017Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 136, nr 17, s. 1588-1597Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Atrial fibrillation (AF) is a common cardiac disease in aging populations with high comorbidity and mortality. Sex differences in AF epidemiology are insufficiently understood.

    Methods: In N=79 793 individuals without AF diagnosis at baseline (median age, 49.6 years; age range, 24.1–97.6 years; 51.7% women) from 4 community-based European studies (FINRISK, DanMONICA, Moli-sani Northern Sweden) of the BiomarCaRE consortium (Biomarker for Cardiovascular Risk Assessment in Europe), we examined AF incidence, its association with mortality, common risk factors, biomarkers, and prevalent cardiovascular disease, and their attributable risk by sex. Median follow-up time was 12.6 (to a maximum of 28.2) years.

    Results: Fewer AF cases were observed in women (N=1796; 4.4%), than in men (N=2465; 6.4%). Cardiovascular risk factor distribution and lipid profile at baseline were less beneficial in men than in women, and cardiovascular disease was more prevalent in men. Cumulative incidence increased markedly after the age of 50 years in men and after 60 years in women. The lifetime risk was similar (>30%) for both sexes. Subjects with incident AF had a 3.5-fold risk of death in comparison with those without AF. Multivariable-adjusted models showed sex differences for the association of body mass index and AF (hazard ratio per standard deviation increase, 1.18; 95% confidence interval [CI], 1.12–1.23 in women versus 1.31; 95% CI 1.25–1.38 in men; interaction P value of 0.001). Total cholesterol was inversely associated with incident AF with a greater risk reduction in women (hazard ratio per SD, 0.86; 95% CI, 0.81–0.90 versus 0.92; 95% CI, 0.88–0.97 in men; interaction P value of 0.023). No sex differences were seen for C-reactive protein and N-terminal pro B-type natriuretic peptide. The population-attributable risk of all risk factors combined was 41.9% in women and 46.0% in men. About 20% of the risk was observed for body mass index.

    Conclusions: Lifetime risk of AF was high, and AF was strongly associated with increased mortality both in women and men. Body mass index explained the largest proportion of AF risk. Observed sex differences in the association of body mass index and total cholesterol with AF need to be evaluated for underlying pathophysiology and relevance to sex-specific prevention strategies.

  • 18. Marklund, Matti
    et al.
    Wu, Jason H Y
    Imamura, Fumiaki
    Del Gobbo, Liana C
    Fretts, Amanda
    de Goede, Janette
    Shi, Peilin
    Tintle, Nathan
    Wennberg, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Aslibekyan, Stella
    Chen, Tzu-An
    de Oliveira Otto, Marcia C
    Hirakawa, Yoichiro
    Eriksen, Helle Højmark
    Kröger, Janine
    Laguzzi, Federica
    Lankinen, Maria
    Murphy, Rachel A
    Prem, Kiesha
    Samieri, Cécilia
    Virtanen, Jyrki
    Wood, Alexis C
    Wong, Kerry
    Yang, Wei-Sin
    Zhou, Xia
    Baylin, Ana
    Boer, Jolanda M A
    Brouwer, Ingeborg A
    Campos, Hannia
    Chaves, Paulo H M
    Chien, Kuo-Liong
    de Faire, Ulf
    Djoussé, Luc
    Eiriksdottir, Gudny
    El-Abbadi, Naglaa
    Forouhi, Nita G
    Gaziano, J Michael
    Geleijnse, Johanna M
    Gigante, Bruna
    Giles, Graham
    Guallar, Eliseo
    Gudnason, Vilmundur
    Harris, Tamara
    Harris, William S
    Helmer, Catherine
    Hellénius, Mai-Lis
    Hodge, Allison
    Hu, Frank B
    Jacques, Paul F
    Jansson, Jan-Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Kalsbeek, Anya
    Khaw, Kay-Tee
    Koh, Woon-Puay
    Laakso, Markku
    Leander, Karin
    Lin, Hung-Ju
    Lind, Lars
    Luben, Robert
    Luo, Juhua
    McKnight, Barbara
    Mursu, Jaakko
    Ninomiya, Toshiharu
    Overvad, Kim
    Psaty, Bruce M
    Rimm, Eric
    Schulze, Matthias B
    Siscovick, David
    Skjelbo Nielsen, Michael
    Smith, Albert V
    Steffen, Brian T
    Steffen, Lyn
    Sun, Qi
    Sundström, Johan
    Tsai, Michael Y
    Tunstall-Pedoe, Hugh
    Uusitupa, Matti I J
    van Dam, Rob M
    Veenstra, Jenna
    Verschuren, W M Monique
    Wareham, Nicholas
    Willett, Walter
    Woodward, Mark
    Yuan, Jian-Min
    Micha, Renata
    Lemaitre, Rozenn N
    Mozaffarian, Dariush
    Risérus, Ulf
    Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality: An Individual-Level Pooled Analysis of 30 Cohort Studies2019Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 139, nr 21, s. 2422-2436Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Global dietary recommendations for and cardiovascular effects of linoleic acid, the major dietary omega-6 fatty acid, and its major metabolite, arachidonic acid, remain controversial. To address this uncertainty and inform international recommendations, we evaluated how in vivo circulating and tissue levels of linoleic acid (LA) and arachidonic acid (AA) relate to incident cardiovascular disease (CVD) across multiple international studies.

    METHODS: We performed harmonized, de novo, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries. Multivariable-adjusted associations of circulating and adipose tissue LA and AA biomarkers with incident total CVD and subtypes (coronary heart disease (CHD), ischemic stroke, cardiovascular mortality) were investigated according to a prespecified analytical plan. Levels of LA and AA, measured as % of total fatty acids, were evaluated linearly according to their interquintile range (i.e., the range between the mid-point of the first and fifth quintiles), and categorically by quintiles. Study-specific results were pooled using inverse-variance weighted meta-analysis. Heterogeneity was explored by age, sex, race, diabetes, statin use, aspirin use, omega-3 levels, and fatty acid desaturase 1 genotype (when available).

    RESULTS: In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659 participants. Higher levels of LA were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI: 0.88-0.99), 0.78 (0.70-0.85), and 0.88 (0.79-0.98), respectively, and nonsignificantly with lower CHD risk (0.94; 0.88-1.00). Relationships were similar for LA evaluated across quintiles. AA levels were not associated with higher risk of cardiovascular outcomes; comparing extreme quintiles, higher levels were associated with lower risk of total CVD (0.92; 0.86-0.99). No consistent heterogeneity by population subgroups was identified in the observed relationships.

    CONCLUSIONS: In pooled global analyses, higher in vivo circulating and tissue levels of LA and possibly AA were associated with lower risk of major cardiovascular events. These results support a favorable role for LA in CVD prevention.

  • 19. Mills, Nicholas L
    et al.
    Robinson, Simon D
    Boon, Nicholas A
    Newby, David E
    Törnqvist, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Gonzalez, Manuel
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Darnley, Kareen
    MacNee, William
    Donaldson, Ken
    Response to letter regarding article "Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis"2006Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 113, nr 24, artikel-id e872Artikel i tidskrift (Övrigt vetenskapligt)
  • 20. Mills, NL
    et al.
    Törnqvist, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Robinson, SD
    Gonzalez, M
    Darnley, K
    MacNee, W
    Boon, NA
    Donaldson, K
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Newby, DE
    Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis.2005Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 112, nr 25, s. 3930-3936Artikel i tidskrift (Refereegranskat)
  • 21. Nielsen, Olav W.
    et al.
    Sajadieh, Ahmad
    Sabbah, Muhammad
    Greve, Anders M.
    Olsen, Michael H.
    Boman, Kurt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Nienaber, Christoph A.
    Kesaniemi, Y. Antero
    Pedersen, Terje R.
    Willenheimer, Ronnie
    Wachtell, Kristian
    Assessing Optimal Blood Pressure in Patients With Asymptomatic Aortic Valve Stenosis The Simvastatin Ezetimibe in Aortic Stenosis Study (SEAS)2016Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 134, nr 6, s. 455-468Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Evidence for treating hypertension in patients with asymptomatic aortic valve stenosis is scarce. We used data from the SEAS trial (Simvastatin Ezetimibe in Aortic Stenosis) to assess what blood pressure (BP) would be optimal. METHODS: A total of 1767 patients with asymptomatic aortic stenosis and no manifest atherosclerotic disease were analyzed. Outcomes were all-cause mortality, cardiovascular death, heart failure, stroke, myocardial infarction, and aortic valve replacement. BP was analyzed in Cox models as the cumulative average of serially measured BP and a time-varying covariate. RESULTS: The incidence of all-cause mortality was highest for average follow-up systolic BP >= 160 mm Hg (4.3 per 100 person-years; 95% confidence interval [CI], 3.1-6.0) and lowest for average systolic BP of 120 to 139 mm Hg (2.0 per 100 person-years; 95% CI, 1.6-2.6). In multivariable analysis, all-cause mortality was associated with average systolic BP < 120 mm Hg (hazard ratio [HR], 3.4; 95% CI, 1.9-6.1), diastolic BP >= 90 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), and pulse pressure < 50 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), with systolic BP of 120 to 139 mm Hg, diastolic BP of 70 to 79 mm Hg, and pulse pressure of 60 to 69 mm Hg taken as reference. Low systolic and diastolic BPs increased risk in patients with moderate aortic stenosis. With a time-varying systolic BP from 130 to 139 mm Hg used as reference, mortality was increased for systolic BP >= 160 mm Hg (HR, 1.7; P=0.033) and BP of 120 to 129 mm Hg (HR, 1.6; P= 0.039). CONCLUSIONS: Optimal BP seems to be systolic BP of 130 to 139 mm Hg and diastolic BP of 70 to 90 mm Hg in these patients with asymptomatic aortic stenosis and no manifest atherosclerotic disease or diabetes mellitus.

  • 22.
    Okin, Peter M
    et al.
    Weill Cornell Med College, New York, NY.
    Kjeldsen, Sverre
    Univ of Oslo, Ullevål Hosp, Oslo, Norway.
    Lindholm, Lars H
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    Dahlöf, Björn
    Sahlgrenska Univ Hosp/Östra, Göteborg, Sweden.
    Devereux, Richard B
    Weill Cornell Med College, New York, NY.
    Competing effects of hypokalemia and hydrochlororothiazide treatment  on regression of Cornell product left ventricular hypertrophy  in hypertensive patients: implications for the development of potassium-sparing diuretics2009Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 120, nr Suppl. 18, s. s1015-s1015Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Background: Hydrochlorothiazide (HCTZ) treatment is associated with blood pressure reduction and regression of left ventricular hypertrophy (LVH). HCTZ is also associated with hypokalemia (hypoK), which increases blood pressure and is associated with a greater likelihood and severity of electrocardiographic (ECG) LVH. However, the competing effects of HCTZ use and concomitant hypoK on LVH regression have not been examined.

    Methods: Baseline and yearly Cornell product (CP) ECG LVH levels were examined in relation to hypoK (serum K 3.90, the lowest quartile) and HCTZ use in 7816 patients in the LIFE study with baseline and year-1 K levels. Patients were randomized to losartan vs atenolol-based treatment and additional HCTZ as needed.

    Results: Patients on HCTZ had lower serum K levels at year 1 (4.05 ± 0.38 vs 4.24 ± 0.38), year 2 (4.04 ± 0.38 vs 4.25 ± 0.38), year 3 (4.04 ± 0.39 vs 4.27 ± 0.39) and year 4 (4.05 ± 0.41 vs 4.26 ± 0.38) of the study (all p < 0.001). In 2-way analysis of covariance adjusting for age, sex, race, prior and randomized treatment, yearly body mass index, serum glucose and creatinine, and for baseline and change in diastolic and systolic pressure, hypoK was associated with less mean reduction of CP LVH whereas HCTZ use was associated with greater regression of CP LVH between baseline and years 1 to 4. Multivariate logistic regression analyses with the same covariates revealed that hypoK was associated with a statistically significant 15 to 19% lower likelihood of median (236 mm·ms) reduction in CP LVH while HCTZ use was associated with an 18 to 33% greater likelihood of CP LVH regression of 236 mm·ms between baseline and years 1 to 4.

    Conclusions: HCTZ therapy is independently associated with a greater likelihood and magnitude of LVH regression whereas concomitant hypoK is associated with a competing lower likelihood and magnitude of LVH regression during antihypertensive therapy. These findings suggest that hypoK may blunt regression of LVH during treatment.

  • 23.
    Oldgren, Jonas
    et al.
    Uppsala Clinical Research Center (J.O.; Department of Medical Sciences, Uppsala University, S.Å.
    Åsberg, Signild
    Department of Medical Sciences, Uppsala University, S.Å.
    Hijazi, Ziad
    Uppsala Clinical Research Center (J.O.; Department of Medical Sciences, Uppsala University, S.Å.
    Wester, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin. Department of Clinical Science, Karolinska Institutet Danderyds sjukhus, Stockholm, Sweden.
    Bertilsson, Maria
    Uppsala Clinical Research Center (J.O..
    Norrving, Bo
    Department of Clinical Sciences' Section of Neurology' Lund University' Skåne University Hospital, Sweden.
    Early versus delayed non-vitamin k antagonist oral anticoagulant therapy after acute ischemic stroke in atrial fibrillation (timing): a registry-based randomized controlled noninferiority study2022Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 146, nr 14, s. 1056-1066Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: There are no evidence-based recommendations on the optimal time point to initiate non-vitamin K antagonist oral anticoagulants (NOACs) after acute ischemic stroke in patients with atrial fibrillation. We aimed to investigate the efficacy and safety of early versus delayed initiation of NOAC in these patients.

    METHODS: TIMING (Timing of Oral Anticoagulant Therapy in Acute Ischemic Stroke With Atrial Fibrillation) was a registry-based, randomized, noninferiority, open-label, blinded end-point study at 34 stroke units using the Swedish Stroke Register for enrollment and follow-up. Within 72 hours from stroke onset, patients were randomized to early (≤4 days) or delayed (5-10 days) NOAC initiation, with choice of NOAC at the investigators' discretion. The primary outcome was the composite of recurrent ischemic stroke, symptomatic intracerebral hemorrhage, or all-cause mortality at 90 days. The prespecified noninferiority margin was 3%. Secondary outcomes included the individual components of the primary outcome.

    RESULTS: Between April 2, 2017, and December 30, 2020, 888 patients were randomized to either early (n=450) or delayed (n=438) initiation of NOAC. No patient was lost to 90-day follow-up. Mean age was 78.3 years (SD, 9.9 years); 46.2% were women; 49.1% had previously known atrial fibrillation; and 17.5% prior stroke. The primary outcome occurred in 31 patients (6.89%) assigned to early initiation and in 38 patients (8.68%) assigned to delayed NOAC initiation (absolute risk difference, -1.79% [95% CI, -5.31% to 1.74%]; Pnoninferiority=0.004). Ischemic stroke rates were 3.11% and 4.57% (risk difference, -1.46% [95% CI, -3.98% to 1.07%]) and all-cause mortality rates were 4.67% and 5.71% (risk difference, -1.04% [95% CI, -3.96% to 1.88%]) in the early and delayed groups, respectively. No patient in either group experienced symptomatic intracerebral hemorrhage.

    CONCLUSIONS: Early initiation was noninferior to delayed start of NOAC after acute ischemic stroke in patients with atrial fibrillation. Numerically lower rates of ischemic stroke and death and the absence of symptomatic intracerebral hemorrhages implied that the early start of NOAC was safe and should be considered for acute secondary stroke prevention in patients eligible for NOAC treatment. 

  • 24.
    Paluch, Amanda E.
    et al.
    Department of Kinesiology, Institute for Applied Life Sciences, University of Massachusetts Amherst (A.E.P., S.B..
    Bajpai, Shivangi
    Department of Kinesiology, Institute for Applied Life Sciences, University of Massachusetts Amherst (A.E.P., S.B..
    Ballin, Marcel
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Bassett, David R.
    Department of Kinesiology, Recreation, Sport Studies, University of Tennessee, University of Alabama at Birmingham.
    Buford, Thomas W.
    Departments of Medicine, University of Alabama at Birmingham; Birmingham/Atlanta Geriatric Research, Education, Clinical Center, Birmingham VA Medical Center, AL (T.W.B.).
    Carnethon, Mercedes R.
    Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Mexico.
    Chernofsky, Ariel
    Department of Biostatistics, Boston University.
    Dooley, Erin E.
    Epidemiology (E.E.D.' K.P.G.), University of Alabama at Birmingham.
    Ekelund, Ulf
    Department of Sport Medicine, Norwegian School of Sport Sciences, Norway; Department of Chronic Diseases and Ageing, Norwegian Institute of Public Health, Norway.
    Evenson, Kelly R.
    Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina Chapel Hill (K.R.E.).
    Galuska, Deborah A.
    Division of Nutrition, Physical Activity, Obesity, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, United States.
    Jefferis, Barbara J.
    Department of Primary Care and Population Health, University College London Medical School, United Kingdom (B.J.J.), London, United Kingdom.
    Kong, Lingsong
    Department of Kinesiology, Institute for Applied Life Sciences, University of Massachusetts Amherst (A.E.P., S.B..
    Kraus, William E.
    Duke Molecular Physiology Institute, Durham, United Kingdom; Department of Medicine, Duke University, Durham, United Kingdom.
    Larson, Martin G.
    Department of Biostatistics, Boston University.
    Lee, I-Min
    Brigham and Women's Hospital, Harvard Medical School and Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, United States.
    Matthews, Charles E.
    Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, United States.
    Newton, Robert L.
    Pennington Biomedical Research Center, Baton Rouge, United States.
    Nordström, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för hållbar hälsa. Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik. School of Sport Sciences, UiT The Arctic University of Norway, Norway.
    Nordström, Peter
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering, Geriatrik.
    Palta, Priya
    Department of Medicine, Columbia University.
    Patel, Alpa V.
    American Cancer Society, Population Science Department, Atlanta, United States.
    Pettee Gabriel, Kelley
    Epidemiology (E.E.D.' K.P.G.), University of Alabama at Birmingham.
    Pieper, Carl F.
    Department of Medicine, Duke University, Durham, United Kingdom.
    Pompeii, Lisa
    Department of Pediatrics, Center for Epidemiology and Population Health, Baylor College of Medicine, Houston, United States.
    Rees-Punia, Erika
    American Cancer Society, Population Science Department, Atlanta, United States.
    Spartano, Nicole L.
    Departments of Endocrinology, Diabetes, Nutrition and Weight Management (N.L.S.), Boston University School of Medicine, MA, United States.
    Vasan, Ramachandran S.
    Medicine and Epidemiology (R.S.V.), Boston University School of Medicine, MA, United States; Department of Medicine and Epidemiology, Boston University School of Public Health.
    Whincup, Peter H.
    Population Health Research Institute, St George's' University of London, United Kingdom (P.H.W.), United Kingdom.
    Yang, Shengping
    Pennington Biomedical Research Center, Baton Rouge, United States.
    Fulton, Janet E.
    Division of Nutrition, Physical Activity, Obesity, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, United States.
    Prospective association of daily steps with cardiovascular disease: a harmonized meta-analysis2023Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 147, nr 2, s. 122-131Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Taking fewer than the widely promoted "10 000 steps per day" has recently been associated with lower risk of all-cause mortality. The relationship of steps and cardiovascular disease (CVD) risk remains poorly described. A meta-analysis examining the dose-response relationship between steps per day and CVD can help inform clinical and public health guidelines.

    METHODS: Eight prospective studies (20 152 adults [ie, ≥18 years of age]) were included with device-measured steps and participants followed for CVD events. Studies quantified steps per day and CVD events were defined as fatal and nonfatal coronary heart disease, stroke, and heart failure. Cox proportional hazards regression analyses were completed using study-specific quartiles and hazard ratios (HR) and 95% CI were meta-analyzed with inverse-variance-weighted random effects models.

    RESULTS: The mean age of participants was 63.2±12.4 years and 52% were women. The mean follow-up was 6.2 years (123 209 person-years), with a total of 1523 CVD events (12.4 per 1000 participant-years) reported. There was a significant difference in the association of steps per day and CVD between older (ie, ≥60 years of age) and younger adults (ie, <60 years of age). For older adults, the HR for quartile 2 was 0.80 (95% CI, 0.69 to 0.93), 0.62 for quartile 3 (95% CI, 0.52 to 0.74), and 0.51 for quartile 4 (95% CI, 0.41 to 0.63) compared with the lowest quartile. For younger adults, the HR for quartile 2 was 0.79 (95% CI, 0.46 to 1.35), 0.90 for quartile 3 (95% CI, 0.64 to 1.25), and 0.95 for quartile 4 (95% CI, 0.61 to 1.48) compared with the lowest quartile. Restricted cubic splines demonstrated a nonlinear association whereby more steps were associated with decreased risk of CVD among older adults.

    CONCLUSIONS: For older adults, taking more daily steps was associated with a progressively decreased risk of CVD. Monitoring and promoting steps per day is a simple metric for clinician-patient communication and population health to reduce the risk of CVD.

  • 25. Solomon, Scott D.
    et al.
    Adams, David
    Kristen, Arnt
    Grogan, Martha
    Gonzalez-Duarte, Alejandra
    Maurer, Mathew S.
    Merlini, Giampaolo
    Damy, Thibaud
    Slama, Michel S.
    Brannagan, Thomas H., III
    Dispenzieri, Angela
    Berk, John L.
    Shah, Amil M.
    Garg, Pushkal
    Vaishnaw, Akshay
    Karsten, Verena
    Chen, Jihong
    Gollob, Jared
    Vest, John
    Suhr, Ole B.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Effects of Patisiran, an RNA Interference Therapeutic, on Cardiac Parameters in Patients With Hereditary Transthyretin-Mediated Amyloidosis: Analysis of the APOLLO Study2019Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 139, nr 4, s. 431-443Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Hereditary transthyretin-mediated (hATTR) amyloidosis is a rapidly progressive, multisystem disease that presents with cardiomyopathy or polyneuropathy. The APOLLO study assessed the efficacy and tolerability of patisiran in patients with hATTR amyloidosis. The effects of patisiran on cardiac structure and function in a prespecified subpopulation of patients with evidence of cardiac amyloid involvement at baseline were assessed.

    Methods: APOLLO was an international, randomized, double-blind, placebo-controlled phase 3 trial in patients with hATTR amyloidosis. Patients were randomized 2:1 to receive 0.3 mg/kg patisiran or placebo via intravenous infusion once every 3 weeks for 18 months. The prespecified cardiac subpopulation comprised patients with a baseline left ventricular wall thickness 13 mm and no history of hypertension or aortic valve disease. Prespecified exploratory cardiac end points included mean left ventricular wall thickness, global longitudinal strain, and N-terminal prohormone of brain natriuretic peptide. Cardiac parameters in the overall APOLLO patient population were also evaluated. A composite end point of cardiac hospitalizations and all-cause mortality was assessed in a post hoc analysis.

    Results: In the cardiac subpopulation (n=126; 56% of total population), patisiran reduced mean left ventricular wall thickness (least-squares mean difference SEM: -0.90.4 mm, P=0.017), interventricular septal wall thickness, posterior wall thickness, and relative wall thickness at month 18 compared with placebo. Patisiran also led to increased end-diastolic volume (8.3 +/- 3.9 mL, P=0.036), decreased global longitudinal strain (-1.4 +/- 0.6%, P=0.015), and increased cardiac output (0.38 +/- 0.19 L/min, P=0.044) compared with placebo at month 18. Patisiran lowered N-terminal prohormone of brain natriuretic peptide at 9 and 18 months (at 18 months, ratio of fold-change patisiran/placebo 0.45, P<0.001). A consistent effect on N-terminal prohormone of brain natriuretic peptide at 18 months was observed in the overall APOLLO patient population (n=225). Median follow-up duration was 18.7 months. The exposure-adjusted rates of cardiac hospitalizations and all-cause death were 18.7 and 10.1 per 100 patient-years in the placebo and patisiran groups, respectively (Andersen-Gill hazard ratio, 0.54; 95% CI, 0.28-1.01).

    Conclusions: Patisiran decreased mean left ventricular wall thickness, global longitudinal strain, N-terminal prohormone of brain natriuretic peptide, and adverse cardiac outcomes compared with placebo at month 18, suggesting that patisiran may halt or reverse the progression of the cardiac manifestations of hATTR amyloidosis.

  • 26.
    Thøgersen, AM
    et al.
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin.
    Jansson, JH
    Boman, K.
    Nilsson, TK
    Weinehall, L.
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin, Epidemiologi och folkhälsovetenskap.
    Huhtasaari, F.
    Hallmans, G.
    High plasminogen activator inhibitor and tissue plasminogen activator levels in plasma precede a first acute myocardial infarction in both men and women.: Evidence for the fibrinolytic system as an independent primary risk factor1998Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 98, nr 21, s. 2241-2247Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: In patients with established ischemic heart disease, prospective cohort studies have indicated that plasminogen activator inhibitor (PAI-1), the inhibitor of the fibrinolytic system, may predict cardiovascular events. So far, there have been no primary prospective studies of PAI-1. METHODS AND RESULTS: The aim of the present study was to test whether plasma levels of PAI-1, tissue-type plasminogen activator (tPA), von Willebrand factor (vWF), and thrombomodulin (TM) could predict the occurrence of a first acute myocardial infarction (AMI) in a population with high prevalence of coronary heart disease by use of a prospective nested case-control design. Mass concentrations of PAI-1 and tPA were significantly higher for the 78 subjects who developed a first AMI compared with the 156 references matched for age, sex, and sampling time; for tPA, this increase was independent of smoking habits, body mass index, hypertension, diabetes, cholesterol, and apolipoprotein A-I. The ratio of quartile 4 to 1 for tPA was 5.9 for a patient to develop a first AMI. The association between tPA and AMI was seen in both men and women. Increased levels of vWF were associated with AMI in a univariate analysis. High levels of TM were associated with AMI in women but not in men. CONCLUSIONS: The plasma levels of PAI-1, tPA, and vWF are associated with subsequent development of a first AMI; for PAI-1 and tPA, this relation was found in both men and women. For tPA but not for PAI-1 and vWF, this association is independent of established risk factors.

  • 27.
    Valham, Fredrik
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mooe, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Rabben, Terje
    Umeå universitet, Medicinska fakulteten, Institutionen för farmakologi och klinisk neurovetenskap, Klinisk neurofysiologi.
    Stenlund, Hans
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och folkhälsovetenskap.
    Wiklund, Urban
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Centrum för medicinsk teknik och fysik (CMTF).
    Franklin, Karl A
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Increased risk of stroke in patients with coronary artery disease and sleep apnea: a 10-year follow-up2008Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 118, nr 9, s. 955-960Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The effect of sleep apnea on mortality and cardiovascular morbidity is mainly unknown. We aimed to study whether sleep apnea is related to stroke, death, or myocardial infarction in patients with symptomatic coronary artery disease.

    Methods and Results A total of 392 men and women with coronary artery disease referred for coronary angiography were examined by use of overnight sleep apnea recordings. Sleep apnea, defined as an apnea-hypopnea index ≥5, was recorded in 54% of the patients. All patients were followed up prospectively for 10 years, and no one was lost to follow-up. Stroke occurred in 47 (12%) of 392 patients during follow-up. Sleep apnea was associated with an increased risk of stroke, with an adjusted hazard ratio of 2.89 (95% confidence interval 1.37 to 6.09, P=0.005), independent of age, body mass index, left ventricular function, diabetes mellitus, gender, intervention, hypertension, atrial fibrillation, a previous stroke or transient ischemic attack, and smoking. Patients with an apnea-hypopnea index of 5 to 15 and patients with an apnea-hypopnea index ≥15 had a 2.44 (95% confidence interval 1.08 to 5.52) and 3.56 (95% confidence interval 1.56 to 8.16) times increased risk of stroke, respectively, than patients without sleep apnea, independent of confounders (P for trend=0.011). Death and myocardial infarction were not related to sleep apnea. Intervention in the form of coronary artery bypass grafting or percutaneous coronary intervention was related to a longer survival but did not affect the incidence of stroke.

    Conclusions Sleep apnea is significantly associated with the risk of stroke among patients with coronary artery disease who are being evaluated for coronary intervention.

  • 28.
    Vejlstrup, Niels
    et al.
    Copenhagen, Denmark .
    Sörensen, Keld
    Aarhus, Denmark .
    Mattsson, Eva
    Stockholm, Sweden .
    Thilen, Ulf
    Lund University, Sweden.
    Kvidal, Per
    Uppsala, Sweden.
    Johansson, Bengt
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Iversen, Kasper
    Herlev County Hospital, Denmark .
    Söndergaard, Lars
    Copenhagen, Denmark .
    Dellborg, Mikael
    Göteborg, Sweden .
    Eriksson, Peter
    Göteborg, Sweden .
    Long-Term Outcome of Mustard/Senning Correction for Transposition of the Great Arteries in Sweden and Denmark2015Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 132, nr 8, s. 633-638Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background The atrial switch operation, the Mustard or Senning operation, for the transposition of the great arteries (TGA) was introduced in the late 1950s and was the preferred surgery for TGA until the early 1990s. The Mustard and Senning operation involves extensive surgery in the atria and leaves the right ventricle as the systemic ventricle. The Mustard and Senning cohort is now well into adulthood and we begin to see the long-term outcome. Methods and Results All the 6 surgical centers that performed Mustard and Senning operations in Sweden and Denmark identified all operated TGA patients. Information about death was obtained in late 2007 and early 2008 from the Danish and Swedish Centralised Civil Register by using the patients' unique national Civil Registration Numbers. Four hundred sixty-eight patients undergoing the atrial switch operation were identified. Perioperative 30-day mortality was 20%, and 60% were alive after 30 years of follow-up. Perioperative mortality was significantly increased by the presence of a ventricular septal defect, left ventricular outflow obstruction, surgery early in the Mustard and Senning era. However, only pacemaker implantation is predictive of long-term outcome (hazard ratio, 1.90; 95% confidence interval, 1.05-3.46, P=0.04), once the TGA patient has survived the perioperative period. The risk of reoperation was correlated to the presence of associated defects and where the first Mustard/Senning operation was performed. Conclusions The long-term survival of patients with Mustard and Senning correction for TGA appears to be primarily determined by factors in the right ventricle and tricuspid valve and not the timing of or the type of surgery in childhood. Cardiac function necessitating the implantation of a pacemaker is associated with an increase in mortality.

  • 29. Wachtell, Kristian
    et al.
    Okin, Peter M
    Olsen, Michael H
    Dahlöf, Björn
    Devereux, Richard B
    Ibsen, Hans
    Kjeldsen, Sverre E
    Lindholm, Lars H
    Department Preventive Medicine, Umeå University Hospital, Umeå, Sweden.
    Nieminen, Markku S
    Thygesen, Kristian
    Regression of electrocardiographic left ventricular hypertrophy during antihypertensive therapy and reduction in sudden cardiac death: the LIFE Study2007Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 116, nr 7, s. 700-705Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Sudden cardiac death (SCD) occurs more often in patients with ECG left ventricular (LV) hypertrophy. However, whether LV hypertrophy regression is associated with a reduced risk of SCD remains unclear.

    Methods and Results: The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study included 9193 patients 55 to 80 years of age with essential hypertension and ECG LV hypertrophy by gender-adjusted Cornell product (CP) (RaVL+SV3 [+6 mm in women]) · QRS duration>2440 mm · ms) and/or Sokolow-Lyon voltage (SLV) (SV1+RV5/6>38 mm). During follow-up (mean, 4.8 years), 190 patients (2%) experienced SCD. In time-dependent Cox analyses, absence of in-treatment LV hypertrophy was associated with a decreased risk of SCD: every 1-SD-lower in-treatment CP (1050 mm · ms) was associated with a 28% lower risk of SCD (hazard ratio [HR], 0.72; 95% CI, 0.66 to 0.79) and 1-SD-lower SLV (10.5 mm) with a 26% lower risk (HR, 0.74; 95% CI, 0.65 to 0.84). After adjustment for time-varying systolic and diastolic blood pressures, treatment allocation, age, gender, baseline Framingham risk score, ECG strain, heart rate, urine albumin/creatinine ratio, smoking, diabetes, congestive heart failure, coronary heart disease, atrial fibrillation, and occurrence of myocardial infarction, atrial fibrillation, heart failure, and noncardiovascular death, both in-treatment CP and SLV remained predictive of SCD: each 1-SD-lower CP was associated with a 19% lower risk of SCD (HR, 0.81; 95% CI, 0.73 to 0.90) and 1-SD-lower SLV with an 18% lower risk (HR, 0.82; 95% CI, 0.70 to 0.98). Absence of in-treatment LV hypertrophy by both SLV and CP was associated with a 30% lower risk of SCD (HR, 0.70; 95% CI, 0.54 to 0.92).

    Conclusions: Absence of in-treatment ECG LV hypertrophy is associated with reduced risk of SCD independently of treatment modality, blood pressure reduction, prevalent coronary heart disease, and other cardiovascular risk factors in hypertensive patients with LV hypertrophy.

  • 30. Wallert, John
    et al.
    Madison, Guy
    Umeå universitet, Samhällsvetenskapliga fakulteten, Institutionen för psykologi.
    Held, Claes
    Olsson, Erik
    Cognitive ability, lifestyle risk factors, and two-year mortality in first myocardial infarction men: a Swedish national registry study2016Ingår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, artikel-id A20831Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Introduction: General cognitive ability (CA) estimated early in life is positively associated with later physical and mental health, health literacy, and longevity.

    Methods: We investigated young adulthood CA as a long-term risk indicator for the lifestyle factors smoking, diabetes, hypertension, obesity, and two-year mortality in the largest sample to date of 60 years or younger Swedish first MI males. CA was estimated from mandatory conscript register data (INSARK) gathered when patients were 18-20 years old. The national quality register SWEDEHEART/RIKS-HIA provided data on cardiac functioning and lifestyle risk factors ~ 30 years later at first MI hospital admission. An additional two years later, the Cause of Death Register provided death dates for those deceased. The 5,680 complete cases including deceased (n = 110) and still alive (n = 5,570) were descriptively compared on CA, lifestyle risk factors and mortality. Logistic regression was used to model crude and adjusted associations.

    Results: Early first MI non-survivors had 0.28 SD lower young adulthood CA (M = 4.38, SD = 1.49) compared to survivors (M = 4.81, SD = 1.51). The whole first MI group CA was also 0.13 SD lower (M = 4.80, SD = 1.51) than the expected population norm (M = 5.00, SD = 1.56). Adjusting for covariates, one SD increase in CA was associated with decreased probability of being a current smoking (OR = 0.62 [0.59, 0.67], P < 0.001), previous smoker (0.79 [0.73, 0.84], P < 0.001), having diabetes (0.81 [0.74, 0.89], P < 0.001), obesity (0.89 [0.84, 0.95], P < 0.001) at hospital admission, and increased odds of being alive two years thereafter (1.27 [1.04, 1.53], P < 0.001). CA was not associated with hypertension at hospital admission (1.04 [0.97, 1.11], P = 0.228).

    Conclusion: This study confirms substantial inverse associations between CA, and lifestyle related cardiovascular risk factors, and mortality in the earliest first MI male patients. Our findings also expand the CA - morbidity association to comorbid diabetes and obesity. Since CA is highly stable from 18-65 years, can be cost-effectively estimated, and is presently not evaluated in clinical care, CA assessment might provide a better risk stratification and possibly aid further tailoring of secondary prevention.

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