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  • 1551. White, Harvey D.
    et al.
    Held, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Stewart, Ralph
    Tarka, Elizabeth
    Brown, Rebekkah
    Davies, Richard Y.
    Budaj, Andrzej
    Harrington, Robert A.
    Steg, P. Gabriel
    Ardis-Sino, Diego
    Armstrong, Paul W.
    Avezum, Alvaro
    Aylward, Philip E.
    Bryce, Alfonso
    Chen, Hong
    Chen, Ming-Fong
    Corbalan, Ramon
    Dalby, Anthony J.
    Danchin, Nicolas
    De Winter, Robbert J.
    Denchev, Stefan
    Diaz, Rafael
    Elisaf, Moses
    Flather, Marcus D.
    Goudev, Assen R.
    Granger, Christopher B.
    Grinfeld, Liliana
    Hochman, Judith S.
    Husted, Steen
    Kim, Hyo-Soo
    Koenig, Wolfgang
    Linhart, Ales
    Lonn, Eva
    Lopez-Sendon, Jose
    Manolis, Athanasios J.
    Mohler, Emile R., III
    Nicolau, Jose C.
    Pais, Prem
    Parkhomenko, Alexander
    Pedersen, Terje R.
    Pella, Daniel
    Ramos-Corrales, Marco A.
    Ruda, Mikhail
    Sereg, Mtys
    Siddique, Saulat
    Sinnaeve, Peter
    Smith, Peter
    Sritara, Piyamitr
    Swart, Henk P.
    Sy, Rody G.
    Teramoto, Tamio
    Tse, Hung-Fat
    Watson, David
    Weaver, W. Douglas
    Weiss, Robert
    Viigimaa, Margus
    Vinereanu, Dragos
    Zhu, Junren
    Cannon, Christopher P.
    Wallentin, Lars
    Survival with Cardiac-Resynchronization Therapy in Mild Heart Failure2014In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 370, no 18, p. 1702-1711Article in journal (Refereed)
    Abstract [en]

    Background: Elevated lipoprotein-associated phospholipase A(2) activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A(2). Methods: In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization). Results: During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02). ConclusionsIn patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.)

  • 1552. White, Harvey D
    et al.
    Held, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Stewart, Ralph
    Tarka, Elizabeth
    Brown, Rebekkah
    Davies, Richard Y
    Budaj, Andrzej
    Harrington, Robert A
    Steg, P Gabriel
    Ardissino, Diego
    Armstrong, Paul W
    Avezum, Alvaro
    Aylward, Philip E
    Bryce, Alfonso
    Chen, Hong
    Chen, Ming-Fong
    Corbalan, Ramon
    Dalby, Anthony J
    Danchin, Nicolas
    De Winter, Robbert J
    Denchev, Stefan
    Diaz, Rafael
    Elisaf, Moses
    Flather, Marcus D
    Goudev, Assen R
    Granger, Christopher B
    Grinfeld, Liliana
    Hochman, Judith S
    Husted, Steen
    Kim, Hyo-Soo
    Koenig, Wolfgang
    Linhart, Ales
    Lonn, Eva
    López-Sendón, José
    Manolis, Athanasios J
    Mohler, Emile R
    Nicolau, José C
    Pais, Prem
    Parkhomenko, Alexander
    Pedersen, Terje R
    Pella, Daniel
    Ramos-Corrales, Marco A
    Ruda, Mikhail
    Sereg, Mátyás
    Siddique, Saulat
    Sinnaeve, Peter
    Smith, Peter
    Sritara, Piyamitr
    Swart, Henk P
    Sy, Rody G
    Teramoto, Tamio
    Tse, Hung-Fat
    Watson, David
    Weaver, W Douglas
    Weiss, Robert
    Viigimaa, Margus
    Vinereanu, Dragos
    Zhu, Junren
    Cannon, Christopher P
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Darapladib for preventing ischemic events in stable coronary heart disease2014In: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 370, no 18, p. 1702-1711Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Elevated lipoprotein-associated phospholipase A2 activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2.

    METHODS:

    In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization).

    RESULTS:

    During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02).

    CONCLUSIONS:

    In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.).

  • 1553. White, Harvey D.
    et al.
    Huang, Zhen
    Tricoci, Pierluigi
    Van de Werf, Frans
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Lokhnygina, Yuliya
    Moliterno, David J.
    Aylward, Philip E.
    Mahaffey, Kenneth W.
    Armstrong, Paul W.
    Reduction in Overall Occurrences of Ischemic Events With Vorapaxar: Results From TRACER2014In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 3, no 4, p. e001032-Article in journal (Refereed)
    Abstract [en]

    Background-Clinical trials traditionally use time-to-first-event analysis embedded within the composite endpoint of cardiovascular death (CVD), myocardial infarction (MI), or stroke. However, many patients have >1 event, and this approach may not reflect overall experience. We addressed this by analyzing all cardiovascular events in TRACER. Methods and Results-TRACER randomized 12 944 patients with non-ST-segment elevation acute coronary syndromes to placebo or to protease-activated receptor 1 antagonist vorapaxar with a median follow-up of 502 days (interquartile range, 349 to 667). Analysis of vorapaxar's effect on recurrent CVD, MI, or stroke was prespecified using the Wei, Lin, and Weissfeld approach. Vorapaxar did not reduce the first occurrence of the primary endpoint of CVD, MI, stroke, revascularization, or rehospitalization for recurrent ischemia, but reduced the secondary composite endpoint of CVD, MI, or stroke (14.7% vorapaxar vs. 16.4% placebo; hazard ratio [HR], 0.89; 95% confidence interval [CI], 0.81 to 0.98; P=0.02; number needed to treat [NNT], 81). Recurrent secondary events occurred in 2.7% of patients. Vorapaxar reduced overall occurrences of ischemic events, first and subsequent (HR, 0.88; 95% CI, 0.80 to 0.98; P=0.02; NNT, 51). Also, there was a trend indicating that vorapaxar reduced the expanded endpoint, including revascularization and rehospitalization for recurrent ischemia (HR, 0.92; 95% CI, 0.84 to 1.01; P=0.09). Vorapaxar increased overall occurrences of moderate and severe Global Use of Strategies to Open Occluded Coronary Arteries bleeding (HR, 1.42; 95% CI, 1.21 to 1.66; P<0.001) and Thrombolysis in Myocardial Infarction clinically significant bleeding (HR, 1.550; 95% CI, 1.403 to 1.713; P<0.001). Conclusions-Vorapaxar reduced overall occurrences of ischemic events, but increased bleeding. These exploratory findings broaden our understanding of vorapaxar's potential and expand our understanding of the value of capturing recurrent events.

  • 1554. White, Harvey
    et al.
    Held, Claes
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Stewart, Ralph
    Watson, David
    Harrington, Robert
    Budaj, Andrzej
    Steg, Ph. Gabriel
    Cannon, Christopher P.
    Krug-Gourley, Susan
    Wittes, Janet
    Trivedi, Trupti
    Tarka, Elizabeth
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Study design and rationale for the clinical outcomes of the STABILITY Trial (STabilization of Atherosclerotic plaque By Initiation of darapLadIb TherapY) comparing darapladib versus placebo in patients with coronary heart disease2010In: American Heart Journal, ISSN 0002-8703, E-ISSN 1097-6744, Vol. 160, no 4, p. 655-661.e2Article in journal (Refereed)
    Abstract [en]

    Background Elevated plasma levels of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) are associated with increased risk of cardiovascular (CV) events. Direct inhibition of this proinflammatory enzyme with darapladib may benefit CV patients when given as an adjunct to standard of care, including lipid-lowering and antiplatelet therapies. Methods STABILITY is a randomized, placebo-controlled, double-blind, international, multicenter, event-driven trial. The study has randomized 15,828 patients with chronic coronary heart disease (CHD) receiving standard of care to darapladib enteric-coated (EC) tablets, 160 mg or placebo. Results The primary end point is the composite of major adverse cardiovascular events (MACE): CV death, nonfatal myocardial infarction, and nonfatal stroke. The key secondary end points will include major coronary events, total coronary events, individual components of MACE, and all-cause mortality. Prespecified substudies include 24-hour ambulatory blood pressure monitoring, albuminuria progression, changes in cognitive function, and pharmacokinetic and biomarker analyses. Health economic outcomes and characterization of baseline lifestyle risk factors also will be assessed. The study will continue until 1,500 primary end points have occurred to achieve 90% power to detect a 15.5% reduction in the primary end point. The median treatment duration is anticipated to be 2.75 years. Conclusions STABILITY will assess whether direct inhibition of Lp-PLA(2) with darapladib added to the standard of care confers clinical benefit to patients with CHD.

  • 1555.
    Wiberg, Bernice
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Kilander, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Cognitive Function Prior to Stroke is a Risk Factor for Post-Stroke Mortality but Not DependencyArticle in journal (Other academic)
  • 1556. Wieloch, Mattias
    et al.
    Jonsson, Karl M.
    Sjalander, Anders
    Lip, Gregory Y. H.
    Eriksson, Niclas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Svensson, Peter J.
    Estimated glomerular filtration rate is associated with major bleeding complications but not thromboembolic events, in anticoagulated patients taking warfarin2013In: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 131, no 6, p. 481-486Article in journal (Refereed)
    Abstract [en]

    Background: Decreased glomerular filtration rate is an established risk factor for bleeding but there are limited data on its association with bleeding risk in well-controlled anticoagulated patients taking warfarin. Objectives: The aim was to investigate the relationship between glomerular filtration rate, major bleeding and thromboembolic complications in patients with tight anticoagulation control. Patients/Methods: A cohort study of patients from a Swedish quality register for anticoagulation, including all the registered patients that received anticoagulation during 2008 in the anticoagulation center of Skane University Hospital, Malmo. Key outcome measures were major bleeding and arterial or venous thrombosis during 2008. A total of 3536 patients (2875 treatment years) were included. Results: Total rates of 2.6 (2.0-3.2) bleeding events and 1.8 (1.3-2.3) thrombotic events per 100 treatment years were recorded (75 bleeding and 51 thromboembolic events). Data on estimated glomerular filtration rate were available in 3349 patients. Mean time in therapeutic range (international normalized ratio 2.0-3.0) was 74.5% (n=2894). Major bleeding events were significantly related to age and percentage of time with international normalized ratio >3.0 (P<0.001). Glomerular filtration rate levels <30 ml/min/1.73 m(2) were particularly associated with high risk of bleeding, especially in elderly patients. No correlation between glomerular filtration rate and thromboembolic events was seen. Conclusions: With good anticoagulation control as measured by time in therapeutic range, patients had a relatively low risk for major bleeding if their renal function is normal. Despite good anticoagulation control, severely impaired kidney function is associated with a very high yearly risk of major bleeding events.

  • 1557. Wieloch, Mattias
    et al.
    Själander, Anders
    Frykman, Viveka
    Rosenqvist, Mårten
    Eriksson, Niclas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research Center.
    Svensson, Peter J.
    Anticoagulation control in Sweden: reports of time in therapeutic range, major bleeding, and thrombo-embolic complications from the national quality registry AuriculA2011In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 32, no 18, p. 2282-2289Article in journal (Refereed)
    Abstract [en]

    Aims: In anticoagulation treatment with warfarin, the risk of thrombo-embolic events must be weighed against the risk of bleeding. Time in therapeutic range (TTR) is an important tool to assess the quality of anticoagulation treatment, and has been shown to correlate with less bleeding and thrombo-embolic complications. AuriculA, the Swedish national quality registry for atrial fibrillation and anticoagulation, is used for follow-up and dosage control of warfarin. This is the first report of TTR in AuriculA and, in a subgroup of two centres, bleeding and thrombo-embolic complications during 2008.

    Methods and results: Prothrombin complex (International normalized ratio) values from 18 391 patients in 67 different centres were analysed. The mean (SD) age was 70 (12) years. The main indications for warfarin treatment were: atrial fibrillation (64%), venous thromboembolism (19%), and heart valve dysfunction (13%). Time in therapeutic range for all patients was 76.2%. The mean weekly dose of warfarin decreased with age and TTR increased with age. In 4273 patients from two centres in AuriculA, the frequency of major bleedings and venous/arterial thrombo-embolism were 2.6 and 1.7% and for atrial fibrillation, 2.6 and 1.4%, per treatment year, respectively. A correlation between age and the risk of major bleeding (P < 0.001), but not thrombo-embolic complications (P = 0.147), was seen.

    Conclusion: Compared with prospective randomized trials of warfarin treatment, TTR in the AuriculA population was higher. Complications were low, probably due to the organization of anticoagulation treatment in Sweden. Use of the AuriculA dosing programme could have contributed to the results by keeping dosing regimens consistent over all centres.

  • 1558. Wijns, William
    et al.
    Kolh, Philippe
    Danchin, Nicolas
    Di Mario, Carlo
    Falk, Volkmar
    Folliguet, Thierry
    Garg, Scot
    Huber, Kurt
    James, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , UCR-Uppsala Clinical Research Center.
    Knuuti, Juhani
    Lopez-Sendon, Jose
    Marco, Jean
    Menicanti, Lorenzo
    Ostojic, Miodrag
    Piepoli, Massimo F
    Pirlet, Charles
    Pomar, Jose L
    Reifart, Nicolaus
    Ribichini, Flavio L
    Schalij, Martin J
    Sergeant, Paul
    Serruys, Patrick W
    Silber, Sigmund
    Sousa Uva, Miguel
    Taggart, David
    Vahanian, Alec
    Auricchio, Angelo
    Bax, Jeroen
    Ceconi, Claudio
    Dean, Veronica
    Filippatos, Gerasimos
    Funck-Brentano, Christian
    Hobbs, Richard
    Kearney, Peter
    McDonagh, Theresa
    Popescu, Bogdan A
    Reiner, Zeljko
    Sechtem, Udo
    Sirnes, Per Anton
    Tendera, Michal
    Vardas, Panos E
    Widimsky, Petr
    Kolh, Philippe
    Alfieri, Ottavio
    Dunning, Joel
    Elia, Stefano
    Kappetein, Pieter
    Lockowandt, Ulf
    Sarris, George
    Vouhe, Pascal
    Kearney, Peter
    von Segesser, Ludwig
    Agewall, Stefan
    Aladashvili, Alexander
    Alexopoulos, Dimitrios
    Antunes, Manuel J
    Atalar, Enver
    Brutel de la Riviere, Aart
    Doganov, Alexander
    Eha, Jaan
    Fajadet, Jean
    Ferreira, Rafael
    Garot, Jerome
    Halcox, Julian
    Hasin, Yonathan
    Janssens, Stefan
    Kervinen, Kari
    Laufer, Gunther
    Legrand, Victor
    Nashef, Samer A M
    Neumann, Franz-Josef
    Niemela, Kari
    Nihoyannopoulos, Petros
    Noc, Marko
    Piek, Jan J
    Pirk, Jan
    Rozenman, Yoseph
    Sabate, Manel
    Starc, Radovan
    Thielmann, Matthias
    Wheatley, David J
    Windecker, Stephan
    Zembala, Marian
    Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)2010In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 31, no 20, p. 2501-2555Article in journal (Refereed)
  • 1559. Willer, Cristen J.
    et al.
    Schmidt, Ellen M.
    Sengupta, Sebanti
    Peloso, Gina M.
    Gustafsson, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Kanoni, Stavroula
    Ganna, Andrea
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Chen, Jin
    Buchkovich, Martin L.
    Mora, Samia
    Beckmann, Jacques S.
    Bragg-Gresham, Jennifer L.
    Chang, Hsing-Yi
    Demirkan, Ayse
    Den Hertog, Heleen M.
    Do, Ron
    Donnelly, Louise A.
    Ehret, Georg B.
    Esko, Tonu
    Feitosa, Mary F.
    Ferreira, Teresa
    Fischer, Krista
    Fontanillas, Pierre
    Fraser, Ross M.
    Freitag, Daniel F.
    Gurdasani, Deepti
    Heikkila, Kauko
    Hyppoenen, Elina
    Isaacs, Aaron
    Jackson, Anne U.
    Johansson, Åsa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Johnson, Toby
    Kaakinen, Marika
    Kettunen, Johannes
    Kleber, Marcus E.
    Li, Xiaohui
    Luan, Jian'an
    Lyytikainen, Leo-Pekka
    Magnusson, Patrik K. E.
    Mangino, Massimo
    Mihailov, Evelin
    Montasser, May E.
    Mueller-Nurasyid, Martina
    Nolte, Ilja M.
    O'Connell, Jeffrey R.
    Palmer, Cameron D.
    Perola, Markus
    Petersen, Ann-Kristin
    Sanna, Serena
    Saxena, Richa
    Service, Susan K.
    Shah, Sonia
    Shungin, Dmitry
    Sidore, Carlo
    Song, Ci
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Strawbridge, Rona J.
    Surakka, Ida
    Tanaka, Toshiko
    Teslovich, Tanya M.
    Thorleifsson, Gudmar
    Van den Herik, Evita G.
    Voight, Benjamin F.
    Volcik, Kelly A.
    Waite, Lindsay L.
    Wong, Andrew
    Wu, Ying
    Zhang, Weihua
    Absher, Devin
    Asiki, Gershim
    Barroso, Ines
    Been, Latonya F.
    Bolton, Jennifer L.
    Bonnycastle, Lori L.
    Brambilla, Paolo
    Burnett, Mary S.
    Cesana, Giancarlo
    Dimitriou, Maria
    Doney, Alex S. F.
    Doering, Angela
    Elliott, Paul
    Epstein, Stephen E.
    Eyjolfsson, Gudmundur Ingi
    Gigante, Bruna
    Goodarzi, Mark O.
    Grallert, Harald
    Gravito, Martha L.
    Groves, Christopher J.
    Hallmans, Goran
    Hartikainen, Anna-Liisa
    Hayward, Caroline
    Hernandez, Dena
    Hicks, Andrew A.
    Holm, Hilma
    Hung, Yi-Jen
    Illig, Thomas
    Jones, Michelle R.
    Kaleebu, Pontiano
    Kastelein, John J. P.
    Khaw, Kay-Tee
    Kim, Eric
    Klopp, Norman
    Komulainen, Pirjo
    Kumari, Meena
    Langenberg, Claudia
    Lehtimaki, Terho
    Lin, Shih-Yi
    Lindstrom, Jaana
    Loos, Ruth J. F.
    Mach, Francois
    McArdle, Wendy L.
    Meisinger, Christa
    Mitchell, Braxton D.
    Mueller, Gabrielle
    Nagaraja, Ramaiah
    Narisu, Narisu
    Nieminen, Tuomo V. M.
    Nsubuga, Rebecca N.
    Olafsson, Isleifur
    Ong, Ken K.
    Palotie, Aarno
    Papamarkou, Theodore
    Pomilla, Cristina
    Pouta, Anneli
    Rader, Daniel J.
    Reilly, Muredach P.
    Ridker, Paul M.
    Rivadeneira, Fernando
    Rudan, Igor
    Ruokonen, Aimo
    Samani, Nilesh
    Scharnagl, Hubert
    Seeley, Janet
    Silander, Kaisa
    Stancakova, Alena
    Stirrups, Kathleen
    Swift, Amy J.
    Tiret, Laurence
    Uitterlinden, Andre G.
    van Pelt, L. Joost
    Vedantam, Sailaja
    Wainwright, Nicholas
    Wijmenga, Cisca
    Wild, Sarah H.
    Willemsen, Gonneke
    Wilsgaard, Tom
    Wilson, James F.
    Young, Elizabeth H.
    Zhao, Jing Hua
    Adair, Linda S.
    Arveiler, Dominique
    Assimes, Themistocles L.
    Bandinelli, Stefania
    Bennett, Franklyn
    Bochud, Murielle
    Boehm, Bernhard O.
    Boomsma, Dorret I.
    Borecki, Ingrid B.
    Bornstein, Stefan R.
    Bovet, Pascal
    Burnier, Michel
    Campbell, Harry
    Chakravarti, Aravinda
    Chambers, John C.
    Chen, Yii-Der Ida
    Collins, Francis S.
    Cooper, Richard S.
    Danesh, John
    Dedoussis, George
    de Faire, Ulf
    Feranil, Alan B.
    Ferrieres, Jean
    Ferrucci, Luigi
    Freimer, Nelson B.
    Gieger, Christian
    Groop, Leif C.
    Gudnason, Vilmundur
    Gyllensten, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Hamsten, Anders
    Harris, Tamara B.
    Hingorani, Aroon
    Hirschhorn, Joel N.
    Hofman, Albert
    Hovingh, G. Kees
    Hsiung, Chao Agnes
    Humphries, Steve E.
    Hunt, Steven C.
    Hveem, Kristian
    Iribarren, Carlos
    Jarvelin, Marjo-Riitta
    Jula, Antti
    Kahonen, Mika
    Kaprio, Jaakko
    Kesaniemi, Antero
    Kivimaki, Mika
    Kooner, Jaspal S.
    Koudstaal, Peter J.
    Krauss, Ronald M.
    Kuh, Diana
    Kuusisto, Johanna
    Kyvik, Kirsten O.
    Laakso, Markku
    Lakka, Timo A.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Lindgren, Cecilia M.
    Martin, Nicholas G.
    Maerz, Winfried
    McCarthy, Mark I.
    McKenzie, Colin A.
    Meneton, Pierre
    Metspalu, Andres
    Moilanen, Leena
    Morris, Andrew D.
    Munroe, Patricia B.
    Njolstad, Inger
    Pedersen, Nancy L.
    Power, Chris
    Pramstaller, Peter P.
    Price, Jackie F.
    Psaty, Bruce M.
    Quertermous, Thomas
    Rauramaa, Rainer
    Saleheen, Danish
    Salomaa, Veikko
    Sanghera, Dharambir K.
    Saramies, Jouko
    Schwarz, Peter E. H.
    Sheu, Wayne H-H
    Shuldiner, Alan R.
    Siegbahn, Agneta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Coagulation and inflammation science.
    Spector, Tim D.
    Stefansson, Kari
    Strachan, David P.
    Tayo, Bamidele O.
    Tremoli, Elena
    Tuomilehto, Jaakko
    Uusitupa, Matti
    van Duijn, Cornelia M.
    Vollenweider, Peter
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Wareham, Nicholas J.
    Whitfield, John B.
    Wolffenbuttel, Bruce H. R.
    Ordovas, Jose M.
    Boerwinkle, Eric
    Palmer, Colin N. A.
    Thorsteinsdottir, Unnur
    Chasman, Daniel I.
    Rotter, Jerome I.
    Franks, Paul W.
    Ripatti, Samuli
    Cupples, L. Adrienne
    Sandhu, Manjinder S.
    Rich, Stephen S.
    Boehnke, Michael
    Deloukas, Panos
    Kathiresan, Sekar
    Mohlke, Karen L.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Abecasis, Goncalo R.
    Discovery and refinement of loci associated with lipid levels2013In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 45, no 11, p. 1274-1283Article in journal (Refereed)
    Abstract [en]

    Levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides and total cholesterol are heritable, modifiable risk factors for coronary artery disease. To identify new loci and refine known loci influencing these lipids, we examined 188,577 individuals using genome-wide and custom genotyping arrays. We identify and annotate 157 loci associated with lipid levels at P < 5 x 10(-8), including 62 loci not previously associated with lipid levels in humans. Using dense genotyping in individuals of European, East Asian, South Asian and African ancestry, we narrow association signals in 12 loci. We find that loci associated with blood lipid levels are often associated with cardiovascular and metabolic traits, including coronary artery disease, type 2 diabetes, blood pressure, waist-hip ratio and body mass index. Our results demonstrate the value of using genetic data from individuals of diverse ancestry and provide insights into the biological mechanisms regulating blood lipids to guide future genetic, biological and therapeutic research.

  • 1560.
    Williams, Rachel
    et al.
    GlaxoSmithKline, Worldwide Epidemiol, Collegeville, PA USA..
    Shearn, Shawn Patrick
    GlaxoSmithKline, Ophthalmol Res & Dev, Philadelphia, PA USA..
    Dowd, Michael
    Bogier Clin & IT Solut Inc, Raleigh, NC USA..
    Cicconetti, Greg
    GlaxoSmithKline, Quantitat Sci, Philadelphia, PA USA..
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    White, Harvey
    Auckland City Hosp, Green Lane Cardiovasc Serv, Auckland, New Zealand.;Univ Auckland, Auckland 1, New Zealand..
    Janmohamed, Salim
    Wurzelmann, John I.
    GlaxoSmithKline, Ophthalmol Res & Dev, Philadelphia, PA USA..
    McLaughlin, Megan M.
    GlaxoSmithKline, Ophthalmol Res & Dev, Philadelphia, PA USA..
    Post-hoc analyses of darapladib, an oral Lp-PLA(2) inhibitor, in phase III cardiovascular outcomes trials may inform investigation in diabetic macular edema2015In: Investigative Ophthalmology and Visual Science, ISSN 0146-0404, E-ISSN 1552-5783, Vol. 56, no 7Article in journal (Other academic)
  • 1561. Wimo, Anders
    et al.
    Religa, Dorota
    Spångberg, Kalle
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Edlund, Ann-Katrin
    Winblad, Bengt
    Eriksdotter, Maria
    Costs of diagnosing dementia: results from SveDem, the Swedish Dementia Registry2013In: International Journal of Geriatric Psychiatry, ISSN 0885-6230, E-ISSN 1099-1166, Vol. 28, no 10, p. 1039-1044Article in journal (Refereed)
    Abstract [en]

    Objective Diagnostic of different dementia disorders is an important part of dementia care. So far, there is limited knowledge about how dementia is diagnosed in clinical routine, and there are few reports on the costs of the dementia work-up leading to a diagnosis. Here, we examine the costs of diagnostic dementia work-up in Sweden. Methods The analyses were made on the data from the Swedish Dementia Registry (SveDem) and included 11,561 dementia patients diagnosed during 2007-2010, mainly not only in specialist care (SC) (n=53) but also some primary care centres (PC). We have studied differences in the use of investigations for dementia diagnostics such as cognitive tests, blood and cerebrospinal fluid analyses, radiological examinations and assessments of functions. Unit costs for each diagnostic investigation were combined with the use of these investigations for all cases in the database. Results are presented versus gender and stratified for age. Results The number of diagnostic tests performed was 2.8 in PC and 4.6 in SC. The average costs (Euro1=SEK9 and US$1=SEK7 in 2010) were SEK6777 in PC and SEK11,682 in SC. Age was the strongest cost predictor while there were no gender differences. There were also regional differences, ranging from SEK8231 to SEK14,734 in SC. Conclusions The SveDem database offers valuable information on the diagnostic procedures for dementia in daily clinical practice. The differences between PC and SC in diagnostic costs reflect national guidelines. The age effect needs to be studied more.

  • 1562.
    Winell, Henric
    et al.
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Lindbäck, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    A general score-independent test for order-restricted inference2018In: Statistics in Medicine, ISSN 0277-6715, E-ISSN 1097-0258, Vol. 37, no 21, p. 3078-3090Article in journal (Refereed)
    Abstract [en]

    In the analysis of ordered categorical data, the categories are often assigned a set of subjectively chosen order-restricted scores. To overcome the arbitrariness involved in the assignment of the scores, several score-independent tests have been proposed. However, these methods are limited to 2 x K contingency tables, where K is the number of ordered categories. We present an efficiency robust score-independent test that is applicable to more general situations. The test is embedded into a flexible framework for conditional inference and provides a natural generalization of many familiar tests involving ordered categorical data, such as the generalized Cochran-Mantel-Haenszel test for singly or doubly ordered contingency tables, the Page test for randomized block designs and the Tarone-Ware trend test for survival data. The proposed method is illustrated by several numerical examples.

  • 1563. Wiren, Sara M.
    et al.
    Drevin, Linda I.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Carlsson, Sigrid V.
    Akre, Olof
    Holmberg, Erik C.
    Robinson, David E.
    Garmo, Hans G.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Stattin, Par E.
    Fatherhood status and risk of prostate cancer: Nationwide, population-based case-control study2013In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 133, no 4, p. 937-943Article in journal (Refereed)
    Abstract [en]

    Previous studies have shown a decreased risk of prostate cancer for childless men; however, the cause of the association remains to be elucidated. The aim of our study was to assess the risk of prostate cancer by fatherhood status, also considering potential confounding factors. In a case-control study in Prostate Cancer data Base Sweden 2.0, a nationwide, population-based cohort, data on number of children, marital status, education, comorbidity and tumor characteristics obtained through nationwide healthcare registers and demographic databases for 117,328 prostate cancer cases and 562,644 controls, matched on birth year and county of residence, were analyzed. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs) for prostate cancer overall and by risk category, adjusting for marital status and education. Childless men had a decreased risk of prostate cancer compared to fathers, OR=0.83 (95% CI=0.82-0.84), and risk was lower for low-risk prostate cancer, OR=0.74 (95% CI=0.72-0.77), than for metastatic prostate cancer, OR=0.93 (95% CI=0.90-0.97). Adjustment for marital status and education attenuated the association in the low-risk category, adjusted OR=0.87 (95% CI=0.84-0.91), whereas OR for metastatic cancer remained virtually unchanged, adjusted OR=0.92 (95% CI=0.88-0.96). Our data indicate that the association between fatherhood status and prostate cancer to a large part is due to socioeconomic factors influencing healthcare-seeking behavior including testing of prostate-specific antigen levels.

  • 1564.
    Witt, Nils
    et al.
    Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, and Unit of Cardiology, Södersjukhuset, Stockholm, Sweden.
    Rück, Andreas
    Department of Medicine, Karolinska Institutet, and Department of Cardiology, Karolinska University Hospital, Stockholm.
    James, Stefan K
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Physiology.
    Koul, Sasha
    Department of Cardiology, Skåne University Hospital, Lund University, Lund, Sweden .
    Lagerqvist, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Sweden: coronary and structural heart interventions from 2010 to 20152017In: EuroIntervention, ISSN 1774-024X, E-ISSN 1969-6213, Vol. 13, no Z, p. Z70-Z74, article id EIJ-D-16-00830Article in journal (Refereed)
    Abstract [en]

    Sparsely populated and with wide non-urbanised areas, Sweden faces specific challenges in providing publicly financed, high-quality and equal healthcare to all parts of the country. As a result, a decentralised organisation for acute coronary care has been developed with coronary care units and catheterisation laboratories in several small- and medium-sized city areas. In contrast, highly specialised non-emergent interventional procedures are centralised to a few high-volume centres, mainly located at university hospitals in large city areas. Nationwide quality registries with nearly complete coverage facilitate healthcare quality improvement and form a basis for clinical research. In this report, we present an overview of demographics, healthcare organisation, quality registries and procedural data for coronary and structural heart interventions in Sweden over the past six years.

  • 1565. Wollert, Kai C
    et al.
    Kempf, Tibor
    Lagerqvist, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lindahl, Bertil
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Olofsson, Sylvia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Allhoff, Tim
    Peter, Timo
    Siegbahn, Agneta
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Venge, Per
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Drexler, Helmut
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Growth Differentiation Factor 15 for Risk Stratification and Selection of an Invasive Treatment Strategy in Non-ST-Elevation Acute Coronary Syndrome2007In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 116, no 14, p. 1540-1548Article in journal (Refereed)
    Abstract [en]

    Background— An invasive treatment strategy improves outcomein patients with non–ST-elevation acute coronary syndromeat moderate to high risk. We hypothesized that the circulatinglevel of growth differentiation factor 15 (GDF-15) may improverisk stratification.

    Methods and Results— The Fast Revascularization duringInStability in Coronary artery disease II (FRISC-II) trial randomizedpatients with non–ST-elevation acute coronary syndrometo an invasive or conservative strategy with a follow-up for2 years. GDF-15 and other biomarkers were determined on admissionin 2079 patients. GDF-15 was moderately elevated (between 1200and 1800 ng/L) in 770 patients (37.0%), and highly elevated(>1800 ng/L) in 493 patients (23.7%). Elevated levels ofGDF-15 independently predicted the risk of the composite endpoint of death or recurrent myocardial infarction in the conservativegroup (P=0.016) but not in the invasive group. A significantinteraction existed between the GDF-15 level on admission andthe effect of treatment strategy on the composite end point.The occurrence of the composite end point was reduced by theinvasive strategy at GDF-15 levels >1800 ng/L (hazard ratio,0.49; 95% confidence interval, 0.33 to 0.73; P=0.001), between1200 and 1800 ng/L (hazard ratio, 0.68; 95% confidence interval,0.46 to 1.00; P=0.048), but not <1200 ng/L (hazard ratio,1.06; 95% confidence interval, 0.68 to 1.65; P=0.81). Patientswith ST-segment depression or a troponin T level >0.01 µg/Lwith a GDF-15 level <1200 ng/L did not benefit from the invasivestrategy.

    Conclusions— GDF-15 is a potential tool for risk stratificationand therapeutic decision making in patients with non–ST-elevationacute coronary syndrome as initially diagnosed by ECG and troponinlevels. A prospective randomized trial is needed to validatethese findings.

  • 1566. Wollert, Kai C.
    et al.
    Kempf, Tibor
    Peter, Timo
    Olofsson, Sylvia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    James, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Johnston, Nina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lindahl, Bertil
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Horn-Wichmann, Rüdiger
    Brabant, Georg
    Simoons, Maarten L.
    Armstrong, Paul W.
    Califf, Robert M.
    Drexler, Helmut
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Prognostic value of growth-differentiation factor-15 in patients with non-ST-elevation acute coronary syndrome2007In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 115, no 8, p. 962-971Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Growth-differentiation factor-15 (GDF-15) is a member of the transforming growth factor-beta cytokine superfamily that is induced in the heart after ischemia-and-reperfusion injury. Circulating levels of GDF-15 may provide prognostic information in patients with non-ST-elevation acute coronary syndrome. METHODS AND RESULTS: Blood samples were obtained on admission from 2081 patients with acute chest pain and either ST-segment depression or troponin elevation who were included in the Global Utilization of Strategies to Open Occluded Arteries (GUSTO)-IV Non-ST-Elevation Acute Coronary Syndrome trial and from a matching cohort of 429 apparently healthy individuals. GDF-15 levels were determined by immunoradiometric assay. Approximately two thirds of patients presented with GDF-15 levels above the upper limit of normal in healthy controls (1200 ng/L); one third presented with levels >1800 ng/L. Increasing tertiles of GDF-15 were associated with an enhanced risk of death at 1 year (1.5%, 5.0%, and 14.1%; P<0.001). By multiple Cox regression analysis, only the levels of GDF-15 and N-terminal pro-B-type natriuretic peptide, together with age and a history of previous myocardial infarction, contributed independently to 1-year mortality risk. Receiver operating characteristic curve analyses further illustrated that GDF-15 is a strong marker of 1-year mortality risk (area under the curve, 0.757; best cutoff, 1808 ng/L). At this cutoff value, GDF-15 added significant prognostic information in patient subgroups defined by age; gender; time from symptom onset to admission; cardiovascular risk factors; previous cardiovascular disease; and the risk markers ST-segment depression, troponin T, N-terminal pro-B-type natriuretic peptide, C-reactive protein, and creatinine clearance. CONCLUSIONS: GDF-15 is a new biomarker of the risk for death in patients with non-ST-elevation acute coronary syndrome that provides prognostic information beyond that provided by established clinical and biochemical markers.

  • 1567.
    Wollert, Kai C.
    et al.
    Hannover Med Sch, Dept Cardiol & Angiol, Div Mol & Translat Cardiol, Hannover, Germany..
    Kempf, Tibor
    Hannover Med Sch, Dept Cardiol & Angiol, Div Mol & Translat Cardiol, Hannover, Germany..
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Growth Differentiation Factor 15 as a Biomarker in Cardiovascular Disease2017In: Clinical Chemistry, ISSN 0009-9147, E-ISSN 1530-8561, Vol. 63, no 1, p. 140-151Article, review/survey (Refereed)
    Abstract [en]

    BACKGROUND: Growth differentiation factor 15 (GDF-15) is expressed and secreted in response to inflammation, oxidative stress, hypoxia, telomere erosion, and oncogene activation. Cardiovascular (CV) disease is a major. driver of GDF-15 production. GDF-15 has favorable preanalytic characteristics and can be measured in serum and plasma by immunoassay. CONTENT: In community-dwelling individuals higher concentrations of GDF-15 are associated with increased risks of developing CV disease, chronic kidney disease, and cancer, independent of traditional CV risk factors, renal function, and other biomarkers (C-reactive protein, B-type natriuretic peptide, cardiac troponin). Low concentrations of GDF-15 are closely associated with longevity. GDF-15 is as an independent marker of all-cause mortality and CV events in patients with coronary artery disease, and may help select patients with non-ST-elevation acute coronary syndrome for early revascularization and more intensive medical therapies. GDF-15 is, independently associated with mortality and nonfatal events in atrial fibrillation and heart failure (HF) with preserved or reduced ejection fraction. GDF-15 reflects chronic disease burden and acute perturbations in HF and responds to improvements in hemodynamic status. GDF-15 is independently associated with major bleeding in patients receiving antithrombotic therapies and has been included in a new bleeding risk score, which may become useful for decision support. SUMMARY: GDF-15 captures distinct aspects of CV disease development, progression, and prognosis, which are not represented by clinical risk predictors and other biomarkers. The usefulness of GDF-15 to guide management decisions and discover new treatment targets should be further explored.

  • 1568. Wormser, David
    et al.
    Kaptoge, Stephen
    Di Angelantonio, Emanuele
    Wood, Angela M
    Pennells, Lisa
    Thompson, Alex
    Sarwar, Nadeem
    Kizer, Jorge R
    Lawlor, Debbie A
    Nordestgaard, Børge G
    Ridker, Paul
    Salomaa, Veikko
    Stevens, June
    Woodward, Mark
    Sattar, Naveed
    Collins, Rory
    Thompson, Simon G
    Whitlock, Gary
    Ärnlöv, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Risérus, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism.
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Danesh, John
    Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies2011In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 377, no 9771, p. 1085-1095Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Guidelines differ about the value of assessment of adiposity measures for cardiovascular disease risk prediction when information is available for other risk factors. We studied the separate and combined associations of body-mass index (BMI), waist circumference, and waist-to-hip ratio with risk of first-onset cardiovascular disease.

    METHODS:

    We used individual records from 58 cohorts to calculate hazard ratios (HRs) per 1 SD higher baseline values (4.56 kg/m(2) higher BMI, 12.6 cm higher waist circumference, and 0.083 higher waist-to-hip ratio) and measures of risk discrimination and reclassification. Serial adiposity assessments were used to calculate regression dilution ratios.

    RESULTS:

    Individual records were available for 221,934 people in 17 countries (14,297 incident cardiovascular disease outcomes; 1.87 million person-years at risk). Serial adiposity assessments were made in up to 63,821 people (mean interval 5.7 years [SD 3.9]). In people with BMI of 20 kg/m(2) or higher, HRs for cardiovascular disease were 1.23 (95% CI 1.17-1.29) with BMI, 1.27 (1.20-1.33) with waist circumference, and 1.25 (1.19-1.31) with waist-to-hip ratio, after adjustment for age, sex, and smoking status. After further adjustment for baseline systolic blood pressure, history of diabetes, and total and HDL cholesterol, corresponding HRs were 1.07 (1.03-1.11) with BMI, 1.10 (1.05-1.14) with waist circumference, and 1.12 (1.08-1.15) with waist-to-hip ratio. Addition of information on BMI, waist circumference, or waist-to-hip ratio to a cardiovascular disease risk prediction model containing conventional risk factors did not importantly improve risk discrimination (C-index changes of -0.0001, -0.0001, and 0.0008, respectively), nor classification of participants to categories of predicted 10-year risk (net reclassification improvement -0.19%, -0.05%, and -0.05%, respectively). Findings were similar when adiposity measures were considered in combination. Reproducibility was greater for BMI (regression dilution ratio 0.95, 95% CI 0.93-0.97) than for waist circumference (0.86, 0.83-0.89) or waist-to-hip ratio (0.63, 0.57-0.70).

    INTERPRETATION:

    BMI, waist circumference, and waist-to-hip ratio, whether assessed singly or in combination, do not importantly improve cardiovascular disease risk prediction in people in developed countries when additional information is available for systolic blood pressure, history of diabetes, and lipids.

    FUNDING:

    British Heart Foundation and UK Medical Research Council.

  • 1569. Woudstra, Pier
    et al.
    Grundeken, Maik J
    van de Hoef, Tim P
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Fox, Keith A
    de Winter, Robbert J
    Damman, Peter
    Prognostic relevance of PCI-related myocardial infarction2013In: Nature Reviews Cardiology, ISSN 1759-5002, E-ISSN 1759-5010, Vol. 10, no 4, p. 231-236Article in journal (Refereed)
    Abstract [en]

    Procedure-related myocardial infarction (pMI) is directly associated with a coronary revascularization procedure, such as percutaneous coronary intervention (PCI) or CABG surgery. In contrast to spontaneous myocardial infarction (MI), the prognostic relevance of pMI is the subject of ongoing debate. Data from retrospective analyses of large, randomized clinical trials, and large, contemporary cohort studies have several shortcomings that limit their extrapolation to clinical practice. In our opinion, the currently available evidence is insufficient to conclude that pMI during PCI, as currently defined, always has important prognostic implications. Until further evidence is available, we recommend adopting the definition for MI given in the third universal definition of MI, which differentiates between pMI and spontaneous MI. This is important not only for clinical decision-making but also for the interpretation of pMI as a surrogate end point in clinical trials. Further studies are essential to understand the pathophysiology and consequences of pMI.

  • 1570. Wu, Alan H B
    et al.
    Packer, Milton
    Smith, Andrew
    Bijou, Rachel
    Fink, Daniel
    Mair, Johannes
    Wallentin, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Johnston, Nina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology.
    Feldcamp, Carolyn S
    Haverstick, Doris M
    Ahnadi, Charaf E
    Grant, Andrew
    Despres, Normand
    Bluestein, Barry
    Ghani, Farooq
    Analytical and clinical evaluation of the Bayer ADVIA Centaur automated B-type natriuretic peptide assay in patients with heart failure: a multisite study2004In: Clinical Chemistry, ISSN 0009-9147, E-ISSN 1530-8561, Vol. 50, no 5, p. 867-873Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    B-Type natriuretic peptide (BNP) is released from the left ventricle of the heart into the circulation in response to ventricular stretching and volume overload. Increased BNP concentrations are associated with heart failure (HF).

    METHODS:

    We evaluated the analytical and clinical performance of the Bayer ADVIA Centaur BNP assay. Studies included precision, analytical correlation (against the Shionogi ShionoRIA and Biosite Triage BNP assays), BNP results for blood collected in plastic tubes containing EDTA vs other collection tubes, high-dose hook effect, detection limits, and interferences. The clinical performance was tested on 2243 blood samples collected from 983 apparently healthy individuals, 538 patients with chronic disease but without HF (renal insufficiency, chronic obstructive pulmonary disease, diabetes, and hypertension), and 722 patients with HF (New York Heart Association classes I-IV).

    RESULTS:

    The ADVIA Centaur assay had total imprecision (CV) of 3.4%, 2.9%, and 2.4% at BNP concentrations of 48, 461, and 1768 ng/L, respectively. The Passing-Bablok correlations to the ShionoRIA and Triage were as follows: ADVIA Centaur = 1.11(ShionoRIA) - 1.19 ng/L (r = 0.98); ADVIA Centaur = 0.78(Triage) + 5.89 ng/L (r = 0.92), respectively. Of the different blood collection tubes, only EDTA plastic tubes (with and without the barrier gel) were acceptable. The lower detection limit was 0.5 ng/L, and there were no interferences from common analytes, other neuropeptides, or unusual antibodies. BNP exhibited different reference intervals according to age and gender. BNP concentrations increased progressively as the severity of HF increased.

    CONCLUSIONS:

    The ADVIA Centaur is the first commercially available BNP assay for use on an automated immunochemistry platform. This assay has good analytical and clinical performance characteristics for diagnosing HF.

  • 1571.
    Wu, Jason H. Y.
    et al.
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia..
    Foote, Celine
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia.;Concord Repatriat Gen Hosp, Sydney, NSW, Australia..
    Blomster, Juuso
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia.;Univ Turku, Turku, Finland.;Univ Gothenberg, Sahlgrenska Acad, Gothenburg, Sweden..
    Toyama, Tadashi
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia..
    Perkovic, Vlado
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia.;Royal Prince Alfred Hosp, Sydney, NSW, Australia..
    Sundström, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiology. Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia..
    Neal, Bruce
    Univ Sydney, George Inst Global Hlth, Sydney, NSW 2050, Australia.;Univ London Imperial Coll Sci Technol & Med, London, England..
    Effects of sodium-glucose cotransporter-2 inhibitors on cardiovascular events, death, and major safety outcomes in adults with type 2 diabetes: a systematic review and meta-analysis2016In: The Lancet Diabetes and Endocrinology, ISSN 2213-8587, E-ISSN 2213-8595, Vol. 4, no 5, p. 411-419Article in journal (Refereed)
    Abstract [en]

    Background In patients with type 2 diabetes, sodium-glucose cotransporter-2 (SGLT2) inhibitors are known to reduce glucose concentrations, blood pressure, and weight, but to increase LDL cholesterol and the incidence of urogenital infections. Protection against cardiovascular events has also been reported, as have possible increased risks of adverse outcomes such as ketoacidosis and bone fracture. We aimed to establish the effects of SGLT2 inhibitors on cardiovascular events, death, and safety outcomes in adults with type 2 diabetes, both overall and separately for individual drugs. Methods In this systematic review and meta-analysis, we searched MEDLINE, Embase, the Cochrane Library, and websites of US, European, and Japanese regulatory authorities from Jan 1, 1950, to Sept 30, 2015, for data from prospective randomised controlled trials assessing the effects of SGLT2 treatment compared with controls. We excluded duplicate reports, trials of compound drugs, trials that lasted 7 days or fewer, trials that did not report on outcomes of interest, and articles that presented pooled trial data for which the individual trials could not be identified. We extracted data in duplicate using a standardised approach. The primary outcome was major adverse cardiovascular events. Secondary outcomes were cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, admission to hospital for unstable angina, heart failure, and all-cause mortality. We estimated summary relative risks with fixed-effects meta-analysis, with the I-2 statistic used to estimate heterogeneity of results beyond chance. Findings The analyses included data from six regulatory submissions (37 525 participants) and 57 published trials (33 385 participants), which provided data for seven different SGLT2 inhibitors. SGLT2 inhibitors protected against the risk of major adverse cardiovascular events (relative risk 0.84 [95% CI 0.75-0.95]; p=0.006), cardiovascular death (0.63 [0.51-0.77]; p<0.0001), heart failure (0.65 [0.50-0.85]; p=0.002), and death from any cause (0.71 [0.61-0.83]; p<0.0001). No clear effect was apparent for non-fatal myocardial infarction (0.88 [0.72-1.07]; p=0.18) or angina (0.95 [0.73-1.23]; p=0.70), but we noted an adverse effect for non-fatal stroke (1.30 [1.00-1.68]; p=0.049). We noted no clear evidence that the individual drugs had different effects on cardiovascular outcomes or death (all I I-2 < 43%). Safety analyses showed consistent increased risks of genital infections (regulatory submissions 4.75 [4.00-5.63]; scientific reports 2.88 [2.48-3.34]), but findings for some safety outcomes varied depending on whether anlayses were based on data extracted from regulatory submissions or trials reported in the scientific literature. Interpretation These data suggest net protection of SGLT2 inhibitors against cardiovascular outcomes and death. The efficacy results were driven by findings for empagliflozin (the only SGLT2 inhibitor for which data from a dedicated long-term cardiovascular safety trial have been reported), although results for the other drugs in the class were not clearly different. Adverse events were more difficult to quantify than was efficacy, with the effects of individual drugs in the class seeming to differ for some safety outcomes. Results from ongoing studies will be crucial to substantiate these findings across the drug class, but the available data provide a strong rationale to expect benefit from use of SGLT2 inhibitors in patients with type 2 diabetes at high risk of cardiovascular events.

  • 1572. Wulaningsih, Wahyu
    et al.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Hammar, Niklas
    Jungner, Ingmar
    Walldius, Göran
    van Hemelrijck, Mieke
    Serum Lipids and the Risk of Gastrointestinal Malignancies in the Swedish AMORIS Study2012In: Journal of cancer epidemiology, ISSN 1687-8566, Vol. 2012, p. 792034-Article in journal (Refereed)
    Abstract [en]

    Background.

    Metabolic syndrome has been linked to an increased cancer risk, but the role of dyslipidaemia in gastrointestinal malignancies is unclear. We aimed to assess the risk of oesophageal, stomach, colon, and rectal cancers using serum levels of lipid components.

    Methods.

    From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected 540,309 participants (> 20 years old) with baseline measurements of total cholesterol (TC), triglycerides (TG), and glucose of whom 84,774 had baseline LDL cholesterol (LDL), HDL cholesterol (HDL), apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I). Multivariate Cox proportional hazards regression was used to assess glucose and lipid components in relation to oesophageal, stomach, colon, and rectal cancer risk.

    Results.

    An increased risk of oesophageal cancer was observed in persons with high TG (e.g. HR: 2.29 (95% CI: 1.42-3.68) for the 4th quartile compared to the 1st) and low LDL, LDL/HDL ratio, TC/HDL ratio, log (TG/HDL), and apoB/apoA-I ratio. High glucose and TG were linked with an increased colon cancer risk, while high TC levels were associated with an increased rectal cancer risk.

    Conclusion.

    The persistent link between TC and rectal cancer risk as well as between TG and oesophageal and colon cancer risk in normoglycaemic individuals may imply their substantiality in gastrointestinal carcinogenesis.

  • 1573.
    Wulaningsih, Wahyu
    et al.
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England.;Gadjah Mada Univ, Fac Med, Div Hematol Oncol, Yogyakarta, Indonesia..
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England..
    Garmo, Hans
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England.;Reg Canc Ctr, Uppsala, Sweden..
    Karagiannis, Sophia N.
    Kings Coll London, Guys & St Thomass Hosp, NIHR Biomed Res Ctr, St Johns Inst Dermatol,Div Genet & Mol Med,Fac Li, London, England.;Kings Coll London, London, England..
    Ahlstedt, Staffan
    Karolinska Inst, Inst Environm Med, Ctr Allergy Res, Stockholm, Sweden..
    Malmstrom, Hakan
    Karolinska Inst, Inst Environm Med, Epidemiol Unit, Stockholm, Sweden..
    Lambe, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Hammar, Niklas
    Karolinska Inst, Inst Environm Med, Epidemiol Unit, Stockholm, Sweden.;AstraZeneca R&D, Molndal, Sweden..
    Walldius, Goran
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, Stockholm, Sweden..
    Jungner, Ingmar
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.;CALAB Res, Stockholm, Sweden..
    Ng, Tony
    Kings Coll London, Randall Div, Richard Dimbleby Dept Canc Res, London, England.;Kings Coll London, Div Canc Studies, London, England..
    Van Hemelrijck, Mieke
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England.;Karolinska Inst, Inst Environm Med, Epidemiol Unit, Stockholm, Sweden..
    Investigating the association between allergen-specific immunoglobulin E, cancer risk and survival2016In: Oncoimmunology, ISSN 2162-4011, E-ISSN 2162-402X, Vol. 5, no 6, article id e1154250Article in journal (Refereed)
    Abstract [en]

    Prior findings linking allergy and cancer have been inconsistent, which may be driven by diverse assessment methods. We used serum specific immunoglobulin E (IgE) against common inhalant allergens that was assessed prior to cancer diagnosis in studying this association. We selected 8,727 Swedish men and women who had measurements of serum allergen-specific IgE and total IgE between 1992 and 1996. Multivariable Cox regression using age as a timescale was performed to assess the associations of IgE sensitization, defined by any levels of serum specific IgE >= 35 kU/L, with risk of overall and specific cancers. A test for trend was performed by assigning scores derived from allergen-specific IgE levels at baseline as an ordinal scale. Kaplan-Meier curves and log-rank test were used to assess cancer survival by IgE sensitization status. During a mean follow-up of 16 year, 689 persons were diagnosed with cancer. We found an inverse association between IgE sensitization and cancer risk, with a hazard ratio (HR) of 0.83 and 95% confidence intervals (CI) of 0.70-0.99. A similar trend was seen with specific IgE scores overall (P-trend = 0.007) and in women (P-trend = 0.01). Although IgE sensitization was not associated with risk of common site-specific cancers, serum specific IgE scores were inversely associated with melanoma risk in men and women combined, and with risk of female breast and gynecological cancers combined. No association with survival was observed. The association between circulating IgE levels and incident cancer may point toward a role of T-helper 2 (T(H)2)-biased response in development of some cancers.

  • 1574. Wulaningsih, Wahyu
    et al.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Malmstrom, Håkan
    Lambe, Mats
    Hammar, Niklas
    Walldius, Göran
    Jungner, Ingmar
    Van Hemelrijck, Mieke
    Prediagnostic serum inflammatory markers in relation to breast cancer risk, severity at diagnosis and survival in breast cancer patients2015In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 36, no 10, p. 1121-1128Article in journal (Refereed)
    Abstract [en]

    Inflammation has been linked to cancer but its role in breast cancer is unclear. We investigated common serum markers of inflammation: C-reactive protein (CRP), albumin, haptoglobin and white blood cells (WBC) in relation to breast cancer incidence, severity and survival. A total of 155179 women aged 20 and older without any history of cancer were selected from a large Swedish cohort. Hazard ratios (HRs) for breast cancer were estimated with Cox regression, adjusting for potential confounders. Ordered and binomial logistic regression models were used to assess the associations of serum inflammatory markers with breast cancer severity and oestrogen receptor (ER) positivity at diagnosis, on the other. Cumulative incidence functions by levels of inflammatory markers were assessed for early death from breast cancer and all causes. During a mean follow-up of 18.3 years, 6606 women were diagnosed with breast cancer, of whom 1474 died. A positive association with incident breast cancer was seen for haptoglobin ≥ 1.4g/l [HR 1.09; 95% confidence interval (CI): 1.00-1.18] compared to lower levels. No association was observed between inflammatory markers and breast cancer severity or ER positivity. Higher haptoglobin was linked to risk of early death from breast cancer (HR: 1.27, 95% CI: 1.02-1.59), whereas higher risk of early death from all causes was additionally found with CRP ≥ 10mg/l (HR: 1.19, 95% CI: 1.04-1.36) and WBC ≥ 10×10(9)/l (HR: 1.57, 1.14-2.16). Our findings indicate that prediagnostic serum inflammatory markers were weakly linked to incident breast cancer but corresponded to worse survival after diagnosis.

  • 1575. Wulaningsih, Wahyu
    et al.
    Michaelsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Hammar, Niklas
    Jungner, Ingmar
    Walldius, Goran
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Van Hemelrijck, Mieke
    Inorganic phosphate and the risk of cancer in the Swedish AMORIS study2013In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 13, p. UNSP 257-Article in journal (Refereed)
    Abstract [en]

    Background: Both dietary and serum levels of inorganic phosphate (Pi) have been linked to development of cancer in experimental studies. This is the first population-based study investigating the relation between serum Pi and risk of cancer in humans. Methods: From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected all participants (>20 years old) with baseline measurements of serum Pi, calcium, alkaline phosphatase, glucose, and creatinine (n = 397,292). Multivariable Cox proportional hazards regression analyses were used to assess serum Pi in relation to overall cancer risk. Similar analyses were performed for specific cancer sites. Results: We found a higher overall cancer risk with increasing Pi levels in men (HR: 1.02 (95% CI: 1.00-1.04) for every SD increase in Pi), and a negative association in women (HR: 0.97 (95% CI: 0.96-0.99) for every SD increase in Pi). Further analyses for specific cancer sites showed a positive link between Pi quartiles and the risk of cancer of the pancreas, lung, thyroid gland and bone in men, and cancer of the oesophagus, lung, and nonmelanoma skin cancer in women. Conversely, the risks for developing breast and endometrial cancer as well as other endocrine cancer in both men and women were lower in those with higher Pi levels. Conclusions: Abnormal Pi levels are related to development of cancer. Furthermore, the inverse association between Pi levels and risk of breast, endometrial and other endocrine cancers may indicate the role of hormonal factors in the relation between Pi metabolism and cancer.

  • 1576. Wulaningsih, Wahyu
    et al.
    Michaelsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Hammar, Niklas
    Jungner, Ingmar
    Walldius, Goran
    Lambe, Mats
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Van Hemelrijck, Mieke
    Serum calcium and risk of gastrointestinal cancer in the Swedish AMORIS study2013In: BMC Public Health, ISSN 1471-2458, E-ISSN 1471-2458, Vol. 13, p. 663-Article in journal (Refereed)
    Abstract [en]

    Background:

    Observational studies have indicated that high calcium intake may prevent colorectal cancer, but as for randomized trials the results are inconclusive. Meanwhile, limited data on the link between serum calcium and cancer risk is available. We investigated the relation between serum calcium and risk of different gastrointestinal cancers in a prospective study.

    Methods:

    A cohort based on 492,044 subjects with baseline information on calcium (mmol/L) and albumin (g/L) was selected from the Swedish Apolipoprotein MOrtality RISk (AMORIS) study. Multivariable Cox proportional hazard models were used to analyse associations between standardised levels, quartiles and age/sex-specific categories of serum calcium and risk of oesophageal, stomach, colon, rectal cancer and also colorectal cancer combined, while taking into account serum albumin and other comorbidities.

    Results:

    During 12 years of follow-up, we identified 323 incident oesophageal cancers, 782 stomach cancers, 2519 colon cancers, and 1495 rectal cancers. A positive association was found between albumin-adjusted serum calcium and risk of oesophageal [HR: 4.82 (95% CI: 2.07 - 11.19) for high compared to normal age-specific calcium levels] and colon cancer [e.g. HR: 1.07 (95% CI: 1.00 - 1.14) for every SD increase of calcium] as well as colorectal cancer [e.g. HR: 1.06 (95% CI: 1.02-1.11) for every SD increase of calcium] in women. In men there were similar but weaker non-statistically significant trends.

    Conclusion:

    The positive relation between serum calcium, oesophageal cancer and colorectal cancer calls for further studies including calcium regulators to evaluate whether there is a true link between calcium metabolism and development of gastrointestinal cancer.

  • 1577.
    Wulaningsih, Wahyu
    et al.
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England..
    Sagoo, Harkiran K.
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England..
    Hamza, Mustafa
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England..
    Melvin, Jennifer
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England..
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England.
    Malmström, Håkan
    Karolinska Inst, Inst Environm Med, Epidemiol Unit, S-17177 Stockholm, Sweden..
    Lambe, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Hammar, Niklas
    Karolinska Inst, Inst Environm Med, Epidemiol Unit, S-17177 Stockholm, Sweden.;AstraZeneca R&D, S-43150 Molndal, Sweden..
    Walldius, Göran
    Karolinska Inst, Inst Environm Med, Unit Cardiovasc Epidemiol, S-17177 Stockholm, Sweden..
    Jungner, Ingmar
    Karolinska Inst, Clin Epidemiol Unit, Dept Med, S-17177 Stockholm, Sweden.;CALAB Res, S-17177 Stockholm, Sweden..
    Van Hemelrijck, Mieke
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London SE1 9RT, England.;Karolinska Inst, Inst Environm Med, Epidemiol Unit, S-17177 Stockholm, Sweden..
    Serum Calcium and the Risk of Breast Cancer: Findings from the Swedish AMORIS Study and a Meta-Analysis of Prospective Studies2016In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 17, no 9, article id 1487Article in journal (Refereed)
    Abstract [en]

    To investigate the association between serum calcium and risk of breast cancer using a large cohort and a systematic review with meta-analysis. From the Swedish Apolipoprotein Mortality Risk (AMORIS) Study we included 229,674 women who had baseline measurements of serum total calcium and albumin. Multivariable Cox regression was used to assess the association between total and albumin-corrected calcium and breast cancer risk. For the systematic review, an electronic search of MEDLINE and EMBASE databases was performed to identify other prospective cohorts assessing the relationship between serum calcium and breast cancer risk. We pooled the results of our AMORIS cohort with other eligible studies in a meta-analysis using a random effects model. I-2 test was used to assess heterogeneity. In the AMORIS study, 10,863 women were diagnosed with breast cancer (mean follow-up: 19 years). We found an inverse association between total serum calcium and breast cancer when comparing the fourth quartile to the first quartile (HR: 0.94, 95% CI: 0.88-0.99, p value for trend 0.04) and similar results using albumin-corrected calcium. In the systematic review, we identified another two prospective cohorts evaluating pre-diagnostic serum total calcium and breast cancer. Combining these studies and our findings in AMORIS in a meta-analysis showed a protective effect of serum calcium against breast cancer, with a summary RR of 0.80 (95% CI: 0.66-0.97). No substantial heterogeneity was observed. Our findings in AMORIS and the meta-analysis support an inverse association between serum calcium and breast cancer risk, which warrants mechanistic investigations.

  • 1578.
    Wulaningsih, Wahyu
    et al.
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London WC2R 2LS, England..
    Vahdaninia, Mariam
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London WC2R 2LS, England..
    Rowley, Mark
    Kings Coll London, Inst Math & Mol Biomed, London WC2R 2LS, England..
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Malmstrom, Hakan
    Karolinska Inst, Inst Environm Med, Dept Epidemiol, S-10401 Stockholm, Sweden..
    Lambe, Mats
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Hammar, Niklas
    Karolinska Inst, Inst Environm Med, Dept Epidemiol, S-10401 Stockholm, Sweden.;AstraZeneca Sverige, Sodertalje, Sweden..
    Walldius, Goran
    Karolinska Inst, Inst Environm Med, Dept Cardiovasc Epidemiol, S-10401 Stockholm, Sweden..
    Jungner, Ingmar
    Karolinska Inst, Dept Med, Clin Epidemiol Unit, Stockholm, Sweden.;CALAB Res, Stockholm, Sweden..
    Coolen, Anthonius C.
    Kings Coll London, Inst Math & Mol Biomed, London WC2R 2LS, England..
    Van Hemelrijck, Mieke
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London WC2R 2LS, England.;Karolinska Inst, Inst Environm Med, Dept Epidemiol, S-10401 Stockholm, Sweden..
    Prediagnostic serum glucose and lipids in relation to survival in breast cancer patients: a competing risk analysis2015In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 15, article id 913Article in journal (Refereed)
    Abstract [en]

    Background: Abnormal glucose and lipids levels may impact survival after breast cancer (BC) diagnosis, but their association to other causes of mortality such as cardiovascular (CV) disease may result in a competing risk problem. Methods: We assessed serum glucose, triglycerides (TG) and total cholesterol (TC) measured prospectively 3 months to 3 years before diagnosis in 1798 Swedish women diagnosed with any type of BC between 1985 and 1999. In addition to using Cox regression, we employed latent class proportional hazards models to capture any heterogeneity of associations between these markers and BC death. The latter method was extended to include the primary outcome (BC death) and competing outcomes (CV death and death from other causes), allowing latent class-specific hazard estimation for cause-specific deaths. Results: A lack of association between prediagnostic glucose, TG or TC with BC death was observed with Cox regression. With latent class proportional hazards model, two latent classes (Class I and II) were suggested. Class I, comprising the majority (81.5 %) of BC patients, had an increased risk of BC death following higher TG levels (HR: 1.87, 95 % CI: 1.01-3.45 for every log TG increase). Lower overall survival was observed in Class II, but no association for BC death was found. On the other hand, TC positively corresponded to CV death in Class II, and similarly, glucose to death from other causes. Conclusion: Addressing cohort heterogeneity in relation to BC survival is important in understanding the relationship between metabolic markers and cause-specific death in presence of competing outcomes.

  • 1579.
    Wuttke, Matthias
    et al.
    Univ Freiburg, Fac Med, Dept Biometry Epidemiol & Med Bioinformat, Inst Genet Epidemiol, Freiburg, Germany;Univ Freiburg, Med Ctr, Freiburg, Germany;Univ Freiburg, Fac Med, Dept Med 4, Renal Div, Freiburg, Germany.
    Li, Yong
    Univ Freiburg, Fac Med, Dept Biometry Epidemiol & Med Bioinformat, Inst Genet Epidemiol, Freiburg, Germany;Univ Freiburg, Med Ctr, Freiburg, Germany.
    Li, Man
    Univ Utah, Dept Med, Div Nephrol & Hypertens, Salt Lake City, UT 84112 USA.
    Sieber, Karsten B.
    GlaxoSmithKline, Target Sci Genet, Collegeville, PA USA.
    Feitosa, Mary F.
    Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
    Gorski, Mathias
    Univ Hosp Regensburg, Dept Nephrol, Regensburg, Germany;Univ Regensburg, Dept Genet Epidemiol, Regensburg, Germany.
    Tin, Adrienne
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA;Welch Ctr Prevent Epidemiol & Clin Res, Baltimore, MD USA.
    Wang, Lihua
    Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
    Chu, Audrey Y.
    Merck & Co Inc, Genet, Kenilworth, NJ USA.
    Hoppmann, Anselm
    Univ Freiburg, Fac Med, Dept Biometry Epidemiol & Med Bioinformat, Inst Genet Epidemiol, Freiburg, Germany;Univ Freiburg, Med Ctr, Freiburg, Germany.
    Kirsten, Holger
    Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany;Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany.
    Giri, Ayush
    Vanderbilt Univ, Med Ctr,Div Quantitat Sci, Dept Obstet & Gynecol,Vanderbilt Genet Inst, Inst Med & Publ Hlth,Vanderbilt Epidemiol Ctr, Nashville, TN 37232 USA;Vanderbilt Univ, Tennessee Valley Healthcare Syst 626, Biomed Lab Res & Dev, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Chai, Jin-Fang
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore;Natl Univ Hlth Syst, Singapore, Singapore.
    Sveinbjornsson, Gardar
    Amgen Inc, deCODE Genet, Reykjavik, Iceland.
    Tayo, Bamidele O.
    Loyola Univ Chicago, Dept Publ Hlth Sci, Maywood, IL USA.
    Nutile, Teresa
    Adriano Buzzati Traverso CNR, Inst Genet & Biophys, Naples, Italy.
    Fuchsberger, Christian
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Marten, Jonathan
    Univ Edinburgh, Inst Genet & Mol Med, Med Res Council, Human Genet Unit, Edinburgh, Midlothian, Scotland.
    Cocca, Massimiliano
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy.
    Ghasemi, Sahar
    Univ Med Greifswald, Inst Community Med, Greifswald, Germany;DZHK German Ctr Cardiovasc Res, Partner Site Greifswald, Greifswald, Germany.
    Xu, Yizhe
    Univ Utah, Dept Med, Div Nephrol & Hypertens, Salt Lake City, UT 84112 USA.
    Horn, Katrin
    Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany;Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany.
    Noce, Damia
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Van der Most, Peter J.
    Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
    Sedaghat, Sanaz
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
    Yu, Zhi
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA;Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
    Akiyama, Masato
    RIKEN, Ctr Integrat Med Sci IMS, Lab Stat Anal, Yokohama, Kanagawa, Japan;Kyushu Univ, Grad Sch Med Sci, Dept Ophthalmol, Fukuoka, Fukuoka, Japan.
    Afaq, Saima
    Imperial Coll London, Sch Publ Hlth, Fac Med, Dept Epidemiol & Biostat, London, England;Khyber Med Univ, Inst Publ Hlth & Social Sci, Peshawar, Pakistan.
    Ahluwalia, Tarunveer S.
    Steno Diabet Ctr Copenhagen, Gentofte, Denmark.
    Almgren, Peter
    Lund Univ, Dept Clincial Sci Malmo, Diabetes & Cardiovasc Disease Genet Epidemi, Malmo, Sweden.
    Amin, Najaf
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
    Arnlov, Johan
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med & Primary Care, Stockholm, Sweden;Dalarna Univ, Sch Hlth & Social Studies, Stockholm, Sweden.
    Bakker, Stephan J. L.
    Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, Groningen, Netherlands.
    Bansal, Nisha
    Univ Washington, Div Nephrol, Seattle, WA 98195 USA;Univ Washington, Kidney Res Inst, Seattle, WA 98195 USA.
    Baptista, Daniela
    Geneva Univ Hosp, Cardiol, Geneva, Switzerland.
    Bergmann, Sven
    Univ Lausanne, Dept Computat Biol, Lausanne, Switzerland;Swiss Inst Bioinformat, Lausanne, Switzerland;Univ Cape Town, Dept Integrat Biomed Sci, Cape Town, South Africa.
    Biggs, Mary L.
    Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA;Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
    Biino, Ginevra
    Natl Res Council Italy, Inst Mol Genet, Pavia, Italy.
    Boehnke, Michael
    Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA;Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
    Boerwinkle, Eric
    Univ Texas Hlth Sci Ctr Houston, Human Genet Ctr, Houston, TX 77030 USA.
    Boissel, Mathilde
    Univ Lille, Inst Pasteur Lille, CNRS, UMR 8199,EGID, Lille, France.
    Bottinger, Erwin P.
    Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA;Hasso Plattner Inst, Digital Hlth Ctr, Potsdam, Germany;Univ Potsdam, Potsdam, Germany.
    Boutin, Thibaud S.
    Univ Edinburgh, Inst Genet & Mol Med, Med Res Council, Human Genet Unit, Edinburgh, Midlothian, Scotland.
    Brenner, Hermann
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany;Heidelberg Univ, Network Aging Res, Heidelberg, Germany.
    Brumat, Marco
    Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
    Burkhardt, Ralph
    Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany;Univ Leipzig, Inst Lab Med Clin Chem & Mol Diagnost, Leipzig, Germany;Univ Hosp Regensburg, Inst Clin Chem & Lab Med, Regensburg, Germany.
    Butterworth, Adam S.
    Univ Cambridge, Dept Publ Hlth & Primary Care, MRC BHF Cardiovasc Epidemiol Unit, Cambridge, England;Univ Cambridge, Natl Inst Hlth Res Blood & Transplant Res Unit Do, Cambridge, England.
    Campana, Eric
    Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
    Campbell, Archie
    Univ Edinburgh, Inst Genet & Mol Med, Ctr Genom & Expt Med, Edinburgh, Midlothian, Scotland.
    Campbell, Harry
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Ctr Global Hlth Res, Edinburgh, Midlothian, Scotland.
    Canouil, Mickael
    Univ Lille, Inst Pasteur Lille, CNRS, UMR 8199,EGID, Lille, France.
    Carroll, Robert J.
    Vanderbilt Univ, Med Ctr, Dept Biomed Informat, Nashville, TN USA.
    Catamo, Eulalia
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy.
    Chambers, John C.
    Imperial Coll London, Sch Publ Hlth, Fac Med, Dept Epidemiol & Biostat, London, England;Nanyang Technol Univ, Lee Kong Chian Sch Med, Singapore, Singapore;Ealing Gen Hosp, Dept Cardiol, Middlesex, England;Imperial Coll London, Imperial Coll Healthcare NHS Trust, London, England;Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England.
    Chee, Miao-Ling
    Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
    Chee, Miao-Li
    Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
    Chen, Xu
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Cheng, Ching-Yu
    Natl Univ Hlth Syst, Singapore, Singapore;Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore;Duke NUS Med Sch, Ophthalmol & Visual Sci Acad Clin Program Eye ACP, Singapore, Singapore;Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Ophthalmol, Singapore, Singapore.
    Cheng, Yurong
    Univ Freiburg, Fac Med, Dept Biometry Epidemiol & Med Bioinformat, Inst Genet Epidemiol, Freiburg, Germany;Univ Freiburg, Med Ctr, Freiburg, Germany.
    Christensen, Kaare
    Southern Denmark Univ, Dept Publ Hlth, Unit Epidemiol Biostat & Biodemog, Odense, Denmark.
    Cifkova, Renata
    Charles Univ Prague, Fac Med 1, Ctr Cardiovasc Prevent, Prague, Czech Republic;Thomayer Hosp, Prague, Czech Republic;Charles Univ Prague, Fac Med 1, Dept Med 2, Prague, Czech Republic.
    Ciullo, Marina
    Adriano Buzzati Traverso CNR, Inst Genet & Biophys, Naples, Italy;IRCCS Neuromed, Pozzilli, Italy.
    Concas, Maria Pina
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy.
    Cook, James P.
    Univ Liverpool, Dept Biostat, Liverpool, Merseyside, England.
    Coresh, Josef
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
    Corre, Tanguy
    Univ Lausanne, Dept Computat Biol, Lausanne, Switzerland;Swiss Inst Bioinformat, Lausanne, Switzerland;Lausanne Univ Hosp, Inst Social & Prevent Med, Lausanne, Switzerland.
    Sala, Cinzia Felicita
    San Raffaele Res Inst, Milan, Italy.
    Cusi, Daniele
    Natl Res Council Italy, Inst Biomed Technol, Milan, Italy;Bio4Dreams Business Nursery Life Sci, Milan, Italy.
    Danesh, John
    Univ Cambridge, Sch Clin Med, Dept Publ Hlth & Primary Care, Cambridge, England.
    Daw, E. Warwick
    Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
    De Borst, Martin H.
    Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, Groningen, Netherlands.
    De Grandi, Alessandro
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    De Mutsert, Renee
    Leiden Univ, Med Ctr, Dept Clin Epidemiol, Leiden, Netherlands.
    De Vries, Aiko P. J.
    Leiden Univ, Med Ctr, Dept Internal Med, Sect Nephrol, Leiden, Netherlands.
    Degenhardt, Frauke
    Christian Albrechts Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
    Delgado, Graciela
    Heidelberg Univ, Med Fac Mannheim, Dept Med, Nephrol,Hypertensiol,Rheumatol,Endocrinol,Diabet, Mannheim, Germany.
    Demirkan, Ayse
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
    Di Angelantonio, Emanuele
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England;NHS Blood & Transplant, Cambridge, England.
    Dittrich, Katalin
    Univ Leipzig, Hosp Children & Adolescents, Dept Women & Child Hlth, Leipzig, Germany;Univ Leipzig, Ctr Pediat Res, Leipzig, Germany.
    Divers, Jasmin
    Wake Forest Sch Med, Publ Hlth Sci Biostat, Winston Salem, NC USA.
    Dorajoo, Rajkumar
    Agcy Sci Technol & Res, Genome Inst Singapore, Singapore, Singapore.
    Eckardt, Kai-Uwe
    Charite, Intens Care Med, Berlin, Germany;Friedrich Alexander Univ Erlangen Nurnberg FAU, Dept Nephrol & Hypertens, Erlangen, Germany.
    Ehret, Georg
    Geneva Univ Hosp, Cardiol, Geneva, Switzerland.
    Elliott, Paul
    Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, Dept Epidemiol & Biostat, London, England;Imperial Coll London, Imperial Coll, NIHR Biomed Res Ctr, London, England;Imperial Coll London, Dementia Res Inst, London, England;Hlth Data Res UK London, London, England.
    Endlich, Karlhans
    DZHK German Ctr Cardiovasc Res, Partner Site Greifswald, Greifswald, Germany;Univ Med Greifswald, Dept Anat & Cell Biol, Greifswald, Germany.
    Evans, Michele K.
    NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, US NIH, Baltimore, MD 21224 USA.
    Felix, Janine F.
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands;Univ Med Ctr Rotterdam, Erasmus MC, Generat R Study Grp, Rotterdam, Netherlands;Univ Med Ctr Rotterdam, Erasmus MC, Dept Pediat, Rotterdam, Netherlands.
    Foo, Valencia Hui Xian
    Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
    Franco, Oscar H.
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands;Univ Bern, ISPM, Bern, Switzerland.
    Franke, Andre
    Christian Albrechts Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
    Freedman, Barry I.
    Wake Forest Sch Med, Internal Med, Sect Nephrol, Winston Salem, NC USA.
    Freitag-Wolf, Sandra
    Univ Kiel, Univ Hosp Schleswig Holstein, Inst Med Informat & Stat, Kiel, Germany.
    Friedlander, Yechiel
    Hebrew Univ Jerusalem, Sch Publ Hlth & Community Med, Jerusalem, Israel.
    Froguel, Philippe
    Univ Lille, Inst Pasteur Lille, CNRS, UMR 8199,EGID, Lille, France;Imperial Coll London, Dept Genom Common Dis, London, England.
    Gansevoort, Ron T.
    Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, Groningen, Netherlands.
    Gao, He
    Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, Dept Epidemiol & Biostat, London, England.
    Gasparini, Paolo
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy;Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
    Gaziano, J. Michael
    VA Boston Healthcare Syst, VA Cooperat Studies Program, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA.
    Giedraitis, Vilmantas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Gieger, Christian
    German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, Neuherberg, Germany;German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany;German Ctr Diabet Res DZD, Neuherberg, Germany.
    Girotto, Giorgia
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy;Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
    Giulianini, Franco
    Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA.
    Gogele, Martin
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Gordon, Scott D.
    QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
    Gudbjartsson, Daniel F.
    Amgen Inc, deCODE Genet, Reykjavik, Iceland.
    Gudnason, Vilmundur
    Iceland Heart Assoc, Kopavogur, Iceland;Univ Iceland, Sch Hlth Sci, Fac Med, Reykjavik, Iceland.
    Haller, Toomas
    Univ Tartu, Inst Genom, Estonian Genome Ctr, Tartu, Estonia.
    Hamet, Pavel
    CHUM, Montreal Univ Hosp, Res Ctr, Montreal, PQ, Canada;Medpharmgene, Montreal, PQ, Canada.
    Harris, Tamara B.
    NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, US NIH, Bethesda, MD 20892 USA.
    Hartman, Catharina A.
    Univ Groningen, Univ Med Ctr Groningen, nterdisciplinary Ctr Psychopathol & Emot Regulat, Groningen, Netherlands.
    Hayward, Caroline
    Univ Edinburgh, Inst Genet & Mol Med, Med Res Council, Human Genet Unit, Edinburgh, Midlothian, Scotland.
    Hellwege, Jacklyn N.
    Vanderbilt Univ, Med Ctr, Vanderbilt Genet Inst, Nashville, TN USA;Vanderbilt Univ, Med Ctr, Dept Med, Div Epidemiol,Vanderbilt Genet Inst, Nashville, TN 37232 USA;Vanderbilt Univ, Tennessee Valley Healthcare Syst 626, Dept Vet Affairs, 221 Kirkland Hall, Nashville, TN 37235 USA.
    Heng, Chew-Kiat
    Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Paediat, Singapore, Singapore;Natl Univ Hlth Syst, Khoo Teck Puat Natl Univ, Childrens Med Inst, Singapore, Singapore.
    Hicks, Andrew A.
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Hofer, Edith
    Med Univ Graz, Dept Neurol, Clin Div Neurogeriatr, Graz, Austria;Med Univ Graz, Inst Med Informat Stat & Documentat, Graz, Austria.
    Huang, Wei
    Chinese Natl Human Genome Ctr, Shanghai MOST Key Lab Hlth & Dis Genom, Dept Genet, Shanghai, Peoples R China;Shanghai Ind Technol Inst, Shanghai, Peoples R China.
    Hutri-Kahonen, Nina
    Tampere Univ Hosp, Dept Pediat, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Dept Pediat, Tampere, Finland.
    Hwang, Shih-Jen
    NHLBIs Framingham Heart Study, Framingham, MA USA;NHLBI, Ctr Populat Studies, Framingham, MA USA.
    Ikram, M. Arfan
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
    Indridason, Olafur S.
    Natl Univ Hosp Iceland, Landspitali, Internal Med Serv, Div Nephrol, Reykjavik, Iceland.
    Ingelsson, Erik
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Stanford Univ, Dept Med, Sch Med, Div Cardiovasc Med, Stanford, CA 94305 USA;Stanford Univ, Stanford Cardiovasc Inst, Stanford, CA 94305 USA;Stanford Univ, Stanford Diabet Res Ctr, Stanford, CA 94305 USA.
    Ising, Marcus
    Max Planck Inst Psychiat, Munich, Germany.
    Jaddoe, Vincent W. V.
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands;Charles Univ Prague, Fac Med 1, Ctr Cardiovasc Prevent, Prague, Czech Republic;Thomayer Hosp, Prague, Czech Republic;Univ Med Ctr Rotterdam, Erasmus MC, Dept Pediat, Rotterdam, Netherlands.
    Jakobsdottir, Johanna
    Univ Iceland, Ctr Publ Hlth Sci, Reykjavik, Iceland.
    Jonas, Jost B.
    Heidelberg Univ, Med Fac Mannheim, Dept Ophthalmol, Mannheim, Germany;Capital Med Univ, Beijing Tongren Hosp, Beijing Key Lab Ophthalmol & Visual Sci, Beijing Inst Ophthalmol, Beijing, Peoples R China.
    Joshi, Peter K.
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Ctr Global Hlth Res, Edinburgh, Midlothian, Scotland.
    Josyula, Navya Shilpa
    Biomed & Translat Informat Inst, Geisinger Res, Rockville, MD USA.
    Jung, Bettina
    Univ Hosp Regensburg, Dept Nephrol, Regensburg, Germany.
    Kahonen, Mika
    Tampere Univ Hosp, Dept Clin Physiol, Tampere, Finland;Tampere Univ, Fac Med & Hlth Technol, Finnish Cardiovasc Res Ctr Tampere, Dept Clin Physiol, Tampere, Finland.
    Kamatani, Yoichiro
    RIKEN, Ctr Integrat Med Sci IMS, Lab Stat Anal, Yokohama, Kanagawa, Japan;Kyoto Univ, Grad Sch Med, Kyoto McGill Int Collaborat Sch Genom Med, Kyoto, Japan.
    Kammerer, Candace M.
    Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15261 USA.
    Kanai, Masahiro
    RIKEN, Ctr Integrat Med Sci IMS, Lab Stat Anal, Yokohama, Kanagawa, Japan;Harvard Med Sch, Dept Biomed Informat, Boston, MA 02115 USA.
    Kastarinen, Mika
    Kuopio Univ Hosp, Dept Med, Kuopio, Finland.
    Kerr, Shona M.
    Univ Edinburgh, Inst Genet & Mol Med, Med Res Council, Human Genet Unit, Edinburgh, Midlothian, Scotland.
    Khor, Chiea-Chuen
    Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore;Agcy Sci Technol & Res, Genome Inst Singapore, Singapore, Singapore.
    Kiess, Wieland
    Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany;Univ Leipzig, Hosp Children & Adolescents, Dept Women & Child Hlth, Leipzig, Germany;Univ Leipzig, Ctr Pediat Res, Leipzig, Germany.
    Kleber, Marcus E.
    Heidelberg Univ, Med Fac Mannheim, Dept Med, Nephrol,Hypertensiol,Rheumatol,Endocrinol,Diabet, Mannheim, Germany.
    Koenig, Wolfgang
    Tech Univ Munich, Deutsches Herzzentrum Munchen, Munich, Germany;DZHK German Ctr Cardiovasc Res, Partner Site Munich Heart Alliance, Munich, Germany;Univ Ulm, Inst Epidemiol & Biostat, Ulm, Germany.
    Kooner, Jaspal S.
    Ealing Gen Hosp, Dept Cardiol, Middlesex, England;Imperial Coll London, Imperial Coll Healthcare NHS Trust, London, England;Imperial Coll London, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England;Imperial Coll London, Natl Heart & Lung Inst, London, England.
    Korner, Antje
    Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany;Univ Leipzig, Hosp Children & Adolescents, Dept Women & Child Hlth, Leipzig, Germany;Univ Leipzig, Ctr Pediat Res, Leipzig, Germany.
    Kovacs, Peter
    Univ Leipzig, Integrated Res & Treatment Ctr Adipos Dis, Leipzig, Germany.
    Kraja, Aldi T.
    Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
    Krajcoviechova, Alena
    Charles Univ Prague, Fac Med 1, Ctr Cardiovasc Prevent, Prague, Czech Republic;Thomayer Hosp, Prague, Czech Republic;Charles Univ Prague, Fac Med 1, Dept Med 2, Prague, Czech Republic.
    Kramer, Holly
    Loyola Univ Chicago, Dept Publ Hlth Sci, Maywood, IL USA;Loyola Univ, Div Nephrol & Hypertens, Chicago, IL 60611 USA.
    Kramer, Bernhard K.
    Heidelberg Univ, Med Fac Mannheim, Dept Med, Nephrol,Hypertensiol,Rheumatol,Endocrinol,Diabet, Mannheim, Germany.
    Kronenberg, Florian
    Med Univ Innsbruck, Dept Med Genet Mol & Clin Pharmacol, Div Genet Epidemiol, Innsbruck, Austria.
    Kubo, Michiaki
    RIKEN, Ctr Integrat Med Sci IMS, Yokohama, Kanagawa, Japan.
    Kuhnel, Brigitte
    German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, Neuherberg, Germany.
    Kuokkanen, Mikko
    Natl Inst Hlth & Welf, Dept Publ Hlth Solut, Helsinki, Finland;Univ Helsinki, Diabet & Obes Res Program, Helsinki, Finland.
    Kuusisto, Johanna
    Kuopio Univ Hosp, Dept Med, Kuopio, Finland;Univ Eastern Finland, Internal Med, Inst Clin Med, Kuopio, Finland.
    La Bianca, Martina
    IRCCS Burlo Garofolo, Inst Maternal & Child Hlth, Trieste, Italy.
    Laakso, Markku
    Kuopio Univ Hosp, Dept Med, Kuopio, Finland;Univ Eastern Finland, Internal Med, Inst Clin Med, Kuopio, Finland.
    Lange, Leslie A.
    Univ Colorado Denver, Sch Med, Div Biomed Informat & Personalized Med, Anschutz Med Campus, Aurora, CO USA.
    Langefeld, Carl D.
    Wake Forest Sch Med, Publ Hlth Sci Biostat, Winston Salem, NC USA.
    Lee, Jeannette Jen-Mai
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore;Natl Univ Hlth Syst, Singapore, Singapore.
    Lehne, Benjamin
    Imperial Coll London, Sch Publ Hlth, Fac Med, Dept Epidemiol & Biostat, London, England.
    Lehtimaki, Terho
    Fimlab Labs, Dept Clin Chem, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Dept Clin Chem, Tampere, Finland.
    Lieb, Wolfgang
    Univ Kiel, Inst Epidemiol & Biobank Popgen, Kiel, Germany.
    Lim, Su-Chi
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore, Singapore;Natl Univ Hlth Syst, Singapore, Singapore;Khoo Teck Puat Hosp, Diabet Ctr, Singapore, Singapore.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Epidemiology.
    Lindgren, Cecilia M.
    Univ Oxford, Nuffield Dept Med, Oxford, England;Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
    Liu, Jun
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
    Liu, Jianjun
    Natl Univ Hlth Syst, Singapore, Singapore;Agcy Sci Technol & Res, Genome Inst Singapore, Singapore, Singapore;Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore, Singapore.
    Loeffler, Markus
    Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany;Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany.
    Loos, Ruth J. F.
    Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Mindich Child Hlth & Dev Inst, New York, NY 10029 USA.
    Lucae, Susanne
    Max Planck Inst Psychiat, Munich, Germany.
    Lukas, Mary Ann
    GlaxoSmithKline, Target Sci Genet, Albuquerque, NM USA.
    Lyytikainen, Leo-Pekka
    Fimlab Labs, Dept Clin Chem, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Dept Clin Chem, Tampere, Finland.
    Magi, Reedik
    Univ Tartu, Inst Genom, Estonian Genome Ctr, Tartu, Estonia.
    Magnusson, Patrik K. E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Mahajan, Anubha
    Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England;Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
    Martin, Nicholas G.
    QIMR Berghofer Med Res Inst, Brisbane, Qld, Australia.
    Martins, Jade
    Max Planck Inst Psychiat, Dept Translat Res Psychiat, Munich, Germany.
    Marz, Winfried
    Synlab Holding Deutschland GmbH, Synlab Acad, Mannheim, Germany;Med Univ Graz, Clin Inst Med & Chem Lab Diagnost, Graz, Austria;Heidelberg Univ, Med Fac Mannheim, Med Clin 5, Mannheim, Germany.
    Mascalzoni, Deborah
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Matsuda, Koichi
    Univ Tokyo, Grad Sch Frontier Sci, Lab Clin Genome Sequencing, Tokyo, Japan.
    Meisinger, Christa
    German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Independent Res Grp Clin Epidemiol, Neuherberg, Germany;Ludwig Maximilians Univ Munchen, UNIKA T Augsburg, Chair Epidemiol, Augsburg, Germany.
    Meitinger, Thomas
    DZHK German Ctr Cardiovasc Res, Partner Site Munich Heart Alliance, Munich, Germany;Helmholtz Zentrum Munchen, Inst Human Genet, Neuherberg, Germany;Tech Univ Munich, Inst Human Genet, Munich, Germany.
    Melander, Olle
    Lund Univ, Dept Clincial Sci Malmo, Hypertens & Cardiovasc Dis, Malmo, Sweden.
    Metspalu, Andres
    Univ Tartu, Inst Genom, Estonian Genome Ctr, Tartu, Estonia.
    Mikaelsdottir, Evgenia K.
    Amgen Inc, deCODE Genet, Reykjavik, Iceland.
    Milaneschi, Yuri
    Vrije Univ Amsterdam, Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
    Miliku, Kozeta
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands;Univ Med Ctr Rotterdam, Erasmus MC, Generat R Study Grp, Rotterdam, Netherlands;Univ Med Ctr Rotterdam, Erasmus MC, Dept Pediat, Rotterdam, Netherlands.
    Mishra, Pashupati P.
    Fimlab Labs, Dept Clin Chem, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Dept Clin Chem, Tampere, Finland.
    Program, V. A. Million Veteran
    Univ Freiburg, Fac Med, Dept Biometry Epidemiol & Med Bioinformat, Inst Genet Epidemiol, Freiburg, Germany;Univ Freiburg, Med Ctr, Freiburg, Germany.
    Mohlke, Karen L.
    Univ N Carolina, Dept Genet, Chapel Hill, NC 27515 USA.
    Mononen, Nina
    Fimlab Labs, Dept Clin Chem, Tampere, Finland;Univ Tampere, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Dept Clin Chem, Tampere, Finland.
    Montgomery, Grant W.
    Univ Queensland, Inst Mol Biosci, St Lucia, Qld, Australia.
    Mook-Kanamori, Dennis O.
    Leiden Univ, Med Ctr, Dept Clin Epidemiol, Leiden, Netherlands;Leiden Univ, Med Ctr, Dept Publ Hlth & Primary Care, Leiden, Netherlands.
    Mychaleckyj, Josyf C.
    Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA USA.
    Nadkarni, Girish N.
    Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Med, Div Nephrol, New York, NY 10029 USA.
    Nalls, Mike A.
    NIA, Lab Neurogenet, NIH, Bethesda, MD 20892 USA;Data Tecn Int, Glen Echo, MD USA.
    Nauck, Matthias
    DZHK German Ctr Cardiovasc Res, Partner Site Greifswald, Greifswald, Germany;Univ Med Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
    Nikus, Kjell
    Tampere Univ Hosp, Heart Ctr, Dept Cardiol, Tampere, Finland;Tampere Univ, Fac Med & Life Sci, Finnish Cardiovasc Res Ctr Tampere, Dept Cardiol, Tampere, Finland.
    Ning, Boting
    Boston Univ, Sch Med, Dept Biostat, Boston, MA 02118 USA.
    Nolte, Ilja M.
    Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
    Noordam, Raymond
    Leiden Univ, Med Ctr, Dept Internal Med, Sect Gerontol & Geriatr, Leiden, Netherlands.
    O'Connell, Jeffrey
    Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
    O'Donoghue, Michelle L.
    Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA;TIMI Study Grp, Boston, MA USA.
    Olafsson, Isleifur
    Landspitali Univ Hosp, Dept Clin Biochem, Reykjavik, Iceland.
    Oldehinkel, Albertine J.
    Univ Groningen, Univ Med Ctr Groningen, nterdisciplinary Ctr Psychopathol & Emot Regulat, Groningen, Netherlands.
    Orho-Melander, Marju
    Lund Univ, Dept Clincial Sci Malmo, Diabetes & Cardiovasc Disease Genet Epidemi, Malmo, Sweden.
    Ouwehand, Willem H.
    Univ Cambridge, Sch Clin Med, Dept Publ Hlth & Primary Care, Cambridge, England.
    Padmanabhan, Sandosh
    Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.
    Palmer, Nicholette D.
    Wake Forest Sch Med, Biochem, Winston Salem, NC USA.
    Palsson, Runolfur
    Univ Iceland, Sch Hlth Sci, Fac Med, Reykjavik, Iceland;Natl Univ Hosp Iceland, Landspitali, Internal Med Serv, Div Nephrol, Reykjavik, Iceland.
    Penninx, Brenda W. J. H.
    Vrije Univ Amsterdam, Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
    Perls, Thomas
    Boston Univ, Sch Med, Dept Med, Geriatr Sect,Boston Med Ctr, Boston, MA 02118 USA.
    Perola, Markus
    Natl Inst Hlth & Welf, Helsinki, Finland.
    Pirastu, Mario
    UOS Sassari, Natl Res Council Italy, Inst Genet & Biomed Res, Sassari, Italy.
    Pirastu, Nicola
    Univ Edinburgh, Usher Inst Populat Hlth Sci & Informat, Ctr Global Hlth Res, Edinburgh, Midlothian, Scotland.
    Pistis, Giorgio
    Univ Hosp Lausanne, Dept Psychiat, Lausanne, Switzerland.
    Podgornaia, Anna I.
    Merck & Co Inc, Genet, Kenilworth, NJ USA.
    Polasek, Ozren
    Univ Split, Fac Med, Split, Croatia;Gen Info Ltd, Zagreb, Croatia.
    Ponte, Belen
    Geneva Univ Hosp, Serv Nephrol, Geneva, Switzerland.
    Porteous, David J.
    Univ Edinburgh, Inst Genet & Mol Med, Ctr Genom & Expt Med, Edinburgh, Midlothian, Scotland;Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland.
    Poulain, Tanja
    Univ Leipzig, LIFE Res Ctr Civilizat Dis, Leipzig, Germany.
    Pramstaller, Peter P.
    Univ Lubeck, Inst Biomed, Eurac Res, Bolzano, Italy.
    Preuss, Michael H.
    Icahn Sch Med Mt Sinai, Charles Bronfman Inst Personalized Med, New York, NY 10029 USA.
    Prins, Bram P.
    Univ Cambridge, Dept Publ Hlth & Primary Care, MRC BHF Cardiovasc Epidemiol Unit, Cambridge, England.
    Province, Michael A.
    Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA.
    Rabelink, Ton J.
    Leiden Univ, Med Ctr, Dept Internal Med, Sect Nephrol, Leiden, Netherlands;Leiden Univ, Med Ctr, Einthoven Lab Expt Vasc Res, Leiden, Netherlands.
    Raffield, Laura M.
    Univ N Carolina, Dept Genet, Chapel Hill, NC 27515 USA.
    Raitakari, Olli T.
    Turku Univ Hosp, Dept Clin Physiol & Nucl Med, Turku, Finland;Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
    Reil