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3 results on '"Kofink, Daniel"'

1. Subsequent Event Risk in Individuals With Established Coronary Heart Disease

Author

Patel, Riyaz S, Tragante, Vinicius, Schmidt, Amand F, McCubrey, Raymond O, Holmes, Michael V, Howe, Laurence J, Direk, Kenan, Åkerblom, Axel, Leander, Karin, Virani, Salim S, Kaminski, Karol A, Muehlschlegel, Jochen D, Allayee, Hooman, Almgren, Peter, Alver, Maris, Baranova, Ekaterina V, Behloui, Hassan, Boeckx, Bram, Braund, Peter S, Breitling, Lutz P, Delgado, Graciela, Duarte, Nubia E, Dubé, Marie-Pierre, Dufresne, Line, Eriksson, Niclas, Foco, Luisa, Scholz, Markus, Gijsberts, Crystel M, Glinge, Charlotte, Gong, Yan, Hartiala, Jaana, Heydarpour, Mahyar, Hubacek, Jaroslav A, Kleber, Marcus, Kofink, Daniel, Kotti, Salma, Kuukasjärvi, Pekka, Lee, Vei-Vei, Leiherer, Andreas, Lenzini, Petra A, Levin, Daniel, Lyytikäinen, Leo-Pekka, Martinelli, Nicola, Mons, Ute, Nelson, Christopher P, Nikus, Kjell, Pilbrow, Anna P, Ploski, Rafal, Klungel, Olaf H, Maitland-van der Zee, Anke H, Afd Pharmacoepi & Clinical Pharmacology, and Pharmacoepidemiology and Clinical Pharmacology

Subjects
myocardial infarction, genetics, prognosis, coronary artery disease, sedundary preventation
Abstract

BACKGROUND: The Genetics of Subsequent Coronary Heart Disease (GENIUS-CHD) consortium was established to facilitate discovery and validation of genetic variants and biomarkers for risk of subsequent CHD events, in individuals with established CHD. METHODS: The consortium currently includes 57 studies from 18 countries, recruiting 185 614 participants with either acute coronary syndrome, stable CHD, or a mixture of both at baseline. All studies collected biological samples and followed-up study participants prospectively for subsequent events. RESULTS: Enrollment into the individual studies took place between 1985 to present day with a duration of follow-up ranging from 9 months to 15 years. Within each study, participants with CHD are predominantly of self-reported European descent (38%-100%), mostly male (44%-91%) with mean ages at recruitment ranging from 40 to 75 years. Initial feasibility analyses, using a federated analysis approach, yielded expected associations between age (hazard ratio, 1.15; 95% CI, 1.14-1.16) per 5-year increase, male sex (hazard ratio, 1.17; 95% CI, 1.13-1.21) and smoking (hazard ratio, 1.43; 95% CI, 1.35-1.51) with risk of subsequent CHD death or myocardial infarction and differing associations with other individual and composite cardiovascular endpoints. CONCLUSIONS: GENIUS-CHD is a global collaboration seeking to elucidate genetic and nongenetic determinants of subsequent event risk in individuals with established CHD, to improve residual risk prediction and identify novel drug targets for secondary prevention. Initial analyses demonstrate the feasibility and reliability of a federated analysis approach. The consortium now plans to initiate and test novel hypotheses as well as supporting replication and validation analyses for other investigators.

Published
2019

2. Subsequent event risk in individuals with established coronary heart disease : design and rationale of the GENIUS-CHD consortium

Author

Patel, Riyaz, Tragante, Vinicius, Schmidt, Amand, McCubrey, Raymond, Holmes, Michael, Howe, Laurence, Direk, Kenan, Akerblom, Axel, Leander, Karin, Virani, Salim, Kaminski, Karol, Muehlschlegel, Jochen, Allayee, Hooman, Almgren, Peter, Alver, Maris, Baranova, Ekaterina, Behlouli, Hassan, Boeckx, Bram, Braund, Peter, Breitling, Lutz, Delgado, Graciela, Duarte, Nubia, Dube, Marie-Pierre, Dufresne, Line, Eriksson, Niclas, Foco, Luisa, Scholz, Markus, Gijsberts, Crystel, Glinge, Charlotte, Gong, Yan, Hartiala, Jaana, Heydarpour, Mahyar, Hubacek, Jaroslav, Kleber, Marcus, Kofink, Daniel, Kotti, Salma, Kuukasjarvi, Pekka, Lee, Vei-Vei, Leiherer, Andreas, Lenzini, Petra, Levin, Daniel, Lyytikainen, Leo-Pekka, Martinelli, Nicola, Mons, Ute, Nelson, Christopher, Nikus, Kjell, Pilbrow, Anna, Ploski, Rafal, Sun, Yan, Tanck, Michael, Tang, W.H., Trompet, Stella, van der Laan, Sander, van Setten, Jessica, Vilmundarson, Ragnar, Anselmi, Chiara, Vlachopoulou, Efthymia, Al Ali, Lawien, Boerwinkle, Eric, Briguori, Carlo, Carlquist, John, Carruthers, Kathryn, Casu, Gavino, Deanfield, John, Deloukas, Panos, Dudbridge, Frank, Engstrom, Thomas, Fitzpatrick, Natalie, Fox, Kim, Gigante, Bruna, James, Stefan, Lokki, Marja-Liisa, Lotufo, Paulo, Marziliano, Nicola, Muhlestein, Joseph, Newton-Cheh, Christopher, Pitha, Jan, Saely, Christoph, Samman-Tahhan, Ayman, Sandesara, Pratik, Teren, Andrej, Timmis, Adam, Van de Werf, Frans, Wauters, Els, Wilde, Arthur, Ford, Ian, Stott, David, Algra, Ale, Andreassi, Maria, Ardissino, Diego, Arsenault, Benoit, Ballantyne, Christie, Bergmeijer, Thomas, Bezzina, Connie, Body, Simon, Boersma, Eric, Bogaty, Peter, Bots, Michiel, Brenner, Hermann, Brugts, Jasper, Burkhardt, Ralph, Carpeggiani, Clara, Condorelli, Gianluigi, Cooper-DeHoff, Rhonda, Cresci, Sharon, Danchin, Nicolas, de Faire, Ulf, Doughty, Robert, Drexel, Heinz, Engert, James, Fox, Keith, Girelli, Domenico, Grobbee, Diederick, Hagstrom, Emil, Hazen, Stanley, Held, Claes, Hemingway, Harry, Hoefer, Imo, Hovingh, G., Jabbari, Reza, Johnson, Julie, Jukema, J., Kaczor, Marcin, Kahonen, Mika, Kettner, Jiri, Kiliszek, Marek, Klungel, Olaf, Lagerqvist, Bo, Lambrechts, Diether, Laurikka, Jari, Lehtimaki, Terho, Lindholm, Daniel, Mahmoodi, B., Maitland-van der Zee, Anke, McPherson, Ruth, Melander, Olle, Metspalu, Andres, Niemcunowicz-Janica, Anna, Olivieri, Oliviero, Opolski, Grzegorz, Palmer, Colin, Pasterkamp, Gerard, Pepine, Carl, Pereira, Alexandre, Pilote, Louise, Quyyumi, Arshed, Richards, A., Sanak, Marek, Siegbahn, Agneta, Simon, Tabassome, Sinisalo, Juha, Smith, J., Spertus, John, Stender, Steen, Stewart, Alexandre, Szczeklik, Wojciech, Szpakowicz, Anna, Tardif, Jean-Claude, ten Berg, Jurrien, Tfelt-Hansen, Jacob, Thanassoulis, George, Thiery, Joachim, Torp-Pedersen, Christian, van der Graaf, Yolanda, Visseren, Frank, Waltenberger, Johannes, van der Harst, Pim, Lang, Chim, Sattar, Naveed, Cameron, Vicky, Anderson, Jeffrey, Brophy, James, Pare, Guillaume, Horne, Benjamin, Marz, Winfried, Wallentin, Lars, Samani, Nilesh, Hingorani, Aroon, and Asselbergs, Folkert

Subjects
myocardial infarction, genetics, prognosis, coronary artery disease, secondary prevention
Abstract

BACKGROUND: The Genetics of Subsequent Coronary Heart Disease (GENIUS-CHD) consortium was established to facilitate discovery and validation of genetic variants and biomarkers for risk of subsequent CHD events, in individuals with established CHD. METHODS: The consortium currently includes 57 studies from 18 countries, recruiting 185 614 participants with either acute coronary syndrome, stable CHD, or a mixture of both at baseline. All studies collected biological samples and followed-up study participants prospectively for subsequent events. RESULTS: Enrollment into the individual studies took place between 1985 to present day with a duration of follow-up ranging from 9 months to 15 years. Within each study, participants with CHD are predominantly of self-reported European descent (38%-100%), mostly male (44%–91%) with mean ages at recruitment ranging from 40 to 75 years. Initial feasibility analyses, using a federated analysis approach, yielded expected associations between age (hazard ratio, 1.15; 95% CI, 1.14-1.16) per 5-year increase, male sex (hazard ratio, 1.17; 95% CI, 1.13-1.21) and smoking (hazard ratio, 1.43; 95% CI, 1.35-1.51) with risk of subsequent CHD death or myocardial infarction and differing associations with other individual and composite cardiovascular endpoints. CONCLUSIONS: GENIUS-CHD is a global collaboration seeking to elucidate genetic and nongenetic determinants of subsequent event risk in individuals with established CHD, to improve residual risk prediction and identify novel drug targets for secondary prevention. Initial analyses demonstrate the feasibility and reliability of a federated analysis approach. The consortium now plans to initiate and test novel hypotheses as well as supporting replication and validation analyses for other investigators.

Published
2019

3. Loss of Y Chromosome in Blood Is Associated With Major Cardiovascular Events During Follow-Up in Men After Carotid Endarterectomy.

Author

Haitjema, Saskia, Kofink, Daniel, van Setten, Jessica, van der Laan, Sander W., Schoneveld, Arjan H., Eales, James, Tomaszewski, Maciej, de Jager, Saskia C. A., Pasterkamp, Gerard, Asselbergs, Folkert W., and den Ruijter, Hester M.

Abstract

Background--Recent studies found an immune regulatory role for Y chromosome and a relationship between loss of Y chromosome (LOY) in blood cells and a higher risk of cancer and mortality. Given involvement of immune cells in atherosclerosis, we hypothesized that LOY is associated with the severity of atherosclerotic plaque characteristics and outcome in men undergoing carotid endarterectomy. Methods and Results--LOY was quantified in blood and plaque from raw intensity genotyping data in men within the Athero-Express biobank study. Plaques were dissected, and the culprit lesions used for histology and the measurement of inflammatory proteins. We tested LOY for association with (inflammatory) atherosclerotic plaque phenotypes and cytokines and assessed the association of LOY with secondary events during 3-year follow-up. Of 366 patients with carotid endarterectomy, 61 exhibited some degree of LOY in blood. LOY was also present in atherosclerotic plaque lesions (n=8/242, 3%). LOY in blood was negatively associated with age (β=-0.03/10 y; r²=0.07; P=1.6x10-7) but not with cardiovascular disease severity at baseline. LOY in blood was associated with a larger atheroma size (odds ratio, 2.15; 95% confidence interval, 1.06-4.76; P=0.04); however, this association was not significant after correction for multiple testing. LOY was independently associated with secondary major cardiovascular events (hazard ratio=2.28; 95% confidence interval, 1.11-4.67; P=0.02) in blood when corrected for confounders. Conclusions--In this hypothesis-generating study, LOY in blood is independently associated with secondary major cardiovascular events in a severely atherosclerotic population. Our data could indicate that LOY affects secondary outcome via other mechanisms than inflammation in the atherosclerotic plaque. [ABSTRACT FROM AUTHOR]

Published
2017
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