@article {8557,
	title = {{Genetic Risk Prediction of Atrial Fibrillation},
	journal = {Circulation},
	volume = {135},
	year = {2017},
	month = {Apr},
	pages = {1311{\textendash}1320},
	abstract = {Atrial fibrillation (AF) has a substantial genetic basis. Identification of individuals at greatest AF risk could minimize the incidence of cardioembolic stroke.\ To determine whether genetic data can stratify risk for development of AF, we examined associations between AF genetic risk scores and incident AF in 5 prospective studies comprising 18 919 individuals of European ancestry. We examined associations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40\%]) and 3028 referents. Scores were based on 11 to 719 common variants ({\^a}{\textperthousand}{\textyen}5\%) associated with AF at P values ranging from <1{\~A}{\textemdash}10-3 to <1{\~A}{\textemdash}10-8 in a prior independent genetic association study.\ Incident AF occurred in 1032 individuals (5.5\%). AF genetic risk scores were associated with new-onset AF after adjustment for clinical risk factors. The pooled hazard ratio for incident AF for the highest versus lowest quartile of genetic risk scores ranged from 1.28 (719 variants; 95\% confidence interval, 1.13-1.46; P=1.5{\~A}{\textemdash}10-4) to 1.67 (25 variants; 95\% confidence interval, 1.47-1.90; P=9.3{\~A}{\textemdash}10-15). Discrimination of combined clinical and genetic risk scores varied across studies and scores (maximum C statistic, 0.629-0.811; maximum {\^I}{\textquotedblright}C statistic from clinical score alone, 0.009-0.017). AF genetic risk was associated with stroke in age- and sex-adjusted models. For example, individuals in the highest versus lowest quartile of a 127-variant score had a 2.49-fold increased odds of cardioembolic stroke (95\% confidence interval, 1.39-4.58; P=2.7{\~A}{\textemdash}10-3). The effect persisted after the exclusion of individuals (n=70) with known AF (odds ratio, 2.25; 95\% confidence interval, 1.20-4.40; P=0.01).\ Comprehensive AF genetic risk scores were associated with incident AF beyond associations for clinical AF risk factors but offered small improvements in discrimination. AF genetic risk was also associated with cardioembolic stroke in age- and sex-adjusted analyses. Efforts are warranted to determine whether AF genetic risk may improve identification of subclinical AF or help distinguish between stroke mechanisms.},
	author = {Lubitz, S. A. and Yin, X. and Lin, H. J. and Kolek, M. and Smith, J. G. and Trompet, S. and Rienstra, M. and Rost, N. S. and Teixeira, P. L. and Almgren, P. and Anderson, C. D. and Chen, L. Y. and Engstr?m, G. and Ford, I. and Furie, K. L. and Guo, X. and Larson, M. G. and Lunetta, K. L. and Macfarlane, P. W. and Psaty, B. M. and Soliman, E. Z. and Sotoodehnia, N. and Stott, D. J. and Taylor, K. D. and Weng, L. C. and Yao, J. and Geelhoed, B. and Verweij, N. and Siland, J. E. and Kathiresan, S. and Roselli, C. and Roden, D. M. and van der Harst, P. and Darbar, D. and Jukema, J. W. and Melander, O. and Rosand, J. and Rotter, J. I. and Heckbert, S. R. and Ellinor, P. T. and Alonso, A. and Benjamin, E. J.}
}
@article {8289,
	title = {{Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure},
	journal = {Nat Commun},
	volume = {11},
	year = {2020},
	month = {01},
	pages = {163},
	abstract = {Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies.},
	author = {Shah, S. and Henry, A. and Roselli, C. and Lin, H. and Sveinbj?rnsson, G. and Fatemifar, G. and Hedman, ?. K. and Wilk, J. B. and Morley, M. P. and Chaffin, M. D. and Helgadottir, A. and Verweij, N. and Dehghan, A. and Almgren, P. and Andersson, C. and Aragam, K. G. and ?rnl?v, J. and Backman, J. D. and Biggs, M. L. and Bloom, H. L. and Brandimarto, J. and Brown, M. R. and Buckbinder, L. and Carey, D. J. and Chasman, D. I. and Chen, X. and Chen, X. and Chung, J. and Chutkow, W. and Cook, J. P. and Delgado, G. E. and Denaxas, S. and Doney, A. S. and D?rr, M. and Dudley, S. C. and Dunn, M. E. and Engstr?m, G. and Esko, T. and Felix, S. B. and Finan, C. and Ford, I. and Ghanbari, M. and Ghasemi, S. and Giedraitis, V. and Giulianini, F. and Gottdiener, J. S. and Gross, S. and Gu?bjartsson, D. F. and Gutmann, R. and Haggerty, C. M. and van der Harst, P. and Hyde, C. L. and Ingelsson, E. and Jukema, J. W. and Kavousi, M. and Khaw, K. T. and Kleber, M. E. and K?ber, L. and Koekemoer, A. and Langenberg, C. and Lind, L. and Lindgren, C. M. and London, B. and Lotta, L. A. and Lovering, R. C. and Luan, J. and Magnusson, P. and Mahajan, A. and Margulies, K. B. and M?rz, W. and Melander, O. and Mordi, I. R. and Morgan, T. and Morris, A. D. and Morris, A. P. and Morrison, A. C. and Nagle, M. W. and Nelson, C. P. and Niessner, A. and Niiranen, T. and O{\textquoteright}Donoghue, M. L. and Owens, A. T. and Palmer, C. N. A. and Parry, H. M. and Perola, M. and Portilla-Fernandez, E. and Psaty, B. M. and Rice, K. M. and Ridker, P. M. and Romaine, S. P. R. and Rotter, J. I. and Salo, P. and Salomaa, V. and van Setten, J. and Shalaby, A. A. and Smelser, D. T. and Smith, N. L. and Stender, S. and Stott, D. J. and Svensson, P. and Tammesoo, M. L. and Taylor, K. D. and Teder-Laving, M. and Teumer, A. and Thorgeirsson, G. and Thorsteinsdottir, U. and Torp-Pedersen, C. and Trompet, S. and Tyl, B. and Uitterlinden, A. G. and Veluchamy, A. and V?lker, U. and Voors, A. A. and Wang, X. and Wareham, N. J. and Waterworth, D. and Weeke, P. E. and Weiss, R. and Wiggins, K. L. and Xing, H. and Yerges-Armstrong, L. M. and Yu, B. and Zannad, F. and Zhao, J. H. and Hemingway, H. and Samani, N. J. and McMurray, J. J. V. and Yang, J. and Visscher, P. M. and Newton-Cheh, C. and Malarstig, A. and Holm, H. and Lubitz, S. A. and Sattar, N. and Holmes, M. V. and Cappola, T. P. and Asselbergs, F. W. and Hingorani, A. D. and Kuchenbaecker, K. and Ellinor, P. T. and Lang, C. C. and Stefansson, K. and Smith, J. G. and Vasan, R. S. and Swerdlow, D. I. and Lumbers, R. T. and Abecasis, G. and Backman, J. and Bai, X. and Balasubramanian, S. and Banerjee, N. and Baras, A. and Barnard, L. and Beechert, C. and Blumenfeld, A. and Cantor, M. and Chai, Y. and Chung, J. and Coppola, G. and Damask, A. and Dewey, F. and Economides, A. and Eom, G. and Forsythe, C. and Fuller, E. D. and Gu, Z. and Gurski, L. and Guzzardo, P. M. and Habegger, L. and Hahn, Y. and Hawes, A. and van Hout, C. and Jones, M. B. and Khalid, S. and Lattari, M. and Li, A. and Lin, N. and Liu, D. and Lopez, A. and Manoochehri, K. and Marchini, J. and Marcketta, A. and Maxwell, E. K. and McCarthy, S. and Mitnaul, L. J. and O{\textquoteright}Dushlaine, C. and Overton, J. D. and Padilla, M. S. and Paulding, C. and Penn, J. and Pradhan, M. and Reid, J. G. and Schleicher, T. D. and Schurmann, C. and Shuldiner, A. and Staples, J. C. and Sun, D. and Toledo, K. and Ulloa, R. H. and Widom, L. and Wolf, S. E. and Yadav, A. and Ye, B.}
}
@article {8925,
	title = {{The genomics of heart failure: design and rationale of the HERMES consortium},
	journal = {ESC Heart Fail},
	year = {2021},
	month = {Sep},
	abstract = {The HERMES (HEart failure Molecular Epidemiology for Therapeutic targetS) consortium aims to identify the genomic and molecular basis of heart failure.\ under an additive genetic model.\ HERMES is a global collaboration aiming to (i) identify the genetic determinants of heart failure; (ii) generate insights into the causal pathways leading to heart failure and enable genetic approaches to target prioritization; and (iii) develop genomic tools for disease stratification and risk prediction.},
	author = {Lumbers, R. T. and Shah, S. and Lin, H. and Czuba, T. and Henry, A. and Swerdlow, D. I. and Malarstig, A. and Andersson, C. and Verweij, N. and Holmes, M. V. and {\"A}rnl{\"o}v, J. and Svensson, P. and Hemingway, H. and Sallah, N. and Almgren, P. and Aragam, K. G. and Asselin, G. and Backman, J. D. and Biggs, M. L. and Bloom, H. L. and Boersma, E. and Brandimarto, J. and Brown, M. R. and Brunner-La Rocca, H. P. and Carey, D. J. and Chaffin, M. D. and Chasman, D. I. and Chazara, O. and Chen, X. and Chen, X. and Chung, J. H. and Chutkow, W. and Cleland, J. G. F. and Cook, J. P. and de Denus, S. and Dehghan, A. and Delgado, G. E. and Denaxas, S. and Doney, A. S. and D{\"o}rr, M. and Dudley, S. C. and Engstr{\"o}m, G. and Esko, T. and Fatemifar, G. and Felix, S. B. and Finan, C. and Ford, I. and Fougerousse, F. and Fouodjio, R. and Ghanbari, M. and Ghasemi, S. and Giedraitis, V. and Giulianini, F. and Gottdiener, J. S. and Gross, S. and Gu{\dh}bjartsson, D. F. and Gui, H. and Gutmann, R. and Haggerty, C. M. and van der Harst, P. and Hedman, {\r A}. K. and Helgadottir, A. and Hillege, H. and Hyde, C. L. and Jacob, J. and Jukema, J. W. and Kamanu, F. and Kardys, I. and Kavousi, M. and Khaw, K. T. and Kleber, M. E. and K{\o}ber, L. and Koekemoer, A. and Kraus, B. and Kuchenbaecker, K. and Langenberg, C. and Lind, L. and Lindgren, C. M. and London, B. and Lotta, L. A. and Lovering, R. C. and Luan, J. and Magnusson, P. and Mahajan, A. and Mann, D. and Margulies, K. B. and Marston, N. A. and M{\"a}rz, W. and McMurray, J. J. V. and Melander, O. and Melloni, G. and Mordi, I. R. and Morley, M. P. and Morris, A. D. and Morris, A. P. and Morrison, A. C. and Nagle, M. W. and Nelson, C. P. and Newton-Cheh, C. and Niessner, A. and Niiranen, T. and Nowak, C. and O{\textquoteright}Donoghue, M. L. and Owens, A. T. and Palmer, C. N. A. and Pare, G. and Perola, M. and Perreault, L. L. and Portilla-Fernandez, E. and Psaty, B. M. and Rice, K. M. and Ridker, P. M. and Romaine, S. P. R. and Roselli, C. and Rotter, J. I. and Ruff, C. T. and Sabatine, M. S. and Salo, P. and Salomaa, V. and van Setten, J. and Shalaby, A. A. and Smelser, D. T. and Smith, N. L. and Stefansson, K. and Stender, S. and Stott, D. J. and Sveinbjornsson, G. and Tammesoo, M. L. and Tardif, J. C. and Taylor, K. D. and Teder-Laving, M. and Teumer, A. and Thorgeirsson, G. and Thorsteinsdottir, U. and Torp-Pedersen, C. and Trompet, S. and Tuckwell, D. and Tyl, B. and Uitterlinden, A. G. and Vaura, F. and Veluchamy, A. and Visscher, P. M. and V{\"o}lker, U. and Voors, A. A. and Wang, X. and Wareham, N. J. and Weeke, P. E. and Weiss, R. and White, H. D. and Wiggins, K. L. and Xing, H. and Yang, J. and Yang, Y. and Yerges-Armstrong, L. M. and Yu, B. and Zannad, F. and Zhao, F. and Wilk, J. B. and Holm, H. and Sattar, N. and Lubitz, S. A. and Lanfear, D. E. and Shah, S. and Dunn, M. E. and Wells, Q. S. and Asselbergs, F. W. and Hingorani, A. D. and Dub{\'e}, M. P. and Samani, N. J. and Lang, C. C. and Cappola, T. P. and Ellinor, P. T. and Vasan, R. S. and Smith, J. G.}
}
@article {9263,
	title = {{A saturated map of common genetic variants associated with human height},
	journal = {Nature},
	volume = {610},
	year = {2022},
	month = {Oct},
	pages = {704{\textendash}712},
	abstract = {) account for 40\% (45\%) of phenotypic variance in populations of European ancestry but only around 10-20\% (14-24\%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries.},
	author = {Yengo, L. and Vedantam, S. and Marouli, E. and Sidorenko, J. and Bartell, E. and Sakaue, S. and Graff, M. and Eliasen, A. U. and Jiang, Y. and Raghavan, S. and Miao, J. and Arias, J. D. and Graham, S. E. and Mukamel, R. E. and Spracklen, C. N. and Yin, X. and Chen, S. H. and Ferreira, T. and Highland, H. H. and Ji, Y. and Karaderi, T. and Lin, K. and ll, K. and Malden, D. E. and Medina-Gomez, C. and Machado, M. and Moore, A. and eger, S. and Sim, X. and Vrieze, S. and Ahluwalia, T. S. and Akiyama, M. and Allison, M. A. and Alvarez, M. and Andersen, M. K. and Ani, A. and Appadurai, V. and Arbeeva, L. and Bhaskar, S. and Bielak, L. F. and Bollepalli, S. and Bonnycastle, L. L. and Bork-Jensen, J. and Bradfield, J. P. and Bradford, Y. and Braund, P. S. and Brody, J. A. and Burgdorf, K. S. and Cade, B. E. and Cai, H. and Cai, Q. and Campbell, A. and adas-Garre, M. and Catamo, E. and Chai, J. F. and Chai, X. and Chang, L. C. and Chang, Y. C. and Chen, C. H. and Chesi, A. and Choi, S. H. and Chung, R. H. and Cocca, M. and Concas, M. P. and Couture, C. and Cuellar-Partida, G. and Danning, R. and Daw, E. W. and Degenhard, F. and Delgado, G. E. and Delitala, A. and Demirkan, A. and Deng, X. and Devineni, P. and Dietl, A. and Dimitriou, M. and Dimitrov, L. and Dorajoo, R. and Ekici, A. B. and Engmann, J. E. and Fairhurst-Hunter, Z. and Farmaki, A. E. and Faul, J. D. and Fernandez-Lopez, J. C. and Forer, L. and Francescatto, M. and Freitag-Wolf, S. and Fuchsberger, C. and Galesloot, T. E. and Gao, Y. and Gao, Z. and Geller, F. and Giannakopoulou, O. and Giulianini, F. and Gjesing, A. P. and Goel, A. and Gordon, S. D. and Gorski, M. and Grove, J. and Guo, X. and Gustafsson, S. and Haessler, J. and Hansen, T. F. and Havulinna, A. S. and Haworth, S. J. and He, J. and Heard-Costa, N. and Hebbar, P. and Hindy, G. and Ho, Y. A. and Hofer, E. and Holliday, E. and Horn, K. and Hornsby, W. E. and Hottenga, J. J. and Huang, H. and Huang, J. and Huerta-Chagoya, A. and Huffman, J. E. and Hung, Y. J. and Huo, S. and Hwang, M. Y. and Iha, H. and Ikeda, D. D. and Isono, M. and Jackson, A. U. and ger, S. and Jansen, I. E. and Johansson, I. and Jonas, J. B. and Jonsson, A. and rgensen, T. and Kalafati, I. P. and Kanai, M. and Kanoni, S. and rhus, L. L. and Kasturiratne, A. and Katsuya, T. and Kawaguchi, T. and Kember, R. L. and Kentistou, K. A. and Kim, H. N. and Kim, Y. J. and Kleber, M. E. and Knol, M. J. and Kurbasic, A. and Lauzon, M. and Le, P. and Lea, R. and Lee, J. Y. and Leonard, H. L. and Li, S. A. and Li, X. and Li, X. and Liang, J. and Lin, H. and Lin, S. Y. and Liu, J. and Liu, X. and Lo, K. S. and Long, J. and Lor{\'e}s-Motta, L. and Luan, J. and Lyssenko, V. and inen, L. P. and Mahajan, A. and Mamakou, V. and Mangino, M. and Manichaikul, A. and Marten, J. and Mattheisen, M. and Mavarani, L. and McDaid, A. F. and Meidtner, K. and Melendez, T. L. and Mercader, J. M. and Milaneschi, Y. and Miller, J. E. and Millwood, I. Y. and Mishra, P. P. and Mitchell, R. E. and llehave, L. T. and Morgan, A. and Mucha, S. and Munz, M. and Nakatochi, M. and Nelson, C. P. and Nethander, M. and Nho, C. W. and Nielsen, A. A. and Nolte, I. M. and Nongmaithem, S. S. and Noordam, R. and Ntalla, I. and Nutile, T. and Pandit, A. and Christofidou, P. and rna, K. and Pauper, M. and Petersen, E. R. B. and Petersen, L. V. and nen, N. and ek, O. and Poveda, A. and Preuss, M. H. and Pyarajan, S. and Raffield, L. M. and Rakugi, H. and Ramirez, J. and Rasheed, A. and Raven, D. and Rayner, N. W. and Riveros, C. and Rohde, R. and Ruggiero, D. and Ruotsalainen, S. E. and Ryan, K. A. and Sabater-Lleal, M. and Saxena, R. and Scholz, M. and Sendamarai, A. and Shen, B. and Shi, J. and Shin, J. H. and Sidore, C. and Sitlani, C. M. and Slieker, R. C. and Smit, R. A. J. and Smith, A. V. and Smith, J. A. and Smyth, L. J. and Southam, L. and Steinthorsdottir, V. and Sun, L. and Takeuchi, F. and Tallapragada, D. S. P. and Taylor, K. D. and Tayo, B. O. and Tcheandjieu, C. and Terzikhan, N. and Tesolin, P. and Teumer, A. and Theusch, E. and Thompson, D. J. and Thorleifsson, G. and Timmers, P. R. H. J. and Trompet, S. and Turman, C. and Vaccargiu, S. and van der Laan, S. W. and van der Most, P. J. and van Klinken, J. B. and van Setten, J. and Verma, S. S. and Verweij, N. and Veturi, Y. and Wang, C. A. and Wang, C. and Wang, L. and Wang, Z. and Warren, H. R. and Bin Wei, W. and Wickremasinghe, A. R. and Wielscher, M. and Wiggins, K. L. and Winsvold, B. S. and Wong, A. and Wu, Y. and Wuttke, M. and Xia, R. and Xie, T. and Yamamoto, K. and Yang, J. and Yao, J. and Young, H. and Yousri, N. A. and Yu, L. and Zeng, L. and Zhang, W. and Zhang, X. and Zhao, J. H. and Zhao, W. and Zhou, W. and Zimmermann, M. E. and Zoledziewska, M. and Adair, L. S. and Adams, H. H. H. and Aguilar-Salinas, C. A. and Al-Mulla, F. and Arnett, D. K. and Asselbergs, F. W. and svold, B. O. and Attia, J. and Banas, B. and Bandinelli, S. and Bennett, D. A. and Bergler, T. and Bharadwaj, D. and Biino, G. and Bisgaard, H. and Boerwinkle, E. and ger, C. A. and nnelykke, K. and Boomsma, D. I. and rglum, A. D. and Borja, J. B. and Bouchard, C. and Bowden, D. W. and Brandslund, I. and Brumpton, B. and Buring, J. E. and Caulfield, M. J. and Chambers, J. C. and Chandak, G. R. and Chanock, S. J. and Chaturvedi, N. and Chen, Y. I. and Chen, Z. and Cheng, C. Y. and Christophersen, I. E. and Ciullo, M. and Cole, J. W. and Collins, F. S. and Cooper, R. S. and Cruz, M. and Cucca, F. and Cupples, L. A. and Cutler, M. J. and Damrauer, S. M. and Dantoft, T. M. and de Borst, G. J. and de Groot, L. C. P. G. M. and De Jager, P. L. and de Kleijn, D. P. V. and Janaka de Silva, H. and Dedoussis, G. V. and den Hollander, A. I. and Du, S. and Easton, D. F. and Elders, P. J. M. and Eliassen, A. H. and Ellinor, P. 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}
