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1. Sequence variants associated with BMI affect disease risk through BMI itself

Author: Einarsson, Gudmundur, Thorleifsson, Gudmar, Steinthorsdottir, Valgerdur, Zink, Florian, Helgason, Hannes, Olafsdottir, Thorhildur, Rognvaldsson, Solvi, Tragante, Vinicius, Ulfarsson, Magnus O., Sveinbjornsson, Gardar, Snaebjarnarson, Audunn S., Einarsson, Hafsteinn, Aegisdottir, Hildur M., Jonsdottir, Gudrun A., Helgadottir, Anna, Gretarsdottir, Solveig, Styrkarsdottir, Unnur, Arnason, Hannes K., Bjarnason, Ragnar, Sigurdsson, Emil, Arnar, David O., Bjornsson, Einar S., Palsson, Runolfur, Bjornsdottir, Gyda, Stefansson, Hreinn, Thorgeirsson, Thorgeir, Sulem, Patrick, Thorsteinsdottir, Unnur, Holm, Hilma, Gudbjartsson, Daniel F., and Stefansson, Kari
Published: 2024
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2. Genetic insights into resting heart rate and its role in cardiovascular disease.

Author: van de Vegte, Yordi, Eppinga, Ruben, van der Ende, M, Hagemeijer, Yanick, Mahendran, Yuvaraj, Salfati, Elias, Smith, Albert, Tan, Vanessa, Arking, Dan, Ntalla, Ioanna, Appel, Emil, Schurmann, Claudia, Brody, Jennifer, Rueedi, Rico, Polasek, Ozren, Sveinbjornsson, Gardar, Lecoeur, Cecile, Ladenvall, Claes, Zhao, Jing, Isaacs, Aaron, Wang, Lihua, Luan, Jianan, Hwang, Shih-Jen, Mononen, Nina, Auro, Kirsi, Jackson, Anne, Bielak, Lawrence, Zeng, Linyao, Shah, Nabi, Nethander, Maria, Campbell, Archie, Rankinen, Tuomo, Pechlivanis, Sonali, Qi, Lu, Zhao, Wei, Rizzi, Federica, Tanaka, Toshiko, Robino, Antonietta, Cocca, Massimiliano, Lange, Leslie, Müller-Nurasyid, Martina, Roselli, Carolina, Zhang, Weihua, Kleber, Marcus, Guo, Xiuqing, Lin, Henry, Pavani, Francesca, Galesloot, Tessel, Noordam, Raymond, Milaneschi, Yuri, Schraut, Katharina, den Hoed, Marcel, Degenhardt, Frauke, Trompet, Stella, van den Berg, Marten, Pistis, Giorgio, Tham, Yih-Chung, Weiss, Stefan, Sim, Xueling, Li, Hengtong, van der Most, Peter, Nolte, Ilja, Lyytikäinen, Leo-Pekka, Said, M, Witte, Daniel, Iribarren, Carlos, Launer, Lenore, Ring, Susan, de Vries, Paul, Sever, Peter, Linneberg, Allan, Bottinger, Erwin, Padmanabhan, Sandosh, Psaty, Bruce, Sotoodehnia, Nona, Kolcic, Ivana, Arnar, David, Gudbjartsson, Daniel, Holm, Hilma, Balkau, Beverley, Silva, Claudia, Newton-Cheh, Christopher, Nikus, Kjell, Salo, Perttu, Mohlke, Karen, Peyser, Patricia, Schunkert, Heribert, Lorentzon, Mattias, Lahti, Jari, Rao, Dabeeru, Cornelis, Marilyn, Faul, Jessica, Smith, Jennifer, Stolarz-Skrzypek, Katarzyna, Bandinelli, Stefania, Concas, Maria, Sinagra, Gianfranco, Meitinger, Thomas, Waldenberger, Melanie, and Sinner, Moritz
Subjects: Humans, Cardiovascular Diseases, Risk Factors, Heart Rate, Genetic Predisposition to Disease, Atrial Fibrillation, Mendelian Randomization Analysis, Genome-Wide Association Study, Polymorphism, Single Nucleotide
Abstract: Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development.
Published: 2023

3. Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study

Author: Chen, Hao Yu, Dina, Christian, Small, Aeron M, Shaffer, Christian M, Levinson, Rebecca T, Helgadóttir, Anna, Capoulade, Romain, Munter, Hans Markus, Martinsson, Andreas, Cairns, Benjamin J, Trudsø, Linea C, Hoekstra, Mary, Burr, Hannah A, Marsh, Thomas W, Damrauer, Scott M, Dufresne, Line, Le Scouarnec, Solena, Messika-Zeitoun, David, Ranatunga, Dilrini K, Whitmer, Rachel A, Bonnefond, Amélie, Sveinbjornsson, Garðar, Daníelsen, Ragnar, Arnar, David O, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Gudbjartsson, Daníel F, Hólm, Hilma, Ghouse, Jonas, Olesen, Morten Salling, Christensen, Alex H, Mikkelsen, Susan, Jacobsen, Rikke Louise, Dowsett, Joseph, Pedersen, Ole Birger Vesterager, Erikstrup, Christian, Ostrowski, Sisse R, Center, Regeneron Genetics, O’Donnell, Christopher J, Budoff, Matthew J, Gudnason, Vilmundur, Post, Wendy S, Rotter, Jerome I, Lathrop, Mark, Bundgaard, Henning, Johansson, Bengt, Ljungberg, Johan, Näslund, Ulf, Le Tourneau, Thierry, Smith, J Gustav, Wells, Quinn S, Söderberg, Stefan, Stefánsson, Kári, Schott, Jean-Jacques, Rader, Daniel J, Clarke, Robert, Engert, James C, and Thanassoulis, George
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Heart Disease - Coronary Heart Disease, Prevention, Heart Disease, Cardiovascular, Genetics, Human Genome, Atherosclerosis, 2.1 Biological and endogenous factors, Humans, Genome-Wide Association Study, Adiposity, Genetic Predisposition to Disease, Aortic Valve Stenosis, Obesity, Risk Factors, Inflammation, Dyslipidemias, Apolipoproteins, Mendelian Randomization Analysis, Polymorphism, Single Nucleotide, Aortic stenosis, Genome-wide association study, Mendelian randomization, Phenome-wide association study, Gene expression, Genetic risk score, Regeneron Genetics Center, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract: AimsAlthough highly heritable, the genetic etiology of calcific aortic stenosis (AS) remains incompletely understood. The aim of this study was to discover novel genetic contributors to AS and to integrate functional, expression, and cross-phenotype data to identify mechanisms of AS.Methods and resultsA genome-wide meta-analysis of 11.6 million variants in 10 cohorts involving 653 867 European ancestry participants (13 765 cases) was performed. Seventeen loci were associated with AS at P ≤ 5 × 10-8, of which 15 replicated in an independent cohort of 90 828 participants (7111 cases), including CELSR2-SORT1, NLRP6, and SMC2. A genetic risk score comprised of the index variants was associated with AS [odds ratio (OR) per standard deviation, 1.31; 95% confidence interval (CI), 1.26-1.35; P = 2.7 × 10-51] and aortic valve calcium (OR per standard deviation, 1.22; 95% CI, 1.08-1.37; P = 1.4 × 10-3), after adjustment for known risk factors. A phenome-wide association study indicated multiple associations with coronary artery disease, apolipoprotein B, and triglycerides. Mendelian randomization supported a causal role for apolipoprotein B-containing lipoprotein particles in AS (OR per g/L of apolipoprotein B, 3.85; 95% CI, 2.90-5.12; P = 2.1 × 10-20) and replicated previous findings of causality for lipoprotein(a) (OR per natural logarithm, 1.20; 95% CI, 1.17-1.23; P = 4.8 × 10-73) and body mass index (OR per kg/m2, 1.07; 95% CI, 1.05-1.9; P = 1.9 × 10-12). Colocalization analyses using the GTEx database identified a role for differential expression of the genes LPA, SORT1, ACTR2, NOTCH4, IL6R, and FADS.ConclusionDyslipidemia, inflammation, calcification, and adiposity play important roles in the etiology of AS, implicating novel treatments and prevention strategies.
Published: 2023

4. Physical and cognitive impact following SARS-CoV-2 infection in a large population-based case-control study

Author: Holm, Hilma, Ivarsdottir, Erna V., Olafsdottir, Thorhildur, Thorolfsdottir, Rosa, Eythorsson, Elias, Norland, Kristjan, Gisladottir, Rosa, Jonsdottir, Gudrun, Unnsteinsdottir, Unnur, Sveinsdottir, Kristin E., Jonsson, Benedikt A., Andresdottir, Margret, Arnar, David O., Arnthorsson, Asgeir O., Birgisdottir, Kolbrún, Bjarnadottir, Kristbjorg, Bjarnadottir, Solveig, Bjornsdottir, Gyda, Einarsson, Gudmundur, Eiriksdottir, Berglind, Gardarsdottir, Elisabet Eir, Gislason, Thorarinn, Gottfredsson, Magnus, Gudmundsdottir, Steinunn, Gudmundsson, Julius, Gunnarsdottir, Kristbjorg, Helgadottir, Anna, Helgason, Dadi, Hinriksdottir, Ingibjorg, Ingvarsson, Ragnar F., Jonasdottir, Sigga S., Jonsdottir, Ingileif, Karlsdottir, Tekla H., Kristinsdottir, Anna M., Kristinsson, Sigurdur Yngvi, Kristjansdottir, Steinunn, Love, Thorvardur J., Ludviksdottir, Dora, Masson, Gisli, Norddahl, Gudmundur, Olafsdottir, Thorunn, Olafsson, Isleifur, Rafnar, Thorunn, Runolfsdottir, Hrafnhildur L., Saemundsdottir, Jona, Sigurbjornsson, Svanur, Sigurdardottir, Kristin, Sigurdsson, Engilbert, Sigurdsson, Martin I., Sigurdsson, Emil L., Steinthorsdottir, Valgerdur, Sveinbjornsson, Gardar, Thorarensen, Emil A., Thorbjornsson, Bjarni, Thorsteinsdottir, Brynja, Tragante, Vinicius, Ulfarsson, Magnus O., Stefansson, Hreinn, Gislason, Thorsteinn, Kristjansson, Mar, Palsson, Runolfur, Sulem, Patrick, Thorsteinsdottir, Unnur, Thorgeirsson, Gudmundur, Gudbjartsson, Daniel F., and Stefansson, Kari
Published: 2023
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5. Complex effects of sequence variants on lipid levels and coronary artery disease

Author: Snaebjarnarson, Audunn S., Helgadottir, Anna, Arnadottir, Gudny A., Ivarsdottir, Erna V., Thorleifsson, Gudmar, Ferkingstad, Egil, Einarsson, Gudmundur, Sveinbjornsson, Gardar, Thorgeirsson, Thorgeir E., Ulfarsson, Magnus O., Halldorsson, Bjarni V., Olafsson, Isleifur, Erikstrup, Christian, Pedersen, Ole B., Nyegaard, Mette, Bruun, Mie T., Ullum, Henrik, Brunak, Søren, Iversen, Kasper Karmark, Christensen, Alex Hoerby, Olesen, Morten S., Ghouse, Jonas, Banasik, Karina, Knowlton, Kirk U., Arnar, David O., Thorgeirsson, Gudmundur, Nadauld, Lincoln, Ostrowski, Sisse Rye, Bundgaard, Henning, Holm, Hilma, Sulem, Patrick, Stefansson, Kari, and Gudbjartsson, Daniel F.
Published: 2023
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6. Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants

Author: Aragam, Krishna G., Jiang, Tao, Goel, Anuj, Kanoni, Stavroula, Wolford, Brooke N., Atri, Deepak S., Weeks, Elle M., Wang, Minxian, Hindy, George, Zhou, Wei, Grace, Christopher, Roselli, Carolina, Marston, Nicholas A., Kamanu, Frederick K., Surakka, Ida, Venegas, Loreto Muñoz, Sherliker, Paul, Koyama, Satoshi, Ishigaki, Kazuyoshi, Åsvold, Bjørn O., Brown, Michael R., Brumpton, Ben, de Vries, Paul S., Giannakopoulou, Olga, Giardoglou, Panagiota, Gudbjartsson, Daniel F., Güldener, Ulrich, Haider, Syed M. Ijlal, Helgadottir, Anna, Ibrahim, Maysson, Kastrati, Adnan, Kessler, Thorsten, Kyriakou, Theodosios, Konopka, Tomasz, Li, Ling, Ma, Lijiang, Meitinger, Thomas, Mucha, Sören, Munz, Matthias, Murgia, Federico, Nielsen, Jonas B., Nöthen, Markus M., Pang, Shichao, Reinberger, Tobias, Schnitzler, Gavin, Smedley, Damian, Thorleifsson, Gudmar, von Scheidt, Moritz, Ulirsch, Jacob C., Arnar, David O., Burtt, Noël P., Costanzo, Maria C., Flannick, Jason, Ito, Kaoru, Jang, Dong-Keun, Kamatani, Yoichiro, Khera, Amit V., Komuro, Issei, Kullo, Iftikhar J., Lotta, Luca A., Nelson, Christopher P., Roberts, Robert, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Webb, Thomas R., Baras, Aris, Björkegren, Johan L. M., Boerwinkle, Eric, Dedoussis, George, Holm, Hilma, Hveem, Kristian, Melander, Olle, Morrison, Alanna C., Orho-Melander, Marju, Rallidis, Loukianos S., Ruusalepp, Arno, Sabatine, Marc S., Stefansson, Kari, Zalloua, Pierre, Ellinor, Patrick T., Farrall, Martin, Danesh, John, Ruff, Christian T., Finucane, Hilary K., Hopewell, Jemma C., Clarke, Robert, Gupta, Rajat M., Erdmann, Jeanette, Samani, Nilesh J., Schunkert, Heribert, Watkins, Hugh, Willer, Cristen J., Deloukas, Panos, Kathiresan, Sekar, and Butterworth, Adam S.
Published: 2022
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7. Multiomics study of nonalcoholic fatty liver disease

Author: Sveinbjornsson, Gardar, Ulfarsson, Magnus O., Thorolfsdottir, Rosa B., Jonsson, Benedikt A., Einarsson, Eythor, Gunnlaugsson, Gylfi, Rognvaldsson, Solvi, Arnar, David O., Baldvinsson, Magnus, Bjarnason, Ragnar G., Eiriksdottir, Thjodbjorg, Erikstrup, Christian, Ferkingstad, Egil, Halldorsson, Gisli H., Helgason, Hannes, Helgadottir, Anna, Hindhede, Lotte, Hjorleifsson, Grimur, Jones, David, Knowlton, Kirk U., Lund, Sigrun H., Melsted, Pall, Norland, Kristjan, Olafsson, Isleifur, Olafsson, Sigurdur, Oskarsson, Gudjon R., Ostrowski, Sisse Rye, Pedersen, Ole Birger, Snaebjarnarson, Auðunn S., Sigurdsson, Emil, Steinthorsdottir, Valgerdur, Schwinn, Michael, Thorgeirsson, Gudmundur, Thorleifsson, Gudmar, Jonsdottir, Ingileif, Bundgaard, Henning, Nadauld, Lincoln, Bjornsson, Einar S., Rulifson, Ingrid C., Rafnar, Thorunn, Norddahl, Gudmundur L., Thorsteinsdottir, Unnur, Sulem, Patrick, Gudbjartsson, Daniel F., Holm, Hilma, and Stefansson, Kari
Published: 2022
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8. Exome-chip meta-analysis identifies novel loci associated with cardiac conduction, including ADAMTS6

Author: Prins, Bram P, Mead, Timothy J, Brody, Jennifer A, Sveinbjornsson, Gardar, Ntalla, Ioanna, Bihlmeyer, Nathan A, van den Berg, Marten, Bork-Jensen, Jette, Cappellani, Stefania, Van Duijvenboden, Stefan, Klena, Nikolai T, Gabriel, George C, Liu, Xiaoqin, Gulec, Cagri, Grarup, Niels, Haessler, Jeffrey, Hall, Leanne M, Iorio, Annamaria, Isaacs, Aaron, Li-Gao, Ruifang, Lin, Honghuang, Liu, Ching-Ti, Lyytikäinen, Leo-Pekka, Marten, Jonathan, Mei, Hao, Müller-Nurasyid, Martina, Orini, Michele, Padmanabhan, Sandosh, Radmanesh, Farid, Ramirez, Julia, Robino, Antonietta, Schwartz, Molly, van Setten, Jessica, Smith, Albert V, Verweij, Niek, Warren, Helen R, Weiss, Stefan, Alonso, Alvaro, Arnar, David O, Bots, Michiel L, de Boer, Rudolf A, Dominiczak, Anna F, Eijgelsheim, Mark, Ellinor, Patrick T, Guo, Xiuqing, Felix, Stephan B, Harris, Tamara B, Hayward, Caroline, Heckbert, Susan R, Huang, Paul L, Jukema, JW, Kähönen, Mika, Kors, Jan A, Lambiase, Pier D, Launer, Lenore J, Li, Man, Linneberg, Allan, Nelson, Christopher P, Pedersen, Oluf, Perez, Marco, Peters, Annette, Polasek, Ozren, Psaty, Bruce M, Raitakari, Olli T, Rice, Kenneth M, Rotter, Jerome I, Sinner, Moritz F, Soliman, Elsayed Z, Spector, Tim D, Strauch, Konstantin, Thorsteinsdottir, Unnur, Tinker, Andrew, Trompet, Stella, Uitterlinden, André, Vaartjes, Ilonca, van der Meer, Peter, Völker, Uwe, Völzke, Henry, Waldenberger, Melanie, Wilson, James G, Xie, Zhijun, Asselbergs, Folkert W, Dörr, Marcus, van Duijn, Cornelia M, Gasparini, Paolo, Gudbjartsson, Daniel F, Gudnason, Vilmundur, Hansen, Torben, Kääb, Stefan, Kanters, Jørgen K, Kooperberg, Charles, Lehtimäki, Terho, Lin, Henry J, Lubitz, Steven A, Mook-Kanamori, Dennis O, Conti, Francesco J, Newton-Cheh, Christopher H, Rosand, Jonathan, Rudan, Igor, and Samani, Nilesh J
Subjects: Biological Sciences, Biomedical and Clinical Sciences, Genetics, Human Genome, Heart Disease, Cardiovascular, 2.1 Biological and endogenous factors, Aetiology, ADAMTS Proteins, Animals, Black People, Connexin 43, Electrocardiography, Exome, Female, Gene Expression, Gene Expression Profiling, Genetic Loci, Genome-Wide Association Study, Heart Conduction System, Humans, Male, Mice, Middle Aged, Myocardium, Open Reading Frames, Polymorphism, Single Nucleotide, White People, Exome Sequencing, Exome chip, Conduction, ADAMTS6, Meta-analysis, Environmental Sciences, Information and Computing Sciences, Bioinformatics
Abstract: BackgroundGenome-wide association studies conducted on QRS duration, an electrocardiographic measurement associated with heart failure and sudden cardiac death, have led to novel biological insights into cardiac function. However, the variants identified fall predominantly in non-coding regions and their underlying mechanisms remain unclear.ResultsHere, we identify putative functional coding variation associated with changes in the QRS interval duration by combining Illumina HumanExome BeadChip genotype data from 77,898 participants of European ancestry and 7695 of African descent in our discovery cohort, followed by replication in 111,874 individuals of European ancestry from the UK Biobank and deCODE cohorts. We identify ten novel loci, seven within coding regions, including ADAMTS6, significantly associated with QRS duration in gene-based analyses. ADAMTS6 encodes a secreted metalloprotease of currently unknown function. In vitro validation analysis shows that the QRS-associated variants lead to impaired ADAMTS6 secretion and loss-of function analysis in mice demonstrates a previously unappreciated role for ADAMTS6 in connexin 43 gap junction expression, which is essential for myocardial conduction.ConclusionsOur approach identifies novel coding and non-coding variants underlying ventricular depolarization and provides a possible mechanism for the ADAMTS6-associated conduction changes.
Published: 2018

9. Improving outpatient care for heart failure through digital innovation: a feasibility study

Author: Arnar, David O., Oddsson, Saemundur J., Gunnarsdottir, Thrudur, Gudlaugsdottir, Gudbjorg Jona, Gudmundsson, Elias Freyr, Ketilsdóttir, Audur, Halldorsdottir, Hulda, Hrafnkelsdottir, Thordis Jona, Hallsson, Hallur, Amundadottir, Maria L., and Thorgeirsson, Tryggvi
Published: 2022
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10. PR interval genome-wide association meta-analysis identifies 50 loci associated with atrial and atrioventricular electrical activity

Author: van Setten, Jessica, Brody, Jennifer A, Jamshidi, Yalda, Swenson, Brenton R, Butler, Anne M, Campbell, Harry, Del Greco, Fabiola M, Evans, Daniel S, Gibson, Quince, Gudbjartsson, Daniel F, Kerr, Kathleen F, Krijthe, Bouwe P, Lyytikäinen, Leo-Pekka, Müller, Christian, Müller-Nurasyid, Martina, Nolte, Ilja M, Padmanabhan, Sandosh, Ritchie, Marylyn D, Robino, Antonietta, Smith, Albert V, Steri, Maristella, Tanaka, Toshiko, Teumer, Alexander, Trompet, Stella, Ulivi, Sheila, Verweij, Niek, Yin, Xiaoyan, Arnar, David O, Asselbergs, Folkert W, Bader, Joel S, Barnard, John, Bis, Josh, Blankenberg, Stefan, Boerwinkle, Eric, Bradford, Yuki, Buckley, Brendan M, Chung, Mina K, Crawford, Dana, den Hoed, Marcel, Denny, Josh C, Dominiczak, Anna F, Ehret, Georg B, Eijgelsheim, Mark, Ellinor, Patrick T, Felix, Stephan B, Franco, Oscar H, Franke, Lude, Harris, Tamara B, Holm, Hilma, Ilaria, Gandin, Iorio, Annamaria, Kähönen, Mika, Kolcic, Ivana, Kors, Jan A, Lakatta, Edward G, Launer, Lenore J, Lin, Honghuang, Lin, Henry J, Loos, Ruth JF, Lubitz, Steven A, Macfarlane, Peter W, Magnani, Jared W, Leach, Irene Mateo, Meitinger, Thomas, Mitchell, Braxton D, Munzel, Thomas, Papanicolaou, George J, Peters, Annette, Pfeufer, Arne, Pramstaller, Peter P, Raitakari, Olli T, Rotter, Jerome I, Rudan, Igor, Samani, Nilesh J, Schlessinger, David, Silva Aldana, Claudia T, Sinner, Moritz F, Smith, Jonathan D, Snieder, Harold, Soliman, Elsayed Z, Spector, Timothy D, Stott, David J, Strauch, Konstantin, Tarasov, Kirill V, Thorsteinsdottir, Unnur, Uitterlinden, Andre G, Van Wagoner, David R, Völker, Uwe, Völzke, Henry, Waldenberger, Melanie, Jan Westra, Harm, Wild, Philipp S, Zeller, Tanja, Alonso, Alvaro, Avery, Christy L, Bandinelli, Stefania, Benjamin, Emelia J, Cucca, Francesco, Dörr, Marcus, and Ferrucci, Luigi
Subjects: Biological Sciences, Genetics, Human Genome, Heart Disease, Biotechnology, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Atrial Function, Atrioventricular Node, Electrocardiography, Electrophysiological Phenomena, Female, Genome-Wide Association Study, Humans, Linkage Disequilibrium, Male, Mutation, Missense, Risk Factors
Abstract: Electrocardiographic PR interval measures atrio-ventricular depolarization and conduction, and abnormal PR interval is a risk factor for atrial fibrillation and heart block. Our genome-wide association study of over 92,000 European-descent individuals identifies 44 PR interval loci (34 novel). Examination of these loci reveals known and previously not-yet-reported biological processes involved in cardiac atrial electrical activity. Genes in these loci are over-represented in cardiac disease processes including heart block and atrial fibrillation. Variants in over half of the 44 loci were associated with atrial or blood transcript expression levels, or were in high linkage disequilibrium with missense variants. Six additional loci were identified either by meta-analysis of ~105,000 African and European-descent individuals and/or by pleiotropic analyses combining PR interval with heart rate, QRS interval, and atrial fibrillation. These findings implicate developmental pathways, and identify transcription factors, ion-channel genes, and cell-junction/cell-signaling proteins in atrio-ventricular conduction, identifying potential targets for drug development.
Published: 2018

11. Genome-Wide Association Study of Accessory Atrioventricular Pathways

Author: Aegisdottir, Hildur M., Andreasen, Laura, Thorolfsdottir, Rosa B., Sveinbjornsson, Gardar, Jonsdottir, Andrea B., Stefansdottir, Lilja, Thorleifsson, Gudmar, Sigurdsson, Asgeir, Halldorsson, Gisli H., Barc, Julien, Simonet, Floriane, Tragante, Vinicius, Oddsson, Asmundur, Ferkingstad, Egil, Svendsen, Jesper Hastrup, Ghouse, Jonas, Ahlberg, Gustav, Paludan-Müller, Christian, Hadji-Turdeghal, Katra, Bustamante, Mariana, Ulfarsson, Magnus O., Helgadottir, Anna, Gretarsdottir, Solveig, Saevarsdottir, Saedis, Jonsdottir, Ingileif, Erikstrup, Christian, Ullum, Henrik, Sørensen, Erik, Brunak, Søren, Jøns, Christian, Zheng, Chaoqun, Bezzina, Connie R., Knowlton, Kirk U., Nadauld, Lincoln D., Sulem, Patrick, Ostrowski, Sisse R., Pedersen, Ole B., Arnar, David O., Gudbjartsson, Daniel F., Olesen, Morten S., Bundgaard, Henning, Holm, Hilma, and Stefansson, Kari
Abstract: IMPORTANCE: Understanding of the genetics of accessory atrioventricular pathways (APs) and affiliated arrhythmias is limited. OBJECTIVE: To investigate the genetics of APs and affiliated arrhythmias. DESIGN, SETTING, AND PARTICIPANTS: This was a genome-wide association study (GWAS) of APs, defined by International Classification of Diseases (ICD) codes and/or confirmed by electrophysiology (EP) study. Genome-wide significant AP variants were tested for association with AP-affiliated arrhythmias: paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation (AF), ventricular tachycardia, and cardiac arrest. AP variants were also tested in data on other heart diseases and measures of cardiac physiology. Individuals with APs and control individuals from Iceland (deCODE Genetics), Denmark (Copenhagen Hospital Biobank, Danish Blood Donor Study, and SupraGen/the Danish General Suburban Population Study [GESUS]), the US (Intermountain Healthcare), and the United Kingdom (UK Biobank) were included. Time of phenotype data collection ranged from January 1983 to December 2022. Data were analyzed from August 2022 to January 2024. EXPOSURES: Sequence variants. MAIN OUTCOMES AND MEASURES: Genome-wide significant association of sequence variants with APs. RESULTS: The GWAS included 2310 individuals with APs (median [IQR] age, 43 [28-57] years; 1252 [54.2%] male and 1058 [45.8%] female) and 1 206 977 control individuals (median [IQR] year of birth, 1955 [1945-1970]; 632 888 [52.4%] female and 574 089 [47.6%] male). Of the individuals with APs, 909 had been confirmed in EP study. Three common missense variants were associated with APs, in the genes CCDC141 (p.Arg935Trp: adjusted odds ratio [aOR], 1.37; 95% CI, 1.24-1.52, and p.Ala141Val: aOR, 1.55; 95% CI 1.34-1.80) and SCN10A (p.Ala1073Val: OR, 1.22; 95% CI, 1.15-1.30). The 3 variants associated with PSVT and the SCN10A variant associated with AF, supporting an effect on AP-affiliated arrhythmias. All 3 AP risk alleles were associated with higher heart rate and shorter PR interval, and have reported associations with chronotropic response. CONCLUSIONS AND RELEVANCE: Associations were found between sequence variants and APs that were also associated with risk of PSVT, and thus likely atrioventricular reentrant tachycardia, but had allele-specific associations with AF and conduction disorders. Genetic variation in the modulation of heart rate, chronotropic response, and atrial or atrioventricular node conduction velocity may play a role in the risk of AP-affiliated arrhythmias. Further research into CCDC141 could provide insights for antiarrhythmic therapeutic targeting in the presence of an AP.
Published: 2024
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12. Distinction between the effects of parental and fetal genomes on fetal growth

Author: Juliusdottir, Thorhildur, Steinthorsdottir, Valgerdur, Stefansdottir, Lilja, Sveinbjornsson, Gardar, Ivarsdottir, Erna V., Thorolfsdottir, Rosa B., Sigurdsson, Jon K., Tragante, Vinicius, Hjorleifsson, Kristjan E., Helgadottir, Anna, Frigge, Michael L., Thorgeirsson, Gudmundur, Benediktsson, Rafn, Sigurdsson, Emil L., Arnar, David O., Steingrimsdottir, Thora, Jonsdottir, Ingileif, Holm, Hilma, Gudbjartsson, Daniel F., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, and Stefansson, Kari
Published: 2021
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13. Variants at the Interleukin 1 Gene Locus and Pericarditis

Author: Thorolfsdottir, Rosa B., Jonsdottir, Andrea B., Sveinbjornsson, Gardar, Aegisdottir, Hildur M., Oddsson, Asmundur, Stefansson, Olafur A., Halldorsson, Gisli H., Saevarsdottir, Saedis, Thorleifsson, Gudmar, Stefansdottir, Lilja, Pedersen, Ole B., Sørensen, Erik, Ghouse, Jonas, Raja, Anna Axelsson, Zheng, Chaoqun, Silajdzija, Elvira, Rand, Søren Albertsen, Erikstrup, Christian, Ullum, Henrik, Mikkelsen, Christina, Banasik, Karina, Brunak, Søren, Ivarsdottir, Erna V., Sigurdsson, Asgeir, Beyter, Doruk, Sturluson, Arni, Einarsson, Hafsteinn, Tragante, Vinicius, Helgason, Hannes, Lund, Sigrun H., Halldorsson, Bjarni V., Sigurpalsdottir, Brynja D., Olafsson, Isleifur, Arnar, David O., Thorgeirsson, Gudmundur, Knowlton, Kirk U., Nadauld, Lincoln D., Gretarsdottir, Solveig, Helgadottir, Anna, Ostrowski, Sisse R., Gudbjartssson, Daniel F., Jonsdottir, Ingileif, Bundgaard, Henning, Holm, Hilma, Sulem, Patrick, Stefansson, Kari, Thorolfsdottir, Rosa B., Jonsdottir, Andrea B., Sveinbjornsson, Gardar, Aegisdottir, Hildur M., Oddsson, Asmundur, Stefansson, Olafur A., Halldorsson, Gisli H., Saevarsdottir, Saedis, Thorleifsson, Gudmar, Stefansdottir, Lilja, Pedersen, Ole B., Sørensen, Erik, Ghouse, Jonas, Raja, Anna Axelsson, Zheng, Chaoqun, Silajdzija, Elvira, Rand, Søren Albertsen, Erikstrup, Christian, Ullum, Henrik, Mikkelsen, Christina, Banasik, Karina, Brunak, Søren, Ivarsdottir, Erna V., Sigurdsson, Asgeir, Beyter, Doruk, Sturluson, Arni, Einarsson, Hafsteinn, Tragante, Vinicius, Helgason, Hannes, Lund, Sigrun H., Halldorsson, Bjarni V., Sigurpalsdottir, Brynja D., Olafsson, Isleifur, Arnar, David O., Thorgeirsson, Gudmundur, Knowlton, Kirk U., Nadauld, Lincoln D., Gretarsdottir, Solveig, Helgadottir, Anna, Ostrowski, Sisse R., Gudbjartssson, Daniel F., Jonsdottir, Ingileif, Bundgaard, Henning, Holm, Hilma, Sulem, Patrick, and Stefansson, Kari
Abstract: Importance: Recurrent pericarditis is a treatment challenge and often a debilitating condition. Drugs inhibiting interleukin 1 cytokines are a promising new treatment option, but their use is based on scarce biological evidence and clinical trials of modest sizes, and the contributions of innate and adaptive immune processes to the pathophysiology are incompletely understood. Objective: To use human genomics, transcriptomics, and proteomics to shed light on the pathogenesis of pericarditis. Design, Setting, and Participants: This was a meta-analysis of genome-wide association studies of pericarditis from 5 countries. Associations were examined between the pericarditis-associated variants and pericarditis subtypes (including recurrent pericarditis) and secondary phenotypes. To explore mechanisms, associations with messenger RNA expression (cis-eQTL), plasma protein levels (pQTL), and CpG methylation of DNA (ASM-QTL) were assessed. Data from Iceland (deCODE genetics, 1983-2020), Denmark (Copenhagen Hospital Biobank/Danish Blood Donor Study, 1977-2022), the UK (UK Biobank, 1953-2021), the US (Intermountain, 1996-2022), and Finland (FinnGen, 1970-2022) were included. Data were analyzed from September 2022 to August 2023. Exposure: Genotype. Main Outcomes and Measures: Pericarditis. Results: In this genome-wide association study of 4894 individuals with pericarditis (mean [SD] age at diagnosis, 51.4 [17.9] years, 2734 [67.6%] male, excluding the FinnGen cohort), associations were identified with 2 independent common intergenic variants at the interleukin 1 locus on chromosome 2q14. The lead variant was rs12992780 (T) (effect allele frequency [EAF], 31%-40%; odds ratio [OR], 0.83; 95% CI, 0.79-0.87; P = 6.67 × 10-16), downstream of IL1B and the secondary variant rs7575402 (A or T) (EAF, 45%-55%; adjusted OR, 0.89; 95% CI, 0.85-0.93; adjusted P = 9.6 × 10-8). The lead variant rs12992780 had a smaller odds ratio for recurrent pericarditis (0.76) tha
Published: 2024

14. Evaluation of Large-Scale Proteomics for Prediction of Cardiovascular Events

Author: Helgason, Hannes, primary, Eiriksdottir, Thjodbjorg, additional, Ulfarsson, Magnus O., additional, Choudhary, Abhishek, additional, Lund, Sigrun H., additional, Ivarsdottir, Erna V., additional, Hjorleifsson Eldjarn, Grimur, additional, Einarsson, Gudmundur, additional, Ferkingstad, Egil, additional, Moore, Kristjan H. S., additional, Honarpour, Narimon, additional, Liu, Thomas, additional, Wang, Huei, additional, Hucko, Thomas, additional, Sabatine, Marc S., additional, Morrow, David A., additional, Giugliano, Robert P., additional, Ostrowski, Sisse Rye, additional, Pedersen, Ole Birger, additional, Bundgaard, Henning, additional, Erikstrup, Christian, additional, Arnar, David O., additional, Thorgeirsson, Gudmundur, additional, Masson, Gísli, additional, Magnusson, Olafur Th., additional, Saemundsdottir, Jona, additional, Gretarsdottir, Solveig, additional, Steinthorsdottir, Valgerdur, additional, Thorleifsson, Gudmar, additional, Helgadottir, Anna, additional, Sulem, Patrick, additional, Thorsteinsdottir, Unnur, additional, Holm, Hilma, additional, Gudbjartsson, Daniel, additional, and Stefansson, Kari, additional
Published: 2023
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15. Screening for Rare Coding Variants That Associate With the QTc Interval in Iceland

Author: Sveinbjornsson, Gardar, primary, Benediktsdottir, Bara D., additional, Sigfusson, Gunnlaugur, additional, Norland, Kristjan, additional, Davidsson, Olafur B., additional, Thorolfsdottir, Rosa B., additional, Tragante, Vinicius, additional, Arnadottir, Gudny A., additional, Jensson, Brynjar O., additional, Katrinardottir, Hildigunnur, additional, Fridriksdottir, Run, additional, Gudmundsdottir, Hallbera, additional, Aegisdottir, Hildur M., additional, Fridriksson, Brynjar, additional, Thorgeirsson, Gudmundur, additional, Magnusson, Vidar, additional, Oddsson, Asmundur, additional, Sulem, Patrick, additional, Gudbjartsson, Daniel F., additional, Holm, Hilma, additional, Arnar, David O., additional, and Stefansson, Kari, additional
Published: 2023
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16. Genetics of common complex diseases: a view from Iceland

Author: Arnar, David O. and Palsson, Runolfur
Published: 2017
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17. Multi-ancestry GWAS of the electrocardiographic PR interval identifies 202 loci underlying cardiac conduction

Author: Ntalla, Ioanna, Weng, Lu-Chen, Cartwright, James H., Hall, Amelia Weber, Sveinbjornsson, Gardar, Tucker, Nathan R., Choi, Seung Hoan, Chaffin, Mark D., Roselli, Carolina, Barnes, Michael R., Mifsud, Borbala, Warren, Helen R., Hayward, Caroline, Marten, Jonathan, Cranley, James J., Concas, Maria Pina, Gasparini, Paolo, Boutin, Thibaud, Kolcic, Ivana, Polasek, Ozren, Rudan, Igor, Araujo, Nathalia M., Lima-Costa, Maria Fernanda, Ribeiro, Antonio Luiz P., Souza, Renan P., Tarazona-Santos, Eduardo, Giedraitis, Vilmantas, Ingelsson, Erik, Mahajan, Anubha, Morris, Andrew P., Del Greco M, Fabiola, Foco, Luisa, Gögele, Martin, Hicks, Andrew A., Cook, James P., Lind, Lars, Lindgren, Cecilia M., Sundström, Johan, Nelson, Christopher P., Riaz, Muhammad B., Samani, Nilesh J., Sinagra, Gianfranco, Ulivi, Sheila, Kähönen, Mika, Mishra, Pashupati P., Mononen, Nina, Nikus, Kjell, Caulfield, Mark J., Dominiczak, Anna, Padmanabhan, Sandosh, Montasser, May E., O’Connell, Jeff R., Ryan, Kathleen, Shuldiner, Alan R., Aeschbacher, Stefanie, Conen, David, Risch, Lorenz, Thériault, Sébastien, Hutri-Kähönen, Nina, Lehtimäki, Terho, Lyytikäinen, Leo-Pekka, Raitakari, Olli T., Barnes, Catriona L. K., Campbell, Harry, Joshi, Peter K., Wilson, James F., Isaacs, Aaron, Kors, Jan A., van Duijn, Cornelia M., Huang, Paul L., Gudnason, Vilmundur, Harris, Tamara B., Launer, Lenore J., Smith, Albert V., Bottinger, Erwin P., Loos, Ruth J. F., Nadkarni, Girish N., Preuss, Michael H., Correa, Adolfo, Mei, Hao, Wilson, James, Meitinger, Thomas, Müller-Nurasyid, Martina, Peters, Annette, Waldenberger, Melanie, Mangino, Massimo, Spector, Timothy D., Rienstra, Michiel, van de Vegte, Yordi J., van der Harst, Pim, Verweij, Niek, Kääb, Stefan, Schramm, Katharina, Sinner, Moritz F., Strauch, Konstantin, Cutler, Michael J., Fatkin, Diane, London, Barry, Olesen, Morten, Roden, Dan M., Benjamin Shoemaker, M., Gustav Smith, J., Biggs, Mary L., Bis, Joshua C., Brody, Jennifer A., Psaty, Bruce M., Rice, Kenneth, Sotoodehnia, Nona, De Grandi, Alessandro, Fuchsberger, Christian, Pattaro, Cristian, Pramstaller, Peter P., Ford, Ian, Wouter Jukema, J., Macfarlane, Peter W., Trompet, Stella, Dörr, Marcus, Felix, Stephan B., Völker, Uwe, Weiss, Stefan, Havulinna, Aki S., Jula, Antti, Sääksjärvi, Katri, Salomaa, Veikko, Guo, Xiuqing, Heckbert, Susan R., Lin, Henry J., Rotter, Jerome I., Taylor, Kent D., Yao, Jie, de Mutsert, Renée, Maan, Arie C., Mook-Kanamori, Dennis O., Noordam, Raymond, Cucca, Francesco, Ding, Jun, Lakatta, Edward G., Qian, Yong, Tarasov, Kirill V., Levy, Daniel, Lin, Honghuang, Newton-Cheh, Christopher H., Lunetta, Kathryn L., Murray, Alison D., Porteous, David J., Smith, Blair H., Stricker, Bruno H., Uitterlinden, André, van den Berg, Marten E., Haessler, Jeffrey, Jackson, Rebecca D., Kooperberg, Charles, Peters, Ulrike, Reiner, Alexander P., Whitsel, Eric A., Alonso, Alvaro, Arking, Dan E., Boerwinkle, Eric, Ehret, Georg B., Soliman, Elsayed Z., Avery, Christy L., Gogarten, Stephanie M., Kerr, Kathleen F., Laurie, Cathy C., Seyerle, Amanda A., Stilp, Adrienne, Assa, Solmaz, Abdullah Said, M., Yldau van der Ende, M., Lambiase, Pier D., Orini, Michele, Ramirez, Julia, Van Duijvenboden, Stefan, Arnar, David O., Gudbjartsson, Daniel F., Holm, Hilma, Sulem, Patrick, Thorleifsson, Gudmar, Thorolfsdottir, Rosa B., Thorsteinsdottir, Unnur, Benjamin, Emelia J., Tinker, Andrew, Stefansson, Kari, Ellinor, Patrick T., Jamshidi, Yalda, Lubitz, Steven A., and Munroe, Patricia B.
Published: 2020
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18. Genetic Variants Close to TTN , NKX2-5 , and MYH6 Associate With AVNRT

Author: Andreasen, Laura, Ahlberg, Gustav, Ægisdóttir, Hildur M., Sveinbjörnsson, Gardar, Lundegaard, Pia R., Hartmann, Jacob P., Paludan-Müller, Christian, Hadji-Turdeghal, Katra, Ghouse, Jonas, Pehrson, Steen, Jensen, Henrik K., Riahi, Sam, Hansen, Jim, Sandgaard, Niels, Sørensen, Erik, Banasik, Karina, Sækmose, Susanne G., Bruun, Mie T., Hjalgrim, Henrik, Erikstrup, Christian, Pedersen, Ole B., Wittig, Michael, Haunsø, Stig, Ostrowski, Sisse R., Genomic Consortium, Dbds, Franke, Andre, Brunak, Søren, Kanters, Jørgen K., Ellervik, Christina, Bundgaard, Henning, Ullum, Henrik, Gudbjartsson, Daniel F., Thorsteinsdottir, Unnur, Holm, Hilma, Arnar, David O., Stefansson, Kari, Svendsen, Jesper H., and Olesen, Morten S.
Subjects: Electrocardiography, supraventricular tachycardia, Heart Conduction System, Physiology, atrioventricular nodal reentry tachycardia, atrioventricular node, genetics, Cardiology and Cardiovascular Medicine
Published: 2022

19. Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study

Author: Yu Chen, Hao, Dina, Christian, Small, Aeron M, Shaffer, Christian M, Levinson, Rebecca T, Helgadóttir, Anna, Capoulade, Romain, Munter, Hans Markus, Martinsson, Andreas, Cairns, Benjamin J, Trudsø, Linea C, Hoekstra, Mary, Burr, Hannah A, Marsh, Thomas W, Damrauer, Scott M, Dufresne, Line, Le Scouarnec, Solena, Messika-Zeitoun, David, Ranatunga, Dilrini K, Whitmer, Rachel A, Bonnefond, Amélie, Sveinbjornsson, Garðar, Daníelsen, Ragnar, Arnar, David O, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Gudbjartsson, Daníel F, Hólm, Hilma, Ghouse, Jonas, Olesen, Morten Salling, Christensen, Alex H, Mikkelsen, Susan, Jacobsen, Rikke Louise, Dowsett, Joseph, Pedersen, Ole Birger Vesterager, Erikstrup, Christian, Ostrowski, Sisse R, Regeneron Genetics Center, O'Donnell, Christopher J, Budoff, Matthew J, Gudnason, Vilmundur, Post, Wendy S, Rotter, Jerome I, Lathrop, Mark, Bundgaard, Henning, Johansson, Bengt, Ljungberg, Johan, Näslund, Ulf, Le Tourneau, Thierry, Smith, J Gustav, Wells, Quinn S, Söderberg, Stefan, Stefánsson, Kári, Schott, Jean-Jacques, Rader, Daniel J, Clarke, Robert, Engert, James C, and Thanassoulis, George
Subjects: Genome-wide association study, Phenome-wide association study, Clinical Sciences, Cardiorespiratory Medicine and Haematology, Cardiovascular, Risk Factors, Mendelian randomization, Genetics, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Obesity, Polymorphism, Aetiology, Adiposity, Dyslipidemias, Inflammation, Aortic stenosis, Prevention, Human Genome, Aortic Valve Stenosis, Single Nucleotide, Mendelian Randomization Analysis, Regeneron Genetics Center, Genetic risk score, Apolipoproteins, Heart Disease, Cardiovascular System & Hematology, Gene expression, Genome-Wide Association Study
Abstract: AimsAlthough highly heritable, the genetic etiology of calcific aortic stenosis (AS) remains incompletely understood. The aim of this study was to discover novel genetic contributors to AS and to integrate functional, expression, and cross-phenotype data to identify mechanisms of AS.Methods and resultsA genome-wide meta-analysis of 11.6 million variants in 10 cohorts involving 653 867 European ancestry participants (13 765 cases) was performed. Seventeen loci were associated with AS at P ≤ 5 × 10-8, of which 15 replicated in an independent cohort of 90 828 participants (7111 cases), including CELSR2-SORT1, NLRP6, and SMC2. A genetic risk score comprised of the index variants was associated with AS [odds ratio (OR) per standard deviation, 1.31; 95% confidence interval (CI), 1.26-1.35; P = 2.7 × 10-51] and aortic valve calcium (OR per standard deviation, 1.22; 95% CI, 1.08-1.37; P = 1.4 × 10-3), after adjustment for known risk factors. A phenome-wide association study indicated multiple associations with coronary artery disease, apolipoprotein B, and triglycerides. Mendelian randomization supported a causal role for apolipoprotein B-containing lipoprotein particles in AS (OR per g/L of apolipoprotein B, 3.85; 95% CI, 2.90-5.12; P = 2.1 × 10-20) and replicated previous findings of causality for lipoprotein(a) (OR per natural logarithm, 1.20; 95% CI, 1.17-1.23; P = 4.8 × 10-73) and body mass index (OR per kg/m2, 1.07; 95% CI, 1.05-1.9; P = 1.9 × 10-12). Colocalization analyses using the GTEx database identified a role for differential expression of the genes LPA, SORT1, ACTR2, NOTCH4, IL6R, and FADS.ConclusionDyslipidemia, inflammation, calcification, and adiposity play important roles in the etiology of AS, implicating novel treatments and prevention strategies.
Published: 2023

20. Biobank-driven genomic discovery yields new insight into atrial fibrillation biology

Author: Nielsen, Jonas B., Thorolfsdottir, Rosa B., Fritsche, Lars G., Zhou, Wei, Skov, Morten W., Graham, Sarah E., Herron, Todd J., McCarthy, Shane, Schmidt, Ellen M., Sveinbjornsson, Gardar, Surakka, Ida, Mathis, Michael R., Yamazaki, Masatoshi, Crawford, Ryan D., Gabrielsen, Maiken E., Skogholt, Anne Heidi, Holmen, Oddgeir L., Lin, Maoxuan, Wolford, Brooke N., Dey, Rounak, Dalen, Håvard, Sulem, Patrick, Chung, Jonathan H., Backman, Joshua D., Arnar, David O., Thorsteinsdottir, Unnur, Baras, Aris, O’Dushlaine, Colm, Holst, Anders G., Wen, Xiaoquan, Hornsby, Whitney, Dewey, Frederick E., Boehnke, Michael, Kheterpal, Sachin, Mukherjee, Bhramar, Lee, Seunggeun, Kang, Hyun M., Holm, Hilma, Kitzman, Jacob, Shavit, Jordan A., Jalife, José, Brummett, Chad M., Teslovich, Tanya M., Carey, David J., Gudbjartsson, Daniel F., Stefansson, Kari, Abecasis, Gonçalo R., Hveem, Kristian, and Willer, Cristen J.
Published: 2018
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21. Evaluation of Large-Scale Proteomics for Prediction of Cardiovascular Events

Author: Helgason, Hannes, Eiriksdottir, Thjodbjorg, Ulfarsson, Magnus O., Choudhary, Abhishek, Lund, Sigrun H., Ivarsdottir, Erna V., Hjorleifsson Eldjarn, Grimur, Einarsson, Gudmundur, Ferkingstad, Egil, Moore, Kristjan H.S., Honarpour, Narimon, Liu, Thomas, Wang, Huei, Hucko, Thomas, Sabatine, Marc S., Morrow, David A., Giugliano, Robert P., Ostrowski, Sisse Rye, Pedersen, Ole Birger, Bundgaard, Henning, Erikstrup, Christian, Arnar, David O., Thorgeirsson, Gudmundur, Masson, Gísli, Magnusson, Olafur Th, Saemundsdottir, Jona, Gretarsdottir, Solveig, Steinthorsdottir, Valgerdur, Thorleifsson, Gudmar, Helgadottir, Anna, Sulem, Patrick, Thorsteinsdottir, Unnur, Holm, Hilma, Gudbjartsson, Daniel, Stefansson, Kari, Helgason, Hannes, Eiriksdottir, Thjodbjorg, Ulfarsson, Magnus O., Choudhary, Abhishek, Lund, Sigrun H., Ivarsdottir, Erna V., Hjorleifsson Eldjarn, Grimur, Einarsson, Gudmundur, Ferkingstad, Egil, Moore, Kristjan H.S., Honarpour, Narimon, Liu, Thomas, Wang, Huei, Hucko, Thomas, Sabatine, Marc S., Morrow, David A., Giugliano, Robert P., Ostrowski, Sisse Rye, Pedersen, Ole Birger, Bundgaard, Henning, Erikstrup, Christian, Arnar, David O., Thorgeirsson, Gudmundur, Masson, Gísli, Magnusson, Olafur Th, Saemundsdottir, Jona, Gretarsdottir, Solveig, Steinthorsdottir, Valgerdur, Thorleifsson, Gudmar, Helgadottir, Anna, Sulem, Patrick, Thorsteinsdottir, Unnur, Holm, Hilma, Gudbjartsson, Daniel, and Stefansson, Kari
Abstract: Importance: Whether protein risk scores derived from a single plasma sample could be useful for risk assessment for atherosclerotic cardiovascular disease (ASCVD), in conjunction with clinical risk factors and polygenic risk scores, is uncertain. Objective: To develop protein risk scores for ASCVD risk prediction and compare them to clinical risk factors and polygenic risk scores in primary and secondary event populations. Design, Setting, and Participants: The primary analysis was a retrospective study of primary events among 13540 individuals in Iceland (aged 40-75 years) with proteomics data and no history of major ASCVD events at recruitment (study duration, August 23, 2000 until October 26, 2006; follow-up through 2018). We also analyzed a secondary event population from a randomized, double-blind lipid-lowering clinical trial (2013-2016), consisting of individuals with stable ASCVD receiving statin therapy and for whom proteomic data were available for 6791 individuals. Exposures: Protein risk scores (based on 4963 plasma protein levels and developed in a training set in the primary event population); polygenic risk scores for coronary artery disease and stroke; and clinical risk factors that included age, sex, statin use, hypertension treatment, type 2 diabetes, body mass index, and smoking status at the time of plasma sampling. Main Outcomes and Measures: Outcomes were composites of myocardial infarction, stroke, and coronary heart disease death or cardiovascular death. Performance was evaluated using Cox survival models and measures of discrimination and reclassification that accounted for the competing risk of non-ASCVD death. Results: In the primary event population test set (4018 individuals [59.0% women]; 465 events; median follow-up, 15.8 years), the protein risk score had a hazard ratio (HR) of 1.93 per SD (95% CI, 1.75 to 2.13). Addition of protein risk score and polygenic risk scores significantly increased the C index when added to a clinical ri
Published: 2023

22. Genetic variants associated with syncope implicate neural and autonomic processes

Author: Aegisdottir, Hildur M., Thorolfsdottir, Rosa B., Sveinbjornsson, Gardar, Stefansson, Olafur A., Gunnarsson, Bjarni, Tragante, Vinicius, Thorleifsson, Gudmar, Stefansdottir, Lilja, Thorgeirsson, Thorgeir E., Ferkingstad, Egil, Sulem, Patrick, Norddahl, Gudmundur, Rutsdottir, Gudrun, Banasik, Karina, Christensen, Alex Hoerby, Mikkelsen, Christina, Pedersen, Ole Birger, Brunak, Søren, Bruun, Mie Topholm, Erikstrup, Christian, Jacobsen, Rikke Louise, Nielsen, Kaspar Rene, Sorensen, Erik, Frigge, Michael L., Hjorleifsson, Kristjan E., Ivarsdottir, Erna, Helgadottir, Anna, Gretarsdottir, Solveig, Steinthorsdottir, Valgerdur, Oddsson, Asmundur, Eggertsson, Hannes P., Halldorsson, Gisli H., Jones, David A., Anderson, Jeffrey L., Knowlton, Kirk U., Nadauld, Lincoln D., DBDS Genomic Consortium, D. B. D. S. Genomic Consortium, Haraldsson, Magnus, Thorgeirsson, Gudmundur, Bundgaard, Henning, Arnar, David O., Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F., Ostrowsk, Sisse R., Holm, Hilma, Stefansson, Kari, Aegisdottir, Hildur M., Thorolfsdottir, Rosa B., Sveinbjornsson, Gardar, Stefansson, Olafur A., Gunnarsson, Bjarni, Tragante, Vinicius, Thorleifsson, Gudmar, Stefansdottir, Lilja, Thorgeirsson, Thorgeir E., Ferkingstad, Egil, Sulem, Patrick, Norddahl, Gudmundur, Rutsdottir, Gudrun, Banasik, Karina, Christensen, Alex Hoerby, Mikkelsen, Christina, Pedersen, Ole Birger, Brunak, Søren, Bruun, Mie Topholm, Erikstrup, Christian, Jacobsen, Rikke Louise, Nielsen, Kaspar Rene, Sorensen, Erik, Frigge, Michael L., Hjorleifsson, Kristjan E., Ivarsdottir, Erna, Helgadottir, Anna, Gretarsdottir, Solveig, Steinthorsdottir, Valgerdur, Oddsson, Asmundur, Eggertsson, Hannes P., Halldorsson, Gisli H., Jones, David A., Anderson, Jeffrey L., Knowlton, Kirk U., Nadauld, Lincoln D., DBDS Genomic Consortium, D. B. D. S. Genomic Consortium, Haraldsson, Magnus, Thorgeirsson, Gudmundur, Bundgaard, Henning, Arnar, David O., Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F., Ostrowsk, Sisse R., Holm, Hilma, and Stefansson, Kari
Abstract: Aims Syncope is a common and clinically challenging condition. In this study, the genetics of syncope were investigated to seek knowledge about its pathophysiology and prognostic implications. Methods and results This genome-wide association meta-analysis included 56 071 syncope cases and 890 790 controls from deCODE genetics (Iceland), UK Biobank (United Kingdom), and Copenhagen Hospital Biobank Cardiovascular Study/Danish Blood Donor Study (Denmark), with a follow-up assessment of variants in 22 412 cases and 286 003 controls from Intermountain (Utah, USA) and FinnGen (Finland). The study yielded 18 independent syncope variants, 17 of which were novel. One of the variants, p.Ser140Thr in PTPRN2, affected syncope only when maternally inherited. Another variant associated with a vasovagal reaction during blood donation and five others with heart rate and/or blood pressure regulation, with variable directions of effects. None of the 18 associations could be attributed to cardiovascular or other disorders. Annotation with regard to regulatory elements indicated that the syncope variants were preferentially located in neural-specific regulatory regions. Mendelian randomization analysis supported a causal effect of coronary artery disease on syncope. A polygenic score (PGS) for syncope captured genetic correlation with cardiovascular disorders, diabetes, depression, and shortened lifespan. However, a score based solely on the 18 syncope variants performed similarly to the PGS in detecting syncope risk but did not associate with other disorders. Conclusion The results demonstrate that syncope has a distinct genetic architecture that implicates neural regulatory processes and a complex relationship with heart rate and blood pressure regulation. A shared genetic background with poor cardiovascular health was observed, supporting the importance of a thorough assessment of individuals presenting with syncope.
Published: 2023

23. GWAS Summary Statistics from a Global Meta-Analysis of Aortic Stenosis

Author: Chen, Hao Yu, PhD, Dina, Christian, PhD, Small, Aeron M., MD, Shaffer, Christian M., Levinson, Rebecca T., PhD, Helgadóttir, Anna, MD, PhD, Capoulade, Romain, PhD, Munter, Hans Markus, PhD, Martinsson, Andreas, MD, Cairns, Benjamin J., PhD, Trudsø, Linea C., Hoekstra, Mary, Burr, Hannah A., Marsh, Thomas W., Damrauer, Scott M., MD, Dufresne, Line, Scouarnec, Solena Le, PhD, Messika-Zeitoun, David, MD, PhD, Ranatunga, Dilrini K., Whitmer, Rachel A., PhD, Bonnefond, Amélie, PhD, Sveinbjornsson, Garðar, Daníelsen, Ragnar, MD, PhD, Arnar, David O., MD, PhD, Thorgeirsson, Gudmundur, MD, PhD, Thorsteinsdottir, Unnur, PhD, Gudbjartsson, Daníel F., PhD, Hólm, Hilma, MD, Ghouse, Jonas, MD, Olesen, Morten Salling, PhD, Christensen, Alex H., MD, Mikkelsen, Susan, MD, Jacobsen, Rikke Louise, Dowsett, Joseph, Pedersen, Ole Birger Vesterager, MD, Erikstrup, Christian, MD, Ostrowski, Sisse R., Regeneron Genetics Center, O'Donnell, Christopher J., MD, Budoff, Matthew J., MD, Gudnason, Vilmundur, MD, Post, Wendy S., MD, Rotter, Jerome I., MD, Lathrop, Mark, PhD, Bundgaard, Henning, Johansson, Bengt, MD, PhD, Ljungberg, Johan, MD, PhD, Näslund, Ulf, MD, PhD, Tourneau, Thierry Le, MD, PhD, Smith, J. Gustav, MD, Wells, Quinn S., MD, Söderberg, Stefan, MD, PhD, Stefánsson, Kári, MD, PhD, Schott, Jean-Jacques, PhD, Rader, Daniel J., MD, Clarke, Robert, MD, Engert, James C., PhD, and Thanassoulis, George
Abstract: GWAS Summary Statistics for a Global Meta-Analysis of Aortic Stenosis in the TARGET Consortium 10.5281/zenodo.7630002 This dataset contains the genome-wide association summary statistics for a Global Meta-Analysis of Aortic Stenosis. For the analysis description and included cohorts, please see Chen et al., the European Heart Journal (2023). The data are provided on an "AS-IS" basis, without warranty of any type, expressed or implied, including but not limited to any warranty as to their performance, merchantability, or fitness for any particular purpose. If investigators use these data, any and all consequences are entirely their responsibility. By downloading and using these data, you agree that you will cite the appropriate publication in any communications or publications arising directly or indirectly from these data. When using this data, please cite the paper and this repository: Chenet al., GWAS Summary Statistics for a Global Meta-Analysis of Aortic Stenosis,the European Heart Journal (2023). Zenodo.10.5281/zenodo.7630002 Column headers: CHR: Chromosome code. Not present with 'no-map' modifier. BP: Base-pair coordinate. Not present with 'no-map' modifier. SNP: Variant identifier A1: Effect Allele A2: Other Allele N_cohort: Number of valid studies for variant P: Fixed-effects meta-analysis p-value P.R.: Random-effects meta-analysis p-value OR: Fixed-effects BETA/OR estimate OR.R.: Random-effects BETA/OR estimate Q: p-value for Cochran's Q statistic I: I2 heterogeneity index (0-100 scale) N_ind: Number of individuals Fundings: Fundings for this study were obtained from the following (listed in alphabetical order): ALFEDIAM Ardix Medical Assistance Publique - Hôpitaux de Paris Association Diabète Risque Vasculaire Bayer Diagnostics Becton Dickinson British Heart Foundation British Heart Foundation Oxford Centre Canadian Institutes for Health Research Capital Regions Research Council Cardionics, Merck Santé, Novo Nordisk CNAMTS, Lilly, Novartis Pharma Cohortes Santé TGIR County Council of Västerbotten Crafoord Foundation Ellison Medical Foundation European Research Council Fédération Française de Cardiologie Fédération Française de Cardiologie, a Fondation Coeur et Recherche Fonds de Recherche du Québec - Santé. French Regional Council of Pays-de-la-Loire (VaCaRMe program) Heart and Stroke Foundation of Canada Heart Foundation of Northern Sweden. Kaiser Permanente Knut and Alice Wallenberg foundation to the Wallenberg Center La Fondation de France Medical Research Council and the University of Oxford National Center for Advancing Translational Sciences (CTSI) National Heart, Lung, and Blood Institute (NHLBI) National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) National Institutes of Health Novo Nordisk Foundation ONIVINS Robert Wood Johnson Foundation Sanofi-Aventis; by INSERM (Réseaux en Santé Publique, Interactions entre les déterminants de la santé) Skåne University Hospital Société francophone du diabète Swedish Foundation for Strategic Research Swedish Heart–Lung Foundation Swedish National Health Service Swedish Research Council The Innovation Fund Denmark Umeå University U.S. Department of Veteran Affairs Vanderbilt University Medical Center’s institutional funding Wayne and Gladys Valley Foundation &nbsp
Published: 2023
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24. Mechanisms of atrial fibrillation: genetics

Author: Arnar, David O., primary and Holm, Hilma, additional
Published: 2018
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25. Sequence variants with large effects on cardiac electrophysiology and disease

Author: Norland, Kristjan, Sveinbjornsson, Gardar, Thorolfsdottir, Rosa B., Davidsson, Olafur B., Tragante, Vinicius, Rajamani, Sridharan, Helgadottir, Anna, Gretarsdottir, Solveig, van Setten, Jessica, Asselbergs, Folkert W., Sverrisson, Jon Th., Stephensen, Sigurdur S., Oskarsson, Gylfi, Sigurdsson, Emil L., Andersen, Karl, Danielsen, Ragnar, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Arnar, David O., Sulem, Patrick, Holm, Hilma, Gudbjartsson, Daniel F., and Stefansson, Kari
Published: 2019
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26. Fiix-prothrombin time versus standard prothrombin time for monitoring of warfarin anticoagulation: a single centre, double-blind, randomised, non-inferiority trial

Author: Onundarson, Páll T, Francis, Charles W, Indridason, Olafur S, Arnar, David O, Bjornsson, Einar S, Magnusson, Magnus K, Juliusson, Sigurdur J, Jensdottir, Hulda M, Vidarsson, Brynjar, Gunnarsson, Petur S, Lund, Sigrun H, and Gudmundsdottir, Brynja R
Published: 2015
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27. Reduced anticoagulation variability in patients on warfarin monitored with Fiix-prothrombin time associates with reduced thromboembolism: The Fiix-trial

Author: Oskarsdóttir, Alma Rut, Gudmundsdottir, Brynja R., Indridason, Olafur S., Lund, Sigrun H., Arnar, David O., Bjornsson, Einar S., Magnusson, Magnus K., Jensdottir, Hulda M., Vidarsson, Brynjar, Francis, Charles W., and Onundarson, Pall T.
Published: 2017
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28. Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants

Author: Aragam, Krishna G, Jiang, Tao, Goel, Anuj, Kanoni, Stavroula, Wolford, Brooke N, Atri, Deepak S, Weeks, Elle M, Wang, Minxian, Hindy, George, Zhou, Wei, Grace, Christopher, Roselli, Carolina, Marston, Nicholas A, Kamanu, Frederick K, Surakka, Ida, Venegas, Loreto Muñoz, Sherliker, Paul, Koyama, Satoshi, Ishigaki, Kazuyoshi, Åsvold, Bjørn O, Brown, Michael R, Brumpton, Ben, De Vries, Paul S, Giannakopoulou, Olga, Giardoglou, Panagiota, Gudbjartsson, Daniel F, Güldener, Ulrich, Haider, Syed M Ijlal, Helgadottir, Anna, Ibrahim, Maysson, Kastrati, Adnan, Kessler, Thorsten, Kyriakou, Theodosios, Konopka, Tomasz, Li, Ling, Ma, Lijiang, Meitinger, Thomas, Mucha, Sören, Munz, Matthias, Murgia, Federico, Nielsen, Jonas B, Nöthen, Markus M, Pang, Shichao, Reinberger, Tobias, Schnitzler, Gavin, Smedley, Damian, Thorleifsson, Gudmar, Von Scheidt, Moritz, Ulirsch, Jacob C, Danesh, John, Arnar, David O, Burtt, Noël P, Costanzo, Maria C, Flannick, Jason, Ito, Kaoru, Jang, Dong-Keun, Kamatani, Yoichiro, Khera, Amit V, Komuro, Issei, Kullo, Iftikhar J, Lotta, Luca A, Nelson, Christopher P, Roberts, Robert, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Webb, Thomas R, Baras, Aris, Björkegren, Johan LM, Boerwinkle, Eric, Dedoussis, George, Holm, Hilma, Hveem, Kristian, Melander, Olle, Morrison, Alanna C, Orho-Melander, Marju, Rallidis, Loukianos S, Ruusalepp, Arno, Sabatine, Marc S, Stefansson, Kari, Zalloua, Pierre, Ellinor, Patrick T, Farrall, Martin, Ruff, Christian T, Finucane, Hilary K, Hopewell, Jemma C, Clarke, Robert, Gupta, Rajat M, Erdmann, Jeanette, Samani, Nilesh J, Schunkert, Heribert, Watkins, Hugh, Willer, Cristen J, Deloukas, Panos, Kathiresan, Sekar, Butterworth, Adam S, Aragam, Krishna G [0000-0003-3223-9131], Goel, Anuj [0000-0003-2307-4021], Kanoni, Stavroula [0000-0002-1691-9615], Wolford, Brooke N [0000-0003-3153-1552], Atri, Deepak S [0000-0001-8139-5419], Weeks, Elle M [0000-0002-4317-4444], Wang, Minxian [0000-0002-3753-508X], Zhou, Wei [0000-0001-7719-0859], Roselli, Carolina [0000-0001-5267-6756], Kamanu, Frederick K [0000-0001-7208-1047], Koyama, Satoshi [0000-0002-9286-0360], Ishigaki, Kazuyoshi [0000-0003-2881-0657], Åsvold, Bjørn O [0000-0003-3837-2101], Brumpton, Ben [0000-0002-3058-1059], Gudbjartsson, Daniel F [0000-0002-5222-9857], Güldener, Ulrich [0000-0001-5052-8610], Helgadottir, Anna [0000-0002-1806-2467], Kessler, Thorsten [0000-0003-3326-1621], Li, Ling [0000-0002-3280-9475], Mucha, Sören [0000-0002-1647-2526], Munz, Matthias [0000-0002-4728-3357], Murgia, Federico [0000-0002-3608-845X], Pang, Shichao [0000-0002-4111-2864], Smedley, Damian [0000-0002-5836-9850], Thorleifsson, Gudmar [0000-0003-4623-9087], von Scheidt, Moritz [0000-0001-7159-8271], Ulirsch, Jacob C [0000-0002-7947-0827], Costanzo, Maria C [0000-0001-9043-693X], Flannick, Jason [0000-0002-3618-795X], Ito, Kaoru [0000-0003-1843-773X], Khera, Amit V [0000-0001-6535-5839], Komuro, Issei [0000-0002-0714-7182], Kullo, Iftikhar J [0000-0002-6524-3471], Roberts, Robert [0000-0002-6792-4633], Webb, Thomas R [0000-0001-5998-8226], Baras, Aris [0000-0002-6830-3396], Björkegren, Johan LM [0000-0003-1945-7425], Holm, Hilma [0000-0002-9517-6636], Morrison, Alanna C [0000-0001-6381-4296], Orho-Melander, Marju [0000-0002-3578-2503], Stefansson, Kari [0000-0003-1676-864X], Farrall, Martin [0000-0003-4564-2165], Finucane, Hilary K [0000-0003-3864-9828], Clarke, Robert [0000-0002-9802-8241], Erdmann, Jeanette [0000-0002-4486-6231], Samani, Nilesh J [0000-0002-3286-8133], Schunkert, Heribert [0000-0001-6428-3001], Watkins, Hugh [0000-0002-5287-9016], Willer, Cristen J [0000-0001-5645-4966], Kathiresan, Sekar [0000-0002-3711-7101], Butterworth, Adam S [0000-0002-6915-9015], and Apollo - University of Cambridge Repository
Subjects: 692/699/75/2, 631/208/205/2138, article, Humans, Coronary Artery Disease, Genome-Wide Association Study
Abstract: Funder: K.G.A. has received support from the American Heart Association Institute for Precision Cardiovascular Medicine (17IFUNP3384001), a KL2/Catalyst Medical Research Investigator Training (CMeRIT) award from the Harvard Catalyst (KL2 TR002542), and the NIH (1K08HL153937)., Funder: B.N.W is supported by the National Science Foundation Graduate Research Program (DGE 1256260)., Funder: I.S. is supported by a Precision Health Scholars Award from the University of Michigan Medical School., Funder: I.K., S.Ko., and K.It. are funded by the Japan Agency for Medical Research and Development, AMED, under Grant Numbers JP16ek0109070h0003, JP18kk0205008h0003, JP18kk0205001s0703, JP20km0405209, and JP20ek0109487. The BioBank Japan is supported by AMED under Grant Number JP20km0605001., Funder: J.L.M.B. acknowledges research support from NIH R01HL125863, American Heart Association (A14SFRN20840000), the Swedish Research Council (2018-02529) and Heart Lung Foundation (20170265) and the Foundation Leducq (PlaqueOmics: Novel Roles of Smooth Muscle and Other Matrix Producing Cells in Atherosclerotic Plaque Stability and Rupture, 18CVD02., Funder: P.S.dV was supported by American Heart Association grant number 18CDA34110116 and National Heart, Lung, and Blood Institute grant R01HL146860. The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services (contract numbers HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I and HHSN268201700005I), R01HL087641, R01HL059367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research., Funder: O.G. has received funding from the British Heart Foundation (BHF) (FS/14/66/3129)., Funder: T.K. is supported by the Corona-Foundation (Junior Research Group Translational Cardiovascular Genomics) and the German Research Foundation (DFG) as part of the Sonderforschungsbereich SFB 1123 (B02)., Funder: D.S.A. has received support from a training grant from the NIH (T32HL007604)., Funder: N.P.B., M.C.C., J.F., and D.-K.J. have been funded by the National Institute of Diabetes and Digestive and Kidney Diseases (2UM1DK105554)., Funder: A.V.K. has been funded by 1K08HG010155 from the National Human Genome Research Institute., Funder: C.P.N. and T.R.W received funding from the British Heart Foundation (SP/16/4/32697)., Funder: The Trøndelag Health Study (The HUNT Study) is a collaboration between HUNT Research Centre (Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology), Trøndelag County Council, Central Norway Regional Health Authority, and the Norwegian Institute of Public Health. The K.G. Jebsen Center for Genetic Epidemiology is financed by Stiftelsen Kristian Gerhard Jebsen; Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology; and Central Norway Regional Health Authority. Whole genome sequencing for the HUNT study was funded by HL109946., Funder: O.M. was funded by the Swedish Heart- and Lung Foundation, the Swedish Research Council, the European Research Council ERC-AdG-2019-885003 and Lund University Infrastructure grant ”Malmö population-based cohorts” (STYR 2019/2046)., Funder: This work was supported by the European Commission (HEALTH-F2–2013-601456) and the TriPartite Immunometabolism Consortium [TrIC]- NovoNordisk Foundation (NNF15CC0018486), VIAgenomics (SP/19/2/344612), the British Heart Foundation, a Wellcome Trust core award (M.F., H.W., 203141/Z/16/Z) and support from the NIHR Oxford Biomedical Research Centre. M.F. and H.W. are members of the Oxford BHF Centre of Research Excellence (RE/13/1/30181). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health., Funder: J.D. is a British Heart Foundation Professor, European Research Council Senior Investigator, and National Institute for Health Research (NIHR) Senior Investigator., Funder: J.C.H. acknowledges personal funding from the British Heart Foundation (FS/14/55/30806) and is a member of the Oxford BHF Centre of Research Excellence (RE/13/1/30181)., Funder: R.C. has received funding from the British Heart Foundation and British Heart Foundation Centre of Research Excellence., Funder: This research was supported by BHF (SP/13/2/30111) and conducted using the UK Biobank Resource (application number 9922)., Funder: The GerMIFs gratefully acknowledge the support of the Bavarian State Ministry of Health and Care, furthermore founded this work within its framework of DigiMed Bayern (grant No: DMB-1805-0001), the German Federal Ministry of Education and Research (BMBF) within the framework of ERA-NET on Cardiovascular Disease (Druggable-MI-genes: 01KL1802), within the scheme of target validation (BlockCAD: 16GW0198K), within the framework of the e:Med research and funding concept (AbCD-Net: 01ZX1706C), the British Heart Foundation (BHF)/German Centre of Cardiovascular Research (DZHK)-collaboration (VIAgenomics) and the German Research Foundation (DFG) as part of the Sonderforschungsbereich SFB 1123 (B02) and the Sonderforschungsbereich SFB TRR 267 (B05)., Funder: C.J.W. is funded by NIH grant R35-HL135824., Funder: This work was supported by the British Heart Foundation (BHF) grant RG/14/5/30893 (P.D.) and forms part of the research themes contributing to the translational research portfolios of the Barts Biomedical Research Centre funded by the UK National Institute for Health Research (NIHR)., The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We prioritized 220 candidate causal genes, combining eight complementary approaches, including 123 supported by three or more approaches. Using CRISPR–Cas9, we experimentally validated the effect of an enhancer in MYO9B, which appears to mediate CAD risk by regulating vascular cell motility. Our analysis identifies and systematically characterizes >250 risk loci for CAD to inform experimental interrogation of putative causal mechanisms for CAD.
Published: 2022
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29. Cholesterol not particle concentration mediates the atherogenic risk conferred by apolipoprotein B particles:A Mendelian randomization analysis

Author: Helgadottir, Anna, Thorleifsson, Gudmar, Snaebjarnarson, Audunn, Stefansdottir, Lilja, Sveinbjornsson, Gardar, Tragante, Vinicius, Björnsson, Eyþór, Steinthorsdottir, Valgerdur, Gretarsdottir, Solveig, Helgason, Hannes, Saemundsdottir, Jona, Olafsson, Isleifur, Thune, Jens Jakob, Axelsson Raja, Anna, Ghouse, Jonas, Olesen, Morten Salling, Christensen, Alex, Jacobsen, Rikke Louise, Dowsett, Joseph, Bruun, Mie Topholm, Nielsen, Kaspar, Knowlton, Kirk, Nadauld, Lincoln, Benediktsson, Rafn, Erikstrup, Christian, Pedersen, Ole B., Banasik, Karina, Brunak, Søren, Bundgaard, Henning, Ostrowski, Sisse R., Sulem, Patrick, Arnar, David O., Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F., Stefansson, Kari, Holm, Hilma, and Nyegaard, Mette
Subjects: Epidemiology, Apolipoproteins B/genetics, Coronary Artery Disease/genetics, Lipoproteins, Cholesterol, HDL, Non-HDL cholesterol, Coronary Artery Disease, Cholesterol, LDL, Mendelian Randomization Analysis, Atherosclerosis, Apolipoprotein, Cholesterol, Apolipoprotein B-100/genetics, Risk Factors, Apolipoprotein B-100, Mendelian randomization, Humans, Cardiology and Cardiovascular Medicine, Apolipoprotein B, Apolipoproteins B
Abstract: Background and aims:The causal contribution of apolipoprotein B (apoB) particles to coronary artery disease (CAD) is established. We examined whether this atherogenic contribution is better reflected by non-high-density lipoprotein cholesterol (non-HDL-C) or apoB particle concentration.Method and results:We performed Mendelian randomization (MR) analysis using 235 variants as genetic instruments; testing the relationship between their effects on the exposures, non-HDL-C and apoB, and on the outcome CAD using weighted regression. Variant effect estimates on the exposures came from the UK Biobank (N = 376 336) and on the outcome from a meta-analysis of five CAD datasets (187 451 cases and 793 315 controls). Subsequently, we carried out sensitivity and replication analyses.In univariate MR analysis, both exposures associated with CAD (βnon-HDL-C = 0.40, P = 2.8 × 10−48 and βapoB = 0.38, P = 1.3 × 10−44). Adding effects on non-HDL-C into a model that already included those on apoB significantly improved the genetically predicted CAD effects (P = 3.9 × 10−5), while adding apoB into the model including non-HDL-C did not (P = 0.69). Thirty-five per cent (82/235) of the variants used as genetic instruments had discordant effects on the exposures, associating with non-HDL-C/apoB ratio at P Conclusion:Many sequence variants have discordant effects on non-HDL-C and apoB. These variants allowed us to show that the causal mechanism underlying the relationship between apolipoprotein B particles and CAD is more associated with non-HDL-C than apoB particle concentration.
Published: 2022

30. Improving outpatient care for heart failure through digital innovation: A feasibility study

Author: Arnar, David O., primary, Oddsson, Saemundur J., additional, Gunnarsdottir, Thrudur, additional, Gudlaugsdottir, Gudbjorg Jona, additional, Gudmundsson, Elias Freyr, additional, Ketilsdóttir, Audur, additional, Halldorsdottir, Hulda, additional, Hrafnkelsdottir, Thordis Jona, additional, Hallsson, Hallur, additional, Amundadottir, Maria L., additional, and Thorgeirsson, Tryggvi, additional
Published: 2022
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31. Integrating new approaches to atrial fibrillation management: the 6th AFNET/EHRA Consensus Conference

Author: Kotecha, Dipak, Breithardt, Günter, Camm, A John, Lip, Gregory Y H, Schotten, Ulrich, Ahlsson, Anders, Arnar, David, Atar, Dan, Auricchio, Angelo, Bax, Jeroen, Benussi, Stefano, Blomstrom-Lundqvist, Carina, Borggrefe, Martin, Boriani, Giuseppe, Brandes, Axel, Calkins, Hugh, Casadei, Barbara, Castellá, Manuel, Chua, Winnie, Crijns, Harry, Dobrev, Dobromir, Fabritz, Larissa, Feuring, Martin, Freedman, Ben, Gerth, Andrea, Goette, Andreas, Guasch, Eduard, Haase, Doreen, Hatem, Stephane, Haeusler, Karl Georg, Heidbuchel, Hein, Hendriks, Jeroen, Hunter, Craig, Kääb, Stefan, Kespohl, Stefanie, Landmesser, Ulf, Lane, Deirdre A, Lewalter, Thorsten, Mont, Lluís, Nabauer, Michael, Nielsen, Jens C, Oeff, Michael, Oldgren, Jonas, Oto, Ali, Pison, Laurent, Potpara, Tatjana, Ravens, Ursula, Richard-Lordereau, Isabelle, Rienstra, Michiel, Savelieva, Irina, Schnabel, Renate, Sinner, Moritz F, Sommer, Philipp, Themistoclakis, Sakis, Van Gelder, Isabelle C, Vardas, Panagiotis E, Verma, Atul, Wakili, Reza, Weber, Evelyn, Werring, David, Willems, Stephan, Ziegler, André, Hindricks, Gerhard, and Kirchhof, Paulus
Published: 2018
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32. Coding variants in RPL3L and MYZAP increase risk of atrial fibrillation

Author: Thorolfsdottir, Rosa B., Sveinbjornsson, Gardar, Sulem, Patrick, Nielsen, Jonas B., Jonsson, Stefan, Halldorsson, Gisli H., Melsted, Pall, Ivarsdottir, Erna V., Davidsson, Olafur B., Kristjansson, Ragnar P., Thorleifsson, Gudmar, Helgadottir, Anna, Gretarsdottir, Solveig, Norddahl, Gudmundur, Rajamani, Sridharan, Torfason, Bjarni, Valgardsson, Atli S., Sverrisson, Jon T., Tragante, Vinicius, Holmen, Oddgeir L., Asselbergs, Folkert W., Roden, Dan M., Darbar, Dawood, Pedersen, Terje R., Sabatine, Marc S., Willer, Cristen J., Løchen, Maja-Lisa, Halldorsson, Bjarni V., Jonsdottir, Ingileif, Hveem, Kristian, Arnar, David O., Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F., Holm, Hilma, and Stefansson, Kari
Published: 2018
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33. Symptoms, physical measures and cognitive tests after SARS-CoV-2 infection in a large population-based case-control study

Author: Holm, Hilma, primary, Ivarsdottir, Erna, additional, Olafsdottir, Thorhildur, additional, Thorolfsdottir, Rosa, additional, Eythorsson, Elias, additional, Norland, Kristjan, additional, Gisladottir, Rosa, additional, Jonsdottir, Gudrun, additional, Unnsteinsdottir, Unnur, additional, Sveinsdottir, Kristin, additional, Jonsson, Benedikt, additional, Andresdottir, Margret, additional, Arnar, David, additional, Arnthorsson, Asgeir, additional, Birgisdottir, Kolbrun, additional, Bjarnadottir, Kristborg, additional, Bjarnadottir, Solveig, additional, Bjornsdottir, Gyda, additional, Einarsson, Gudmundur, additional, Eiriksdottir, Berglind, additional, Gardarsdottir, Elisabet, additional, Gislason, Thorarinn, additional, Gottfredsson, Magnus, additional, Gudmunsdottir, Steinunn, additional, Gudmundsson, Julius, additional, Gunnarsdottir, Kristbjorg, additional, Helgadóttir, Anna, additional, Helgason, Dadi, additional, Hinriksdottir, Ingibjorg, additional, Ingvarsson, Ragnar, additional, Jonasdottir, Sigga, additional, Jonsdottir, Ingileif, additional, Karlsdottir, Tekla, additional, Kristinsdottir, Anna, additional, Kristinsson, Sigurdur, additional, Kristjansdottir, Steinunn, additional, Love, Thorvardur, additional, Ludviksdottir, Dora, additional, Masson, Gisli, additional, Nordahl, Gudmundur, additional, Olafsdottir, Thorunn, additional, Olafsson, Isleifur, additional, Rafnar, Thorunn, additional, Runolfsdottir, Hrafnhildur, additional, Saemundsdottir, Jona, additional, Sigurbjornsson, Svanur, additional, Sigurdardottir, Kristin, additional, Sigurdsson, Engilbert, additional, Steinthorsdottir, Valgerdur, additional, Sveinbjornsson, Gardar, additional, Thorarensen, Emil, additional, Thorbjornsson, Bjarni, additional, Thorsteinsdottir, Brynja, additional, Tragante, Vinicius, additional, Ulfarsson, Magnus, additional, Sigurdsson, Martin, additional, Sigurdsson, Emil, additional, Stefansson, Hreinn, additional, Gislason, Thorsteinn, additional, Palsson, Runolfur, additional, Kristjansson, Mar, additional, Sulem, Patrick, additional, Thorsteinsdottir, Unnur, additional, Thorgeirsson, Gudmundur, additional, Gudbjartsson, Daniel, additional, and Stefansson, Kari, additional
Published: 2022
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34. Abstract P049: A Digital Therapeutic Intervention Is Feasible For Outpatient Care In Coronary Artery Disease

Author: Arnar, David O, primary, Oddsson, Saemundur, additional, Gunnarsdottir, Thrudur, additional, Olafsdottir, Inga V, additional, Gudmundsdottir, Maria V, additional, Loftsson, Kjartan H, additional, Gudmundsson, Elias F, additional, Kaernested, Bylgja, additional, Amundadottir, Maria L, additional, Sigurdardottir, Svala, additional, Mogensen, Brynjolfur, additional, Libungan, Berglind, additional, and Thorgeirsson, Tryggvi, additional
Published: 2022
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35. Abstract 13222: Genetic Variants Close to NKX2-5 and MYH6 Are Associated With AV Nodal Reentry Tachycardia in First Genome-Wide Association Study

Author: Andreasen, Laura, primary, Ahlberg, Gustav, additional, Lundegaard, Pia Rengtved, additional, Ægisdottir, Hildur, additional, Hartmann, Jacob Peter, additional, Paludan-Mueller, Christian, additional, Hadji-Turdeghal, Katra, additional, Ghouse, Jonas, additional, Pehrson, Steen, additional, Jensen, Henrik, additional, Riahi, Sam, additional, Hansen, Jim, additional, Sandgaard, Niels, additional, Haunso, stig, additional, Kanters, Jorgen, additional, Ellervik, Christina, additional, Bundgaard, Henning, additional, Ullum, Henrik, additional, Holm, Hilma, additional, Arnar, David, additional, Svendsen, Jesper Hastrup, additional, and Olesen, Morten, additional
Published: 2021
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36. Statistics on the use of cardiac electronic devices and electrophysiological procedures in the European Society of Cardiology countries: 2014 report from the European Heart Rhythm Association

Author: Raatikainen, M.J. Pekka, Arnar, David O., Zeppenfeld, Katja, Merino, Jose Luis, Levya, Francisco, Hindriks, Gerhardt, and Kuck, Karl-Heinz
Published: 2015
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37. Major Bleeding of Transjugular Native Kidney Biopsies. A French Nationwide Cohort Study

Author: Hindricks, Gerhard, Potpara, Tatjana, Dagres, Nikolaos, Arbelo, Elena, Bax, Jeroen, Blomström-Lundqvist, Carina, Boriani, Giuseppe, Castella, Manuel, Dan, Gheorghe-Andrei, Dilaveris, Polychronis, Fauchier, Laurent, Filippatos, Gerasimos, Kalman, Jonathan, La Meir, Mark, Lane, Deirdre, Lebeau, Jean-Pierre, Lettino, Maddalena, Lip, Gregory, Pinto, Fausto, Thomas, G Neil, Valgimigli, Marco, van Gelder, Isabelle, van Putte, Bart, Watkins, Caroline, Kirchhof, Paulus, Kühne, Michael, Aboyans, Victor, Ahlsson, Anders, Balsam, Pawel, Bauersachs, Johann, Benussi, Stefano, Brandes, Axel, Braunschweig, Frieder, Camm, a John, Capodanno, Davide, Casadei, Barbara, Conen, David, Crijns, Harry, Delgado, Victoria, Dobrev, Dobromir, Drexel, Heinz, Eckardt, Lars, Fitzsimons, Donna, Folliguet, Thierry, Gale, Chris, Gorenek, Bulent, Haeusler, Karl Georg, Heidbuchel, Hein, Iung, Bernard, Katus, Hugo, Kotecha, Dipak, Landmesser, Ulf, Leclercq, Christophe, Lewis, Basil, Mascherbauer, Julia, Merino, Jose Luis, Merkely, Béla, Mont, Lluís, Mueller, Christian, Nagy, Klaudia, Oldgren, Jonas, Pavlović, Nikola, Pedretti, Roberto, Petersen, Steffen, Piccini, Jonathan, Popescu, Bogdan, Pürerfellner, Helmut, Richter, Dimitrios, Roffi, Marco, Rubboli, Andrea, Scherr, Daniel, Schnabel, Renate, Simpson, Iain, Shlyakhto, Evgeny, Sinner, Moritz, Steffel, Jan, Sousa-Uva, Miguel, Suwalski, Piotr, Svetlosak, Martin, Touyz, Rhian, Neil Thomas, G, Delassi, Tahar, Sisakian, Hamayak, Chasnoits, Alexandr, Pauw, Michel De, Smajić, Elnur, Shalganov, Tchavdar, Avraamides, Panayiotis, Kautzner, Josef, Gerdes, Christian, Alaziz, Ahmad Abd, Kampus, Priit, Raatikainen, Pekka, Boveda, Serge, Papiashvili, Giorgi, Vassilikos, Vassilios, Csanádi, Zoltán, Arnar, David, Galvin, Joseph, Barsheshet, Alon, Caldarola, Pasquale, Rakisheva, Amina, Bytyçi, Ibadete, Kerimkulova, Alina, Kalejs, Oskars, Njeim, Mario, Puodziukynas, Aras, Groben, Laurent, Sammut, Mark, Grosu, Aurel, Boskovic, Aneta, Moustaghfir, Abdelhamid, Groot, Natasja De, Poposka, Lidija, Anfinsen, Ole-Gunnar, Mitkowski, Przemyslaw, Cavaco, Diogo Magalhães, Siliste, Calin, Mikhaylov, Evgeny, Bertelli, Luca, Kojic, Dejan, Hatala, Robert, Fras, Zlatko, Arribas, Fernando, Juhlin, Tord, Sticherling, Christian, Abid, Leila, Atar, Ilyas, Sychov, Oleg, Bates, Matthew, Zakirov, Nodir, Halimi, Jean-Michel, Gatault, Philippe, Longuet, Hélène, Barbet, Christelle, Goumard, Annabelle, Gueguen, Juliette, Goin, Nicolas, Sautenet, Bénédicte, Herbert, Julien, Bisson, Arnaud, Universität Leipzig [Leipzig], University of Belgrade [Belgrade], Leiden University Medical Center (LUMC), Uppsala University, Università degli Studi di Modena e Reggio Emilia, Colentina University Hospital, University of Medicine and Pharmacy 'Carol Davila' Bucharest (UMPCD), CHU Trousseau [Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours), Éducation Éthique Santé EA 7505 (EES), Université de Tours (UT), National and Kapodistrian University of Athens (NKUA), Université d'Athènes (UOA), Attikon University Hospital, The Royal Melbourne Hospital, University of Liverpool, San Gerardo Hospital of Monza, Aalborg University [Denmark] (AAU), Universidade Nova de Lisboa = NOVA University Lisbon (NOVA), Faculdade de Medicina [Lisboa], Universidade de Lisboa (ULISBOA), Hospital de Santa Maria [Lisboa], Service de néphrologie et immunologie clinique [CHRU Tours], Centre Hospitalier Régional Universitaire de Tours (CHRU Tours)-Hôpital Bretonneau-Université de Tours (UT), Centre de recherche en épidémiologie et santé des populations (CESP), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, MethodS in Patients-centered outcomes and HEalth ResEarch (SPHERE), Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR des Sciences Pharmaceutiques et Biologiques, and Université de Nantes (UN)-Université de Nantes (UN)
Subjects: medicine.medical_specialty, Framingham Risk Score, Percutaneous, business.industry, medicine.medical_treatment, kidney biopsy, Retrospective cohort study, Odds ratio, Lower risk, medicine.disease, transjugular, Nephrectomy, Surgery, [SHS]Humanities and Social Sciences, bleeding score, Hematoma, percutaneous, Nephrology, Clinical Research, medicine, epidemiology, business, ComputingMilieux_MISCELLANEOUS, Cohort study
Abstract: Introduction The risk of bleeding associated with transjugular kidney biopsies is unclear, and which patients are the best candidates for this route is unknown. Methods This was a retrospective cohort study comparing proportion of bleeding associated with transjugular versus percutaneous native kidney biopsies in all patients in France in the 2010–2019 period. Major bleeding at day 8 (i.e., blood transfusions, hemorrhage/hematoma, angiographic intervention, nephrectomy) and risk of death at day 30 were assessed, and we used a bleeding risk score initially developed for the percutaneous route. Results Our analysis included 60,331 patients (transjugular route: 5305; percutaneous route: 55,026 patients). The observed proportion of major bleeding varied widely (transjugular vs. percutaneous): 0.4% versus 0.5% for the lowest risk scores (0–4) to 19.1% versus 30.8% for the highest risk scores (≥35). Transjugular was more frequently used than percutaneous route (39% vs. 24%) when the risk score was ≥20 (15,133/60,331; 25% of all patients). Transjugular was associated with a lower risk of major bleeding than percutaneous route in multivariate analyses (odds ratio [OR]: 0.88 [0.78–0.99]), especially for scores ≥20 (OR: 0.83 [0.72–0.96], (i.e., 25% of patients). Major bleeding was associated with an increased risk of death both for transjugular (OR: 1.77 [1.00–3.14]) and percutaneous (OR: 1.80 [1.43–2.28]) routes. Conclusions The transjugular route is independently associated with a lower risk of bleeding than the percutaneous route, especially in high-risk patients identified by a preprocedure risk score ≥20 (i.e., 25% of patients). Major bleeding is associated with an increased risk of death for both routes., Graphical abstract
Published: 2021

38. Genetic insight into sick sinus syndrome

Author: Thorolfsdottir, Rosa B, Sveinbjornsson, Gardar, Aegisdottir, Hildur M, Benonisdottir, Stefania, Stefansdottir, Lilja, Ivarsdottir, Erna V, Halldorsson, Gisli H, Sigurdsson, Jon K, Torp-Pedersen, Christian, Weeke, Peter E, Brunak, Søren, Westergaard, David, Pedersen, Ole B., Sørensen, Erik, Nielsen, Kaspar R, Burgdorf, Kristoffer S., Banasik, Karina, Brumpton, Ben, Zhou, Wei, Oddsson, Asmundur, Tragante, Vinicius, Hjorleifsson, Kristjan E, Davidsson, Olafur B, Rajamani, Sridharan, Jonsson, Stefan, Torfason, Bjarni, Valgardsson, Atli S, Thorgeirsson, Gudmundur, Frigge, Michael L, Thorleifsson, Gudmar, Norddahl, Gudmundur L, Helgadottir, Anna, Gretarsdottir, Solveig, Sulem, Patrick, Jonsdottir, Ingileif, Willer, Cristen J, Hveem, Kristian, Bundgaard, Henning, Ullum, Henrik, Arnar, David O, Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F, Holm, Hilma, Stefansson, Kari, Thorolfsdottir, Rosa B, Sveinbjornsson, Gardar, Aegisdottir, Hildur M, Benonisdottir, Stefania, Stefansdottir, Lilja, Ivarsdottir, Erna V, Halldorsson, Gisli H, Sigurdsson, Jon K, Torp-Pedersen, Christian, Weeke, Peter E, Brunak, Søren, Westergaard, David, Pedersen, Ole B., Sørensen, Erik, Nielsen, Kaspar R, Burgdorf, Kristoffer S., Banasik, Karina, Brumpton, Ben, Zhou, Wei, Oddsson, Asmundur, Tragante, Vinicius, Hjorleifsson, Kristjan E, Davidsson, Olafur B, Rajamani, Sridharan, Jonsson, Stefan, Torfason, Bjarni, Valgardsson, Atli S, Thorgeirsson, Gudmundur, Frigge, Michael L, Thorleifsson, Gudmar, Norddahl, Gudmundur L, Helgadottir, Anna, Gretarsdottir, Solveig, Sulem, Patrick, Jonsdottir, Ingileif, Willer, Cristen J, Hveem, Kristian, Bundgaard, Henning, Ullum, Henrik, Arnar, David O, Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F, Holm, Hilma, and Stefansson, Kari
Abstract: AIMS: The aim of this study was to use human genetics to investigate the pathogenesis of sick sinus syndrome (SSS) and the role of risk factors in its development.METHODS AND RESULTS: We performed a genome-wide association study of 6469 SSS cases and 1 000 187 controls from deCODE genetics, the Copenhagen Hospital Biobank, UK Biobank, and the HUNT study. Variants at six loci associated with SSS, a reported missense variant in MYH6, known atrial fibrillation (AF)/electrocardiogram variants at PITX2, ZFHX3, TTN/CCDC141, and SCN10A and a low-frequency (MAF = 1.1-1.8%) missense variant, p.Gly62Cys in KRT8 encoding the intermediate filament protein keratin 8. A full genotypic model best described the p.Gly62Cys association (P = 1.6 × 10-20), with an odds ratio (OR) of 1.44 for heterozygotes and a disproportionally large OR of 13.99 for homozygotes. All the SSS variants increased the risk of pacemaker implantation. Their association with AF varied and p.Gly62Cys was the only variant not associating with any other arrhythmia or cardiovascular disease. We tested 17 exposure phenotypes in polygenic score (PGS) and Mendelian randomization analyses. Only two associated with the risk of SSS in Mendelian randomization, AF, and lower heart rate, suggesting causality. Powerful PGS analyses provided convincing evidence against causal associations for body mass index, cholesterol, triglycerides, and type 2 diabetes (P > 0.05).CONCLUSION: We report the associations of variants at six loci with SSS, including a missense variant in KRT8 that confers high risk in homozygotes and points to a mechanism specific to SSS development. Mendelian randomization supports a causal role for AF in the development of SSS.
Published: 2021

39. Cholesterol not particle concentration mediates the atherogenic risk conferred by apolipoprotein B particles: a Mendelian randomization analysis

Author: Helgadottir, Anna, Thorleifsson, Gudmar, Snaebjarnarson, Audunn, Stefansdottir, Lilja, Sveinbjornsson, Gardar, Tragante, Vinicius, Björnsson, Eyþór, Steinthorsdottir, Valgerdur, Gretarsdottir, Solveig, Helgason, Hannes, Saemundsdottir, Jona, Olafsson, Isleifur, Thune, Jens Jakob, Raja, Anna Axelsson, Ghouse, Jonas, Olesen, Morten Salling, Christensen, Alex, Jacobsen, Rikke Louise, Dowsett, Joseph, Bruun, Mie Topholm, Nielsen, Kaspar, Knowlton, Kirk, Nadauld, Lincoln, Benediktsson, Rafn, Erikstrup, Christian, Pedersen, Ole B, Banasik, Karina, Brunak, Søren, Bundgaard, Henning, Ostrowski, Sisse R, Sulem, Patrick, Arnar, David O, Thorgeirsson, Gudmundur, Thorsteinsdottir, Unnur, Gudbjartsson, Daniel F, Stefansson, Kari, and Holm, Hilma
Abstract: Graphical Abstract
Published: 2022
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40. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association of Cardio-Thoracic Surgery (EACTS) : the Task Force for the diagnosis and management of atrialfibrillation of the European Society of Cardiology (ESC) : developed with the special contribution of the European HeartRhythm Association (EHRA) of the ESC

Author: Hindricks, Gerhard, Potpara, Tatjana, Dagres, Nikolaos, Arbelo, Elena, Bax, Jeroen J., Blomström-Lundqvist, Carina, Boriani, Giuseppe, Castella, Manuel, Dan, Gheorghe-Andrei, Dilaveris, Polychronis E., Fauchier, Laurent, Petersen, Steffen E., Piccini, Jonathan P., Popescu, Bogdan A., Pürerfellner, Helmut, Richter, Dimitrios J., Roffi, Marco, Rubboli, Andrea, Scherr, Daniel, Schnabel, Renate B., Simpson, Iain A., Raatikainen, Pekka, Shlyakhto, Evgeny, Sinner, Moritz F., Steffel, Jan, Suwalski, Piotr, Svetlosak, Martin, Touyz, Rhian M., Windecker, Stephan, Baigent, Colin, Collet, Jean-Philippe, Dean, Veronica, Boveda, Serge, Fitzsimons, Donna, Gale, Chris P., Grobbee, Diederick E., Halvorsen, Sigrun, Lung, Bernard, Jüni, Peter, Petronio, Anna Sonia, Sousa Uva, Miguel, Delassi, Tahar, Sisakian, Hamayak S., Papiashvili, Giorgi, Chasnoits, Alexandr, De Pauw, Michel, Smajić, Elnur, Shalganov, Tchavdar, Avraamides, Panayiotis, Kautzner, Josef, Gerdes, Christian, Alaziz, Ahmad Abd, Kampus, Priit, Vassilikos, Vassilios P., Csanádi, Zoltán, Arnar, David O., Galvin, Joseph, Barsheshet, Alon, Caldarola, Pasquale, Rakisheva, Amina, Filippatos, Gerasimos, Bytyçi, Ibadete, Kerimkulova, Alina, Kalejs, Oskars, Njeim, Mario, Puodziukynas, Aras, Groben, Laurent, Sammut, Mark A., Grosu, Aurel, Boskovic, Aneta, Moustaghfir, Abdelhamid, Kalman, Jonathan M., de Groot, Natasja, Poposka, Lidija, Anfinsen, Ole-Gunnar, Mitkowski, Przemyslaw P., Cavaco, Diogo, Siliste, Calin, Mikhaylov, Evgeny N., Bertelli, Luca, Kojic, Dejan, Hatala, Robert, La Meir, Mark, Fras, Zlatko, Arribas, Fernando, Juhlin, Tord, Sticherling, Christian, Abid, Leila, Atar, Ilyas, Sychov, Oleg, Bates, Matthew G. D., Zakirov, Nodir U., Lane, Deirdre A., Lebeau, Jean-Pierre, Lettino, Maddalena, Lip, Gregory Y. H., Pinto, Fausto J., Thomas, G. Neil, Valgimigli, Marco, Van Gelder, Isabelle C., Van Putte, Bart P., Watkins, Caroline L., Kirchhof, Paulus, Kühne, Michael, Aboyans, Victor, Ahlsson, Anders, Balsam, Pawel, Bauersachs, Johann, Benussi, Stefano, Brandes, Axel, Braunschweig, Frieder, Camm, A. John, Capodanno, Davide, Casadei, Barbara, Conen, David, Crijns, Harry J. G. M., Delgado, Victoria, Dobrev, Dobromir, Drexel, Heinz, Eckardt, Lars, Folliguet, Thierry, Gorenek, Bulent, Haeusler, Karl Georg, Heidbuchel, Hein, Iung, Bernard, Katus, Hugo A., Kotecha, Dipak, Landmesser, Ulf, Leclercq, Christophe, Lewis, Basil S., Mascherbauer, Julia, Merino, Jose Luis, Merkely, Béla, Mont, Lluís, Mueller, Christian, Nagy, Klaudia V., Oldgren, Jonas, Pavlović, Nikola, Pedretti, Roberto F. E., and Repositório da Universidade de Lisboa
Subjects: Rate control, AF surgery, Guidelines, Upstream therapy, Recommendations, Left atrial appendage occlusion, Atrial fibrillation, Pulmonary vein isolation, Left atrial ablation, Antiarrhythmic drugs, Cardioversion, Stroke, Anticoagulation, Vitamin K antagonists, Screening, Non-vitamin K antagonist oral anticoagulants, Rhythm control, Catheter ablation, ABC pathway
Abstract: © 2020 European Society of Cardiology. All rights reserved., Atrial fibrillation (AF) poses significant burden to patients, physicians, and healthcare systems globally. Substantial research efforts and resources are being directed towards gaining detailed information about the mechanisms underlying AF, its natural course and effective treatments (see also the ESC Textbook of Cardiovascular Medicine: CardioMed) and new evidence is continuously generated and published. The complexity of AF requires a multifaceted, holistic, and multidisciplinary approach to the management of AF patients, with their active involvement in partnership with clinicians. Streamlining the care of patients with AF in daily clinical practice is a challenging but essential requirement for effective management of AF. In recent years, substantial progress has been made in the detection of AF and its management, and new evidence is timely integrated in this third edition of the ESC guidelines on AF. The 2016 ESC AF Guidelines introduced the concept of the five domains to facilitate an integrated structured approach to AF care and promote consistent, guideline-adherent management for all patients. The Atrial Fibrillation Better Care (ABC) approach in the 2020 ESC AF Guidelines is a continuum of this approach, with the goal to further improve the structured management of AF patients, promote patient values, and finally improve patient outcomes.
Published: 2020

41. Genetic variability in the absorption of dietary sterols affects the risk of coronary artery disease

Author: Helgadottir, Anna, Thorleifsson, Gudmar, Alexandersson, Kristjan F, Tragante, Vinicius, Thorsteinsdottir, Margret, Eiriksson, Finnur F, Gretarsdottir, Solveig, Björnsson, Eythór, Magnusson, Olafur, Sveinbjornsson, Gardar, Jonsdottir, Ingileif, Steinthorsdottir, Valgerdur, Ferkingstad, Egil, Jensson, Brynjar Ö, Stefansson, Hreinn, Olafsson, Isleifur, Christensen, Alex H, Torp-Pedersen, Christian, Køber, Lars, Pedersen, Ole B, Erikstrup, Christian, Sørensen, Erik, Brunak, Søren, Banasik, Karina, Hansen, Thomas F., Nyegaard, Mette, Eyjolfssson, Gudmundur I, Sigurdardottir, Olof, Thorarinsson, Bjorn L, Matthiasson, Stefan E, Steingrimsdottir, Thora, Bjornsson, Einar S, Danielsen, Ragnar, Asselbergs, Folkert W, Arnar, David O, Ullum, Henrik, Bundgaard, Henning, Sulem, Patrick, Thorsteinsdottir, Unnur, Thorgeirsson, Gudmundur, Holm, Hilma, Gudbjartsson, Daniel F, Stefansson, Kari, Helgadottir, Anna, Thorleifsson, Gudmar, Alexandersson, Kristjan F, Tragante, Vinicius, Thorsteinsdottir, Margret, Eiriksson, Finnur F, Gretarsdottir, Solveig, Björnsson, Eythór, Magnusson, Olafur, Sveinbjornsson, Gardar, Jonsdottir, Ingileif, Steinthorsdottir, Valgerdur, Ferkingstad, Egil, Jensson, Brynjar Ö, Stefansson, Hreinn, Olafsson, Isleifur, Christensen, Alex H, Torp-Pedersen, Christian, Køber, Lars, Pedersen, Ole B, Erikstrup, Christian, Sørensen, Erik, Brunak, Søren, Banasik, Karina, Hansen, Thomas F., Nyegaard, Mette, Eyjolfssson, Gudmundur I, Sigurdardottir, Olof, Thorarinsson, Bjorn L, Matthiasson, Stefan E, Steingrimsdottir, Thora, Bjornsson, Einar S, Danielsen, Ragnar, Asselbergs, Folkert W, Arnar, David O, Ullum, Henrik, Bundgaard, Henning, Sulem, Patrick, Thorsteinsdottir, Unnur, Thorgeirsson, Gudmundur, Holm, Hilma, Gudbjartsson, Daniel F, and Stefansson, Kari
Abstract: AIMS: To explore whether variability in dietary cholesterol and phytosterol absorption impacts the risk of coronary artery disease (CAD) using as instruments sequence variants in the ABCG5/8 genes, key regulators of intestinal absorption of dietary sterols.METHODS AND RESULTS: We examined the effects of ABCG5/8 variants on non-high-density lipoprotein (non-HDL) cholesterol (N up to 610 532) and phytosterol levels (N = 3039) and the risk of CAD in Iceland, Denmark, and the UK Biobank (105 490 cases and 844 025 controls). We used genetic scores for non-HDL cholesterol to determine whether ABCG5/8 variants confer greater risk of CAD than predicted by their effect on non-HDL cholesterol. We identified nine rare ABCG5/8 coding variants with substantial impact on non-HDL cholesterol. Carriers have elevated phytosterol levels and are at increased risk of CAD. Consistent with impact on ABCG5/8 transporter function in hepatocytes, eight rare ABCG5/8 variants associate with gallstones. A genetic score of ABCG5/8 variants predicting 1 mmol/L increase in non-HDL cholesterol associates with two-fold increase in CAD risk [odds ratio (OR) = 2.01, 95% confidence interval (CI) 1.75-2.31, P = 9.8 × 10-23] compared with a 54% increase in CAD risk (OR = 1.54, 95% CI 1.49-1.59, P = 1.1 × 10-154) associated with a score of other non-HDL cholesterol variants predicting the same increase in non-HDL cholesterol (P for difference in effects = 2.4 × 10-4).CONCLUSIONS: Genetic variation in cholesterol absorption affects levels of circulating non-HDL cholesterol and risk of CAD. Our results indicate that both dietary cholesterol and phytosterols contribute directly to atherogenesis.
Published: 2020

42. Genetic variability in the absorption of dietary sterols affects the risk of coronary artery disease

Author: Onderzoek Precision medicine, Circulatory Health, Team Medisch, Helgadottir, Anna, Thorleifsson, Gudmar, Alexandersson, Kristjan F, Tragante, Vinicius, Thorsteinsdottir, Margret, Eiriksson, Finnur F, Gretarsdottir, Solveig, Björnsson, Eythór, Magnusson, Olafur, Sveinbjornsson, Gardar, Jonsdottir, Ingileif, Steinthorsdottir, Valgerdur, Ferkingstad, Egil, Jensson, Brynjar Ö, Stefansson, Hreinn, Olafsson, Isleifur, Christensen, Alex H, Torp-Pedersen, Christian, Køber, Lars, Pedersen, Ole B, Erikstrup, Christian, Sørensen, Erik, Brunak, Søren, Banasik, Karina, Hansen, Thomas F, Nyegaard, Mette, Eyjolfssson, Gudmundur I, Sigurdardottir, Olof, Thorarinsson, Bjorn L, Matthiasson, Stefan E, Steingrimsdottir, Thora, Bjornsson, Einar S, Danielsen, Ragnar, Asselbergs, Folkert W, Arnar, David O, Ullum, Henrik, Bundgaard, Henning, Sulem, Patrick, Thorsteinsdottir, Unnur, Thorgeirsson, Gudmundur, Holm, Hilma, Gudbjartsson, Daniel F, Stefansson, Kari, Onderzoek Precision medicine, Circulatory Health, Team Medisch, Helgadottir, Anna, Thorleifsson, Gudmar, Alexandersson, Kristjan F, Tragante, Vinicius, Thorsteinsdottir, Margret, Eiriksson, Finnur F, Gretarsdottir, Solveig, Björnsson, Eythór, Magnusson, Olafur, Sveinbjornsson, Gardar, Jonsdottir, Ingileif, Steinthorsdottir, Valgerdur, Ferkingstad, Egil, Jensson, Brynjar Ö, Stefansson, Hreinn, Olafsson, Isleifur, Christensen, Alex H, Torp-Pedersen, Christian, Køber, Lars, Pedersen, Ole B, Erikstrup, Christian, Sørensen, Erik, Brunak, Søren, Banasik, Karina, Hansen, Thomas F, Nyegaard, Mette, Eyjolfssson, Gudmundur I, Sigurdardottir, Olof, Thorarinsson, Bjorn L, Matthiasson, Stefan E, Steingrimsdottir, Thora, Bjornsson, Einar S, Danielsen, Ragnar, Asselbergs, Folkert W, Arnar, David O, Ullum, Henrik, Bundgaard, Henning, Sulem, Patrick, Thorsteinsdottir, Unnur, Thorgeirsson, Gudmundur, Holm, Hilma, Gudbjartsson, Daniel F, and Stefansson, Kari
Published: 2020

43. Unexplained sudden death: next-generation sequencing to the rescue?

Author: Arnadottir, Gudny A, primary and Arnar, David O, additional
Published: 2021
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44. Effects of a 5-lipoxygenase-activating protein inhibitor on biomarkers associated with risk of myocardial infarction: A randomized trial

Author: Hakonarson, Hakon, Andresdottir, Margret, Zink, Florian, Gudbjartsson, Daniel, Helgadottir, Anna, Thorvaldsson, Sverrir, Manolescu, Andrei, Jonsson, Asgeir, Thorgeirsson, Gestur, Sigurdsson, Axel, Andersen, Karl, Arnar, David O., Agnarsson, Uggi, Adalsteinsdottir, Asdis E., Gudmundsdottir, Hrefna, Einarsson, Atli, Gottskalksson, Gizur, Bjornsdottir, Halldora, Gudmundsson, Kolbeinn, Gulcher, Jeffrey, Topol, Eric J., Kristinsson, Arni, Hardarson, Thordur, Kristjansson, Kristleifur, Kong, Augustine, Stefansson, Kari, Thorgeirssonj, Gudmundur, and Gurney Mark
Subjects: Leukotrienes -- Research, Biological markers -- Research, Heart attack -- Risk factors, Heart attack -- Research, Leukotrienes -- Synthesis
Abstract: A study is conducted to determine the effect of an inhibitor of 5-lipoxygenase-activating protein (FLAP) on levels of biomarkers associated with myocardial infarction (MI) risk. It is concluded that in patients with specific at-risk variants of 2 genes in the leukotriene pathway, DG-031 led to significant and dose-dependent suppression of biomarkers that are associated with increased risk of MI events.
Published: 2005

45. Do High Levels of n-3 Polyunsaturated Fatty Acids in Cell Membranes Increase the Risk of Postoperative Atrial Fibrillation?

Author: Bjorgvinsdottir, Lara, Arnar, David O., Indridason, Olafur S., Heidarsdottir, Ragnhildur, Skogstrand, Kristin, Torfason, Bjarni, Hougaard, David M., Palsson, Runolfur, and Skuladottir, Gudrun V.
Published: 2013
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46. Atrial Fibrillation is Associated With Reduced Brain Volume and Cognitive Function Independent of Cerebral Infarcts

Author: Stefansdottir, Hrafnhildur, Arnar, David O., Aspelund, Thor, Sigurdsson, Sigurdur, Jonsdottir, Maria K., Hjaltason, Haukur, Launer, Lenore J., and Gudnason, Vilmundur
Published: 2013
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47. Syncope in patients with structural heart disease

Author: Arnar, David O.
Published: 2013
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48. Purkinje involvement in arrhythmias after coronary artery reperfusion

Author: Arnar, David O. and Martins, James B.
Subjects: Arrhythmia -- Physiological aspects, Reperfusion (Physiology) -- Physiological aspects, Purkinje cells -- Physiological aspects, Ventricular tachycardia -- Physiological aspects, Biological sciences
Abstract: Previous studies have indicated that the endocardium may be responsible for a large portion of ventricular tachycardia (VT) seen with reperfusion of ischemic myocardium. To evaluate the role of the Purkinje system in nonreentrant VT arising from the endocardium after reperfusion, the anterior descending coronary artery was occluded for 20 min and then reperfused in 23 dogs after instrumentation of the risk zone with 21 multipolar plunge needles. VT with focal Purkinje origin was defined as a focal endocardial VT with Purkinje potentials recorded before the earliest endocardial myopotential. A total of 19 VTs (mean cycle length 214 [+ or -] 2 ms) were observed with 11 (58%) having focal Purkinje origin. Fifty-eight percent of the VTs degenerated to ventricular fibrillation, with occurrences of two or more independent foci per complex (seen in 7 of 11 compared with 1 of 8 nonsustained VTs). In conclusion, these data show that Purkinje tissue may be important in the genesis of reperfusion VT. mapping; ventricles
Published: 2002

49. Third universal definition of myocardial infarction

Author: Thygesen, Kristian, Alpert, Joseph S., Jaffe, Allan S., Simoons, Maarten L., Chaitman, Bernard R., White, Harvey D., Thygesen, Kristian, Alpert, Joseph S., White, Harvey D., Jaffe, Allan S., Katus, Hugo A., Apple, Fred S., Lindahl, Bertil, Morrow, David A., Chaitman, Bernard R., Clemmensen, Peter M., Johanson, Per, Hod, Hanoch, Underwood, Richard, Bax, Jeroen J., Bonow, Robert O., Pinto, Fausto, Gibbons, Raymond J., Fox, Keith A., Atar, Dan, Newby, L. Kristin, Galvani, Marcello, Hamm, Christian W., Uretsky, Barry F., Gabriel Steg, Ph., Wijns, William, Bassand, Jean-Pierre, Menasché, Phillippe, Ravkilde, Jan, Ohman, E. Magnus, Antman, Elliott M., Wallentin, Lars C., Armstrong, Paul W., Simoons, Maarten L., Januzzi, James L., Nieminen, Markku S., Gheorghiade, Mihai, Filippatos, Gerasimos, Luepker, Russell V., Fortmann, Stephen P., Rosamond, Wayne D., Levy, Dan, Wood, David, Smith, Sidney C., Hu, Dayi, Lopez-Sendon, José-Luis, Robertson, Rose Marie, Weaver, Douglas, Tendera, Michal, Bove, Alfred A., Parkhomenko, Alexander N., Vasilieva, Elena J., Mendis, Shanti, Bax, Jeroen J., Baumgartner, Helmut, Ceconi, Claudio, Dean, Veronica, Deaton, Christi, Fagard, Robert, Funck-Brentano, Christian, Hasdai, David, Hoes, Arno, Kirchhof, Paulus, Knuuti, Juhani, Kolh, Philippe, McDonagh, Theresa, Moulin, Cyril, Popescu, Bogdan A., Reiner, Željko, Sechtem, Udo, Sirnes, Per Anton, Tendera, Michal, Torbicki, Adam, Vahanian, Alec, Windecker, Stephan, Morais, Joao, Aguiar, Carlos, Almahmeed, Wael, Arnar, David O., Barili, Fabio, Bloch, Kenneth D., Bolger, Ann F., Bøtker, Hans Erik, Bozkurt, Biykem, Bugiardini, Raffaele, Cannon, Christopher, de Lemos, James, Eberli, Franz R., Escobar, Edgardo, Hlatky, Mark, James, Stefan, Kern, Karl B., Moliterno, David J., Mueller, Christian, Neskovic, Aleksandar N., Pieske, Burkert Mathias, Schulman, Steven P., Storey, Robert F., Taubert, Kathryn A., Vranckx, Pascal, and Wagner, Daniel R.
Published: 2012
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50. Plasma n-3 and n-6 fatty acids and the incidence of atrial fibrillation following coronary artery bypass graft surgery

Author: Skuladottir, Gudrun V., Heidarsdottir, Ragnhildur, Arnar, David O., Torfason, Bjarni, Edvardsson, Vidar, Gottskalksson, Gizur, Palsson, Runolfur, and Indridason, Olafur S.
Published: 2011
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