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Your search keyword '"Martina Müller-Nurasyid"' showing total 2 results
Start Over Author "Martina Müller-Nurasyid" Journal circulation. genomic and precision medicine
2 results on '"Martina Müller-Nurasyid"'

1. Genetic Determinants of Electrocardiographic P-Wave Duration and Relation to Atrial Fibrillation

Author

Michiel L. Bots, Annette Peters, Jennifer A. Brody, Pim van der Harst, Niek Verweij, Torben Hansen, Lu-Chen Weng, Marco V Perez, Honghuang Lin, Nona Sotoodehnia, Katharina Schramm, Dennis O. Mook-Kanamori, Marcus Dörr, Susan R. Heckbert, Henry J. Lin, Jie Yao, Paul L. Huang, Melanie Waldenberger, Bruno H. Stricker, Cornelia M. van Duijn, Jelena Kornej, Kent D. Taylor, Stephan B. Felix, Julia Ramirez, Xiuqing Guo, Peter van der Meer, Patrick T. Ellinor, Emelia J. Benjamin, Amelia W. Hall, Martina Müller-Nurasyid, Steven A. Lubitz, Alexander Teumer, Ilonca Vaartjes, Niels Grarup, Kathryn L. Lunetta, Marten E. van den Berg, Aaron Isaacs, Uwe Völker, Bruce M. Psaty, Jan A. Kors, Alvaro Alonso, Seung Hoan Choi, Rudolf A. de Boer, Allan Linneberg, Sandosh Padmanabhan, Helen R. Warren, Jerome I. Rotter, Nathan A. Bihlmeyer, Man Li, Jeffrey Haessler, Charles Kooperberg, Moritz F. Sinner, Sean J. Jurgens, Folkert W. Asselbergs, Dan E. Arking, Ruifang Li-Gao, Jessica van Setten, Patricia B. Munroe, Jørgen K. Kanters, Stefan Kääb, Fysiologie, RS: FHML MaCSBio, RS: Carim - B01 Blood proteins & engineering, Erasmus MC other, Medical Informatics, Internal Medicine, Epidemiology, and Cardiology

Subjects
0301 basic medicine, PROTEIN, population, 030204 cardiovascular system & hematology, Cardiovascular, Electrocardiography, 0302 clinical medicine, MYH6, Atrial Fibrillation, 2.1 Biological and endogenous factors, Connectin, atrial fibrillation, Aetiology, Exome, MYOSIN HEAVY-CHAIN, RISK, education.field_of_study, NAV1.8 Voltage-Gated Sodium Channel/genetics, Connectin/genetics, Atrial fibrillation, General Medicine, ASSOCIATION, Heart Disease, Duration (music), Cardiology, EXPRESSION, medicine.medical_specialty, HMGA2, Population, INDEXES, Quantitative Trait Loci, Transcription Factors/genetics, Electrophysiology, Genetic, Genome-wide Association Studies, Article, NAV1.8 Voltage-Gated Sodium Channel, 03 medical and health sciences, Myosin Heavy Chains/genetics, Clinical Research, Internal medicine, Cardiac conduction, Cardiac Myosins/genetics, P wave duration, medicine, Genetics, Humans, education, RECURRENCE, Homeodomain Proteins, Myosin Heavy Chains, business.industry, Human Genome, Genetic Variation, medicine.disease, electrophysiology, Atrial Fibrillation/ethnology, 030104 developmental biology, genome-wide association studies, Homeodomain Proteins/genetics, genetic, business, Cardiac Myosins, exome, Transcription Factors, Genome-Wide Association Study
Abstract

Background: The P-wave duration (PWD) is an electrocardiographic measurement that represents cardiac conduction in the atria. Shortened or prolonged PWD is associated with atrial fibrillation (AF). We used exome-chip data to examine the associations between common and rare variants with PWD. Methods: Fifteen studies comprising 64 440 individuals (56 943 European, 5681 African, 1186 Hispanic, 630 Asian) and ≈230 000 variants were used to examine associations with maximum PWD across the 12-lead ECG. Meta-analyses summarized association results for common variants; gene-based burden and sequence kernel association tests examined low-frequency variant-PWD associations. Additionally, we examined the associations between PWD loci and AF using previous AF genome-wide association studies. Results: We identified 21 common and low-frequency genetic loci (14 novel) associated with maximum PWD, including several AF loci ( TTN , CAND2 , SCN10A , PITX2 , CAV1 , SYNPO2L , SOX5 , TBX5, MYH6, RPL3L ). The top variants at known sarcomere genes ( TTN, MYH6 ) were associated with longer PWD and increased AF risk. However, top variants at other loci (eg, PITX2 and SCN10A ) were associated with longer PWD but lower AF risk. Conclusions: Our results highlight multiple novel genetic loci associated with PWD, and underscore the shared mechanisms of atrial conduction and AF. Prolonged PWD may be an endophenotype for several different genetic mechanisms of AF.

Published
2020

2. Common and Rare Coding Genetic Variation Underlying the Electrocardiographic PR Interval

Author

Tamara B. Harris, Niels Grarup, Marcus Dörr, Martina Müller-Nurasyid, Torben Hansen, Lu-Chen Weng, Honghuang Lin, Thibaud Boutin, Joshua C. Bis, Farid Radmanesh, Jie Yao, Nilesh J. Samani, Ozren Polašek, Massimo Mangino, Charles Kooperberg, Vilmundur Gudnason, Stephan B. Felix, Bruno H. Stricker, Elsayed Z. Soliman, Nathan A. Bihlmeyer, Jette Bork-Jensen, Dan E. Arking, J. Marten, Mika Kähönen, Kenneth Rice, Nona Sotoodehnia, Heather Jameson, Henry J. Lin, Jørgen K. Kanters, Jared W. Magnani, Mark Eijgelsheim, Hao Mei, Tim D. Spector, Oluf Pedersen, Allan Linneberg, G. Homuth, Chengping Wen, Olli T. Raitakari, Blair H. Smith, Marco V Perez, Melanie Waldenberger, Bram P. Prins, James G. Wilson, Xiuqing Guo, Sandosh Padmanabhan, Peter van der Meer, Stefan Weiss, Leo-Pekka Lyytikäinen, Colleen M. Sitlani, Alvaro Alonso, Leanne M. Hall, Cornelia M. van Duijn, Jessica van Setten, Helen R. Warren, Kent D. Taylor, Niek Verweij, Man Li, Moritz F. Sinner, Igor Rudan, Christopher P. Nelson, Emelia J. Benjamin, William J. Hucker, Marten E. van den Berg, Alan Hanley, Jerome I. Rotter, D. O. Mook-Kanamori, Susan R. Heckbert, Bruce M. Psaty, Caroline Hayward, Yalda Jamshidi, Patrick T. Ellinor, John M. C. Connell, Patricia B. Munroe, Lenore J. Launer, Stefan Kääb, Uwe Völker, Ruifang Li-Gao, Jan A. Kors, Annette Peters, J. Wouter Jukema, Jeffrey Haessler, Aaron Isaacs, Folkert W. Asselbergs, Rudolf A. de Boer, Konstantin Strauch, Albert V. Smith, Jonathan Rosand, Steven A. Lubitz, F. Rivadeneira, Nathan R. Tucker, Michiel L. Bots, Zhijun Xie, Jennifer A. Brody, Stella Trompet, Thomas Meitinger, André G. Uitterlinden, Pim van der Harst, Paul L. Huang, Henry Völzke, Terho Lehtimäki, Yii-Der Ida Chen, Cardiovascular Centre (CVC), Restoring Organ Function by Means of Regenerative Medicine (REGENERATE), Epidemiology, Medical Informatics, Clinical Chemistry, Medical Biochemistry, ACS - Atherosclerosis & ischemic syndromes, ACS - Diabetes & metabolism, AII - Infectious diseases, AGEM - Endocrinology, metabolism and nutrition, AGEM - Inborn errors of metabolism, Amsterdam institute for Infection and Immunity, Amsterdam Gastroenterology Endocrinology Metabolism, Gastroenterology and Hepatology, Intensive Care Medicine, Experimental Immunology, Radiotherapy, Graduate School, Cardiology, Biochemie, RS: CARIM - R1.01 - Blood proteins & engineering, RS: CARIM - R1.06 - Genetic Epidemiology and Genomics of cardiovascular diseases, and RS: FHML MaCSBio

Subjects
Adult, Male, 0301 basic medicine, SCN10A, Heart morphogenesis, Quantitative Trait Loci, LOCI, Locus (genetics), Genome-wide association study, atrioventricular node, SUSCEPTIBILITY, Regulatory Sequences, Nucleic Acid, 030204 cardiovascular system & hematology, Quantitative trait locus, Biology, VARIANTS, Atrioventricular Node, Genetic Loci, Genome-wide Association Study, Article, genome-wide, 03 medical and health sciences, Electrocardiography, 0302 clinical medicine, Genetic variation, Humans, Genetic Predisposition to Disease, PR interval, GENOME-WIDE ASSOCIATION, SCN5A GENE, Aged, Genetic association, Genetics, genome-wide association study, HERITABILITY, MUTATIONS, Genetic Variation, genetic loci, General Medicine, Middle Aged, ta3121, Heritability, DILATED CARDIOMYOPATHY, 030104 developmental biology, LONG QT SYNDROME, CONDUCTION, ATRIAL-FIBRILLATION, Female, QRS DURATION, SUDDEN CARDIAC DEATH
Abstract

Background: Electrical conduction from the cardiac sinoatrial node to the ventricles is critical for normal heart function. Genome-wide association studies have identified more than a dozen common genetic loci that are associated with PR interval. However, it is unclear whether rare and low-frequency variants also contribute to PR interval heritability. Methods: We performed large-scale meta-analyses of the PR interval that included 83 367 participants of European ancestry and 9436 of African ancestry. We examined both common and rare variants associated with the PR interval. Results: We identified 31 genetic loci that were significantly associated with PR interval after Bonferroni correction ( P −6 ), including 11 novel loci that have not been reported previously. Many of these loci are involved in heart morphogenesis. In gene-based analysis, we found that multiple rare variants at MYH6 ( P =5.9×10 −11 ) and SCN5A ( P =1.1×10 −7 ) were associated with PR interval. SCN5A locus also was implicated in the common variant analysis, whereas MYH6 was a novel locus. Conclusions: We identified common variants at 11 novel loci and rare variants within 2 gene regions that were significantly associated with PR interval. Our findings provide novel insights to the current understanding of atrioventricular conduction, which is critical for cardiac activity and an important determinant of health.

Published
2018
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