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4. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Peh, C. Au, Chakera, A., Cooper, B., Kurtkoti, J., Langguth, D., Levidiotis, V., Luxton, G., Mount, P., Mudge, D., Noble, E., Phoon, R., Ranganathan, D., Ritchie, A., Ryan, J., Suranyi, M., Rosenkranz, A., Lhotta, K., Kronbichler, A., Demoulin, N., Bovy, C., Hellemans, R., Hougardy, J., Sprangers, B., Wissing, K., Pagnoux, C., Barbour, S., Brachemi, S., Cournoyer, S., Girard, L., Laurin, L., Liang, P., Philibert, D., Walsh, M., Tesar, V., Becvar, R., Horak, P., Rychlik, I., Szpirt, W., Dieperink, H., Gregersen, J., Ivarsen, P., Krarup, E., Lyngsoe, C., Rigothier, C., Augusto, J., Belot, A., Chauveau, D., Cornec, D., Jourde-Chiche, N., Ficheux, M., Karras, A., Klein, A., Maurier, F., Mesbah, R., Moranne, O., Neel, A., Quemeneur, T., Saadoun, D., Terrier, B., Zaoui, P., Schaier, M., Benck, U., Bergner, R., Busch, M., Floege, J., Grundmann, F., Haller, H., Haubitz, M., Hellmich, B., Henes, J., Hohenstein, B., Hugo, C., Iking-Konert, C., Arndt, F., Kubacki, T., Kotter, I., Lamprecht, P., Lindner, T., Halbritter, J., Mehling, H., Schönermarck, U., Venhoff, N., Vielhauer, V., Witzke, O., Szombati, I., Szucs, G., Garibotto, G., Alberici, F., Brunetta, E., Dagna, L., De Vita, S., Emmi, G., Gabrielli, A., Manenti, L., Pieruzzi, F., Roccatello, D., Salvarani, C., Dobashi, H., Atsumi, T., Fujimoto, S., Hagino, N., Ihata, A., Kaname, S., Kaneko, Y., Katagiri, A., Katayama, M., Kirino, Y., Kitagawa, K., Komatsuda, A., Kono, H., Kurasawa, T., Matsumura, R., Mimura, T., Morinobu, A., Murakawa, Y., Naniwa, T., Nanki, T., Ogawa, N., Oshima, H., Sada, K., Sugiyama, E., Takeuchi, T., Taki, H., Tamura, N., Tsukamoto, T., Yamagata, K., Yamamura, M., van Daele, P., Rutgers, A., Teng, Y., Walker, R., Chua, I., Collins, M., Rabindranath, K., de Zoysa, J., Svensson, M., Grevbo, B., Kalstad, S., Little, M., Clarkson, M., Molloy, E., Pamplona, I. Agraz, Anton, J., Lucia, V. Barrio, Ciggaran, S., Cid, M. Cinta, Encarnacion, M. Diaz, Oliveras, X. Fulladosa, Soler, M. Jose, Rusinol, H. Marco, Praga, M., Porras, L. Quintana, Segarra, A., Bruchfeld, A., Segelmark, M., Soveri, I., Thomaidi, E., Westman, K., Neumann, T., Burnier, M., Daikeler, T., Dudler, J., Hauser, T., Seeger, H., Vogt, B., Jayne, D., Burton, J., Al Jayyousi, R., Amin, T., Andrews, J., Baines, L., Brogan, P., Dasgupta, B., Doulton, T., Flossmann, O., Griffin, S., Harper, J., Harper, L., Kidder, D., Klocke, R., Lanyon, P., Luqmani, R., McLaren, J., Makanjuola, D., McCann, L., Nandagudi, A., Selvan, S., O'Riordan, E., Patel, M., Patel, R., Pusey, C., Rajakariar, R., Robson, J., Robson, M., Salama, A., Smyth, L., Sznajd, J., Taylor, J., Merkel, P., Sreih, A., Belilos, E., Bomback, A., Carlin, J., Chen Lin, Y. Chang, Derebail, V., Dragoi, S., Dua, A., Forbess, L., Geetha, D., Gipson, P., Gohh, R., Greenwood, G.T., Hugenberg, S., Jimenez, R., Kaskas, M., Kermani, T., Kivitz, A., Koening, C., Langford, C., Marder, G., Mohamed, A., Monach, P., Neyra, N., Niemer, G., Niles, J., Obi, R., Owens, C., Parks, D., Podoll, A., Rovin, B., Sam, R., Shergy, W., Silva, A., Specks, U., Spiera, R., Springer, J., Striebich, C., Swarup, A., Thakar, S., Tiliakos, A., Tsai, Y., Waguespack, D., Wasko, M. Chester, Cortazar, Frank B., Niles, John L., Jayne, David R.W., Merkel, Peter A., Bruchfeld, Annette, Yue, Huibin, Schall, Thomas J., and Bekker, Pirow

Published
2023
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6. Abstract 13711: Clonal Hematopoiesis Driven by TET2 and ASXL1 but Not DNMT3A is Associated With Interleukin 6 Levels, Cardiac Biomarkers, Cardiac Remodeling, and Risk of Atrial Fibrillation

Author

Saadatagah, Seyedmohammad, Naderian, Mohammadreza, Uddin, Md Mesbah, Dikilitas, Ozan, Schuermans, Art, Niroula, Abhishek, Selvin, Elizabeth, Hoogeveen, Ron C, Matsushita, Kuni, NAMBI, VIJAY, Yu, Bing, Chen, Lin Y, Bick, Alexander G, Ebert, Benjamin L, Honigberg, Michael C, Li, Na, Shah, Amil M, Natarajan, Pradeep, Kullo, Iftikhar J, and Ballantyne, Christie M

Published
2023
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10. Abstract 13089: Plasma Proteomics and Risk of Incident Ischemic Stroke: Meta-Analysis of the Atherosclerosis Risk in Communities (ARIC) Study and the Cardiovascular Health Study (CHS)

Author

Wang, Wendy, Kalani, Rizwan, Zhang, Michael J, Pankow, Jim S, Lakshminarayan, Kamakshi, Alonso, Alvaro, Lutsey, Pamela L, Longstreth, W T, Ballantyne, Christie M, Matsushita, Kuni, Tin, Adrienne, Johansen, Michelle C, Gottesman, Rebecca F, Coresh, Josef, Pan, Wei, Walker, Keenan, Heckbert, Susan R, and Chen, Lin Y

Published
2023
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15. NT‐proBNP as a Mediator of the Racial Difference in Incident Atrial Fibrillation and Heart Failure

Author

Whitman, Isaac R, Vittinghoff, Eric, DeFilippi, Christopher R, Gottdiener, John S, Alonso, Alvaro, Psaty, Bruce M, Heckbert, Susan R, Hoogeveen, Ron C, Arking, Dan E, Selvin, Elizabeth, Chen, Lin Y, Dewland, Thomas A, and Marcus, Gregory M

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Research, Prevention, Cardiovascular, Heart Disease, Good Health and Well Being, Black or African American, Aged, Atrial Fibrillation, Female, Heart Failure, Humans, Incidence, Male, Middle Aged, Natriuretic Peptide, Brain, Peptide Fragments, Proportional Hazards Models, United States, White People, atrial fibrillation arrhythmia, congestive heart failure, mechanisms, mediation, natriuretic peptide, NT-proBNP, NT‐proBNP, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Abstract

Background Blacks harbor more cardiovascular risk factors than whites, but experience less atrial fibrillation ( AF ). Conversely, whites may have a lower risk of heart failure ( CHF ). N-terminal pro-B-type natriuretic peptide ( NT -pro BNP) levels are higher in whites, predict incident AF , and have diuretic effects in the setting of increased ventricular diastolic pressures, potentially providing a unifying explanation for these racial differences. Methods and Results We used data from the CHS (Cardiovascular Health Study) to determine the degree to which baseline NT -pro BNP levels mediate the relationships between race and incident AF and CHF by comparing beta estimates between models with and without NT -pro BNP . The ARIC (Atherosclerosis Risk in Communities) study was used to assess reproducibility. Among 4731 CHS (770 black) and 12 418 ARIC (3091 black) participants, there were 1277 and 1253 incident AF events, respectively. Whites had higher baseline NT -pro BNP ( CHS : 40% higher than blacks; 95% CI , 29-53; ARIC : 39% higher; 95% CI , 33-46) and had a greater risk of incident AF compared with blacks ( CHS : adjusted hazard ratio, 1.60; 95% CI , 1.31-1.93; ARIC : hazard ratio, 1.93; 95% CI , 1.57-2.27). NT -pro BNP levels explained a significant proportion of the racial difference in AF risk ( CHS : 36.2%; 95% CI , 23.2-69.2%; ARIC : 24.6%; 95% CI , 14.8-39.6%). Contrary to our hypothesis, given an increased risk of CHF among whites in CHS (adjusted hazard ratio, 1.20; 95% CI , 1.05-1.47) and the absence of a significant association between race and CHF in ARIC (adjusted hazard ratio, 1.07; 95% CI , 0.94-1.23), CHF -related mediation analyses were not performed. Conclusions A substantial portion of the relationship between race and AF was statistically explained by baseline NT -pro BNP levels. No consistent relationship between race and CHF was observed.

Published
2019

19. Multi-ethnic genome-wide association study for atrial fibrillation

Author

Roselli, Carolina, Chaffin, Mark D, Weng, Lu-Chen, Aeschbacher, Stefanie, Ahlberg, Gustav, Albert, Christine M, Almgren, Peter, Alonso, Alvaro, Anderson, Christopher D, Aragam, Krishna G, Arking, Dan E, Barnard, John, Bartz, Traci M, Benjamin, Emelia J, Bihlmeyer, Nathan A, Bis, Joshua C, Bloom, Heather L, Boerwinkle, Eric, Bottinger, Erwin B, Brody, Jennifer A, Calkins, Hugh, Campbell, Archie, Cappola, Thomas P, Carlquist, John, Chasman, Daniel I, Chen, Lin Y, Chen, Yii-Der Ida, Choi, Eue-Keun, Choi, Seung Hoan, Christophersen, Ingrid E, Chung, Mina K, Cole, John W, Conen, David, Cook, James, Crijns, Harry J, Cutler, Michael J, Damrauer, Scott M, Daniels, Brian R, Darbar, Dawood, Delgado, Graciela, Denny, Joshua C, Dichgans, Martin, Dörr, Marcus, Dudink, Elton A, Dudley, Samuel C, Esa, Nada, Esko, Tonu, Eskola, Markku, Fatkin, Diane, Felix, Stephan B, Ford, Ian, Franco, Oscar H, Geelhoed, Bastiaan, Grewal, Raji P, Gudnason, Vilmundur, Guo, Xiuqing, Gupta, Namrata, Gustafsson, Stefan, Gutmann, Rebecca, Hamsten, Anders, Harris, Tamara B, Hayward, Caroline, Heckbert, Susan R, Hernesniemi, Jussi, Hocking, Lynne J, Hofman, Albert, Horimoto, Andrea RVR, Huang, Jie, Huang, Paul L, Huffman, Jennifer, Ingelsson, Erik, Ipek, Esra Gucuk, Ito, Kaoru, Jimenez-Conde, Jordi, Johnson, Renee, Jukema, J Wouter, Kääb, Stefan, Kähönen, Mika, Kamatani, Yoichiro, Kane, John P, Kastrati, Adnan, Kathiresan, Sekar, Katschnig-Winter, Petra, Kavousi, Maryam, Kessler, Thorsten, Kietselaer, Bas L, Kirchhof, Paulus, Kleber, Marcus E, Knight, Stacey, Krieger, Jose E, Kubo, Michiaki, Launer, Lenore J, Laurikka, Jari, Lehtimäki, Terho, Leineweber, Kirsten, Lemaitre, Rozenn N, Li, Man, Lim, Hong Euy, Lin, Henry J, and Lin, Honghuang

Subjects
Biological Sciences, Genetics, Heart Disease, Cardiovascular, Human Genome, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Atrial Fibrillation, Case-Control Studies, Ethnicity, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Quantitative Trait Loci, Transcriptome, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Atrial fibrillation (AF) affects more than 33 million individuals worldwide1 and has a complex heritability2. We conducted the largest meta-analysis of genome-wide association studies (GWAS) for AF to date, consisting of more than half a million individuals, including 65,446 with AF. In total, we identified 97 loci significantly associated with AF, including 67 that were novel in a combined-ancestry analysis, and 3 that were novel in a European-specific analysis. We sought to identify AF-associated genes at the GWAS loci by performing RNA-sequencing and expression quantitative trait locus analyses in 101 left atrial samples, the most relevant tissue for AF. We also performed transcriptome-wide analyses that identified 57 AF-associated genes, 42 of which overlap with GWAS loci. The identified loci implicate genes enriched within cardiac developmental, electrophysiological, contractile and structural pathways. These results extend our understanding of the biological pathways underlying AF and may facilitate the development of therapeutics for AF.

Published
2018

22. Association Between QT-Interval Components and Sudden Cardiac Death

Author

O'Neal, Wesley T, Singleton, Matthew J, Roberts, Jason D, Tereshchenko, Larisa G, Sotoodehnia, Nona, Chen, Lin Y, Marcus, Gregory M, and Soliman, Elsayed Z

Subjects
Biomedical and Clinical Sciences, Medical Physiology, Cardiovascular Medicine and Haematology, Clinical Sciences, Clinical Research, Heart Disease, Cardiovascular, Action Potentials, Arrhythmias, Cardiac, Death, Sudden, Cardiac, Electrocardiography, Female, Heart Conduction System, Heart Rate, Humans, Male, Middle Aged, Proportional Hazards Models, Prospective Studies, Risk Factors, Time Factors, United States, death, sudden, cardiac, follow-up studies, humans, risk, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences, Medical physiology
Abstract

Several reports have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD). However, it is unknown whether any of the components within the QT interval are responsible for its association with SCD. We examined the association of the individual QT-interval components (R-wave onset to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave end) with SCD in 12 241 participants (54±5.7 years; 26% black; 55% women) from the ARIC study (Atherosclerosis Risk in Communities). The QT interval and its components were measured at baseline (1987-1989) from 12-lead ECGs. SCD cases were adjudicated by a group of physicians through December 31, 2012. During a median follow-up of 23.6 years, a total of 346 cases of SCD were identified. Although prolongation of the QT interval was associated with a 49% increased risk of SCD (hazard ratio, 1.49; 95% confidence interval, 1.01-2.18), only the T-wave onset to T-peak component (per 1-SD increase: hazard ratio, 1.19; 95% confidence interval, 1.06-1.34) was associated with SCD and not any of the other components in separate models. When all of the QT-interval components were included in the same model, T-wave onset to T-peak remained the strongest predictor of SCD (per 1-SD increase: hazard ratio, 1.21; 95% confidence interval, 1.06-1.37). The risk of SCD with the QT interval is driven by prolongation of the T-wave onset to T-peak component. This suggests that shifting the focus from the overall QT interval to its individual components will refine SCD prediction in the community.

Published
2017

23. Ectopy on a Single 12-Lead ECG, Incident Cardiac Myopathy, and Death in the Community.

Author

Nguyen, Kaylin T, Vittinghoff, Eric, Dewland, Thomas A, Dukes, Jonathan W, Soliman, Elsayed Z, Stein, Phyllis K, Gottdiener, John S, Alonso, Alvaro, Chen, Lin Y, Psaty, Bruce M, Heckbert, Susan R, and Marcus, Gregory M

Subjects
Humans, Atrial Fibrillation, Atrial Premature Complexes, Ventricular Premature Complexes, Cardiomyopathies, Electrocardiography, Prognosis, Incidence, Risk Factors, Prospective Studies, Aged, Middle Aged, United States, Female, Male, Heart Failure, atrial fibrillation, heart failure, mortality, premature atrial contractions, premature ventricular contractions, Cardiovascular, Heart Disease, Patient Safety, Aging, Prevention, Clinical Research, Cardiorespiratory Medicine and Haematology
Abstract

BackgroundAtrial fibrillation and heart failure are 2 of the most common diseases, yet ready means to identify individuals at risk are lacking. The 12-lead ECG is one of the most accessible tests in medicine. Our objective was to determine whether a premature atrial contraction observed on a standard 12-lead ECG would predict atrial fibrillation and mortality and whether a premature ventricular contraction would predict heart failure and mortality.Methods and resultsWe utilized the CHS (Cardiovascular Health) Study, which followed 5577 participants for a median of 12 years, as the primary cohort. The ARIC (Atherosclerosis Risk in Communities Study), the replication cohort, captured data from 15 792 participants over a median of 22 years. In the CHS, multivariable analyses revealed that a baseline 12-lead ECG premature atrial contraction predicted a 60% increased risk of atrial fibrillation (hazard ratio, 1.6; 95% CI, 1.3-2.0; P

Published
2017

24. Electrocardiographic intervals associated with incident atrial fibrillation: Dissecting the QT interval

Author

Roberts, Jason D, Soliman, Elsayed Z, Alonso, Alvaro, Vittinghoff, Eric, Chen, Lin Y, Loehr, Laura, and Marcus, Gregory M

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Cardiovascular, Heart Disease, Action Potentials, Atrial Fibrillation, Electrocardiography, Heart Conduction System, Humans, Atrial fibrillation, QT interval, Epidemiology, Arrhythmia, Biomedical Engineering, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundProlongation of the QT interval has been associated with an increased risk of developing atrial fibrillation (AF), but the responsible mechanism remains unknown.ObjectivesThe aims of this study were to subdivide the QT interval into its components and identify the resultant electrocardiographic interval(s) responsible for the association with AF.MethodsPredefined QT-interval components were assessed for association with incident AF in the Atherosclerosis Risk in Communities study using Cox proportional hazards models. Hazard ratios (HRs) were calculated per 1-SD increase in each component. Among QT-interval components exhibiting significant associations, additional analyses evaluating long extremes, defined as greater than the 95th percentile, were performed.ResultsOf the 14,625 individuals, 1505 (10.3%) were diagnosed with incident AF during a mean follow-up period of 17.6 years. After multivariable adjustment, QT-interval components involved in repolarization, but not depolarization, exhibited significant associations with incident AF, including a longer ST segment (HR 1.27; 95% confidence interval [CI] 1.14-1.41; P < .001) and a prolonged T-wave onset to T-wave peak (T-onset to T-peak) (HR 1.13; 95% CI 1.07-1.20; P < .001). Marked prolongation of the ST segment (HR 1.31; 95% CI 1.04-1.64; P = .022) and T-onset to T-peak (HR 1.36; 95% CI 1.09-1.69; P = .006) was also associated with an increased risk of incident AF.ConclusionThe association between a prolonged QT interval and incident AF is primarily explained by components involved in ventricular repolarization: prolongation of the ST segment and T-onset to T-peak. These observations suggest that prolongation of phases 2 and 3 of the cardiac action potential drives the association between the QT interval and AF risk.

Published
2017

25. Genetic Risk Prediction of Atrial Fibrillation

Author

Lubitz, Steven A, Yin, Xiaoyan, Lin, Henry J, Kolek, Matthew, Smith, J Gustav, Trompet, Stella, Rienstra, Michiel, Rost, Natalia S, Teixeira, Pedro L, Almgren, Peter, Anderson, Christopher D, Chen, Lin Y, Engström, Gunnar, Ford, Ian, Furie, Karen L, Guo, Xiuqing, Larson, Martin G, Lunetta, Kathryn L, Macfarlane, Peter W, Psaty, Bruce M, Soliman, Elsayed Z, Sotoodehnia, Nona, Stott, David J, Taylor, Kent D, Weng, Lu-Chen, Yao, Jie, Geelhoed, Bastiaan, Verweij, Niek, Siland, Joylene E, Kathiresan, Sekar, Roselli, Carolina, Roden, Dan M, van der Harst, Pim, Darbar, Dawood, Jukema, J Wouter, Melander, Olle, Rosand, Jonathan, Rotter, Jerome I, Heckbert, Susan R, Ellinor, Patrick T, Alonso, Alvaro, and Benjamin, Emelia J

Subjects
Epidemiology, Health Sciences, Stroke, Cardiovascular, Prevention, Brain Disorders, Heart Disease, Genetics, Clinical Research, Aged, Atrial Fibrillation, Female, Humans, Incidence, Male, Middle Aged, Risk Factors, atrial fibrillation, atrial flutter, forecasting, genetic association studies, stroke, AFGen Consortium, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences, Sports science and exercise
Abstract

BackgroundAtrial fibrillation (AF) has a substantial genetic basis. Identification of individuals at greatest AF risk could minimize the incidence of cardioembolic stroke.MethodsTo determine whether genetic data can stratify risk for development of AF, we examined associations between AF genetic risk scores and incident AF in 5 prospective studies comprising 18 919 individuals of European ancestry. We examined associations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40%]) and 3028 referents. Scores were based on 11 to 719 common variants (≥5%) associated with AF at P values ranging from

Published
2017

27. Past alcohol consumption and incident atrial fibrillation: The Atherosclerosis Risk in Communities (ARIC) Study

Author

Dixit, Shalini, Alonso, Alvaro, Vittinghoff, Eric, Soliman, Elsayed, Chen, Lin Y, and Marcus, Gregory M

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Health Sciences, Cardiovascular, Substance Misuse, Heart Disease, Clinical Research, Alcoholism, Alcohol Use and Health, Prevention, Atherosclerosis, Cancer, Oral and gastrointestinal, Stroke, Good Health and Well Being, Alcohol Drinking, Atrial Fibrillation, Female, Humans, Incidence, Kaplan-Meier Estimate, Male, Middle Aged, Risk Factors, General Science & Technology
Abstract

BackgroundAlthough current alcohol consumption is a risk factor for incident atrial fibrillation (AF), the more clinically relevant question may be whether alcohol cessation is associated with a reduced risk.Methods and resultsWe studied participants enrolled in the Atherosclerosis Risk in Communities Study (ARIC) between 1987 and 1989 without prevalent AF. Past and current alcohol consumption were ascertained at baseline and at 3 subsequent visits. Incident AF was ascertained via study ECGs, hospital discharge ICD-9 codes, and death certificates. Of 15,222 participants, 2,886 (19.0%) were former drinkers. During a median follow-up of 19.7 years, there were 1,631 cases of incident AF, 370 occurring in former consumers. Former drinkers had a higher rate of AF compared to lifetime abstainers and current drinkers. After adjustment for potential confounders, every decade abstinent from alcohol was associated with an approximate 20% (95% CI 11-28%) lower rate of incident AF; every additional decade of past alcohol consumption was associated with a 13% (95% CI 3-25%) higher rate of AF; and every additional drink per day during former drinking was associated with a 4% (95% CI 0-8%) higher rate of AF.ConclusionsAmong former drinkers, the number of years of drinking and the amount of alcohol consumed may each confer an increased risk of AF. Given that a longer duration of abstinence was associated with a decreased risk of AF, earlier modification of alcohol use may have a greater influence on AF prevention.

Published
2017

34. Shared Decision-Making in Cardiac Electrophysiology Procedures and Arrhythmia Management

Author

Chung, Mina K., Fagerlin, Angela, Wang, Paul J., Ajayi, Tinuola B., Allen, Larry A., Baykaner, Tina, Benjamin, Emelia J., Branda, Megan, Cavanaugh, Kerri L., Chen, Lin Y., Crossley, George H., Delaney, Rebecca K., Eckhardt, Lee L., Grady, Kathleen L., Hargraves, Ian G., True Hills, Mellanie, Kalscheur, Matthew M., Kramer, Daniel B., Kunneman, Marleen, Lampert, Rachel, Langford, Aisha T., Lewis, Krystina B., Lu, Ying, Mandrola, John M., Martinez, Kathryn, Matlock, Daniel D., McCarthy, Sarah R., Montori, Victor M., Noseworthy, Peter A., Orland, Kate M., Ozanne, Elissa, Passman, Rod, Pundi, Krishna, Roden, Dan M., Saarel, Elizabeth V., Schmidt, Monika M., Sears, Samuel F., Stacey, Dawn, Stafford, Randall S., Steinberg, Benjamin A., Youn Wass, Sojin, and Wright, Jennifer M.

Published
2021
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35. 52 Genetic Loci Influencing Myocardial Mass

Author

van der Harst, Pim, van Setten, Jessica, Verweij, Niek, Vogler, Georg, Franke, Lude, Maurano, Matthew T, Wang, Xinchen, Leach, Irene Mateo, Eijgelsheim, Mark, Sotoodehnia, Nona, Hayward, Caroline, Sorice, Rossella, Meirelles, Osorio, Lyytikäinen, Leo-Pekka, Polašek, Ozren, Tanaka, Toshiko, Arking, Dan E, Ulivi, Sheila, Trompet, Stella, Müller-Nurasyid, Martina, Smith, Albert V, Dörr, Marcus, Kerr, Kathleen F, Magnani, Jared W, Del Greco M., Fabiola, Zhang, Weihua, Nolte, Ilja M, Silva, Claudia T, Padmanabhan, Sandosh, Tragante, Vinicius, Esko, Tõnu, Abecasis, Gonçalo R, Adriaens, Michiel E, Andersen, Karl, Barnett, Phil, Bis, Joshua C, Bodmer, Rolf, Buckley, Brendan M, Campbell, Harry, Cannon, Megan V, Chakravarti, Aravinda, Chen, Lin Y, Delitala, Alessandro, Devereux, Richard B, Doevendans, Pieter A, Dominiczak, Anna F, Ferrucci, Luigi, Ford, Ian, Gieger, Christian, Harris, Tamara B, Haugen, Eric, Heinig, Matthias, Hernandez, Dena G, Hillege, Hans L, Hirschhorn, Joel N, Hofman, Albert, Hubner, Norbert, Hwang, Shih-Jen, Iorio, Annamaria, Kähönen, Mika, Kellis, Manolis, Kolcic, Ivana, Kooner, Ishminder K, Kooner, Jaspal S, Kors, Jan A, Lakatta, Edward G, Lage, Kasper, Launer, Lenore J, Levy, Daniel, Lundby, Alicia, Macfarlane, Peter W, May, Dalit, Meitinger, Thomas, Metspalu, Andres, Nappo, Stefania, Naitza, Silvia, Neph, Shane, Nord, Alex S, Nutile, Teresa, Okin, Peter M, Olsen, Jesper V, Oostra, Ben A, Penninger, Josef M, Pennacchio, Len A, Pers, Tune H, Perz, Siegfried, Peters, Annette, Pinto, Yigal M, Pfeufer, Arne, Pilia, Maria Grazia, Pramstaller, Peter P, Prins, Bram P, Raitakari, Olli T, Raychaudhuri, Soumya, Rice, Ken M, Rossin, Elizabeth J, Rotter, Jerome I, Schafer, Sebastian, Schlessinger, David, and Schmidt, Carsten O

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Genetics, Heart Disease - Coronary Heart Disease, Cardiovascular, Heart Disease, Biotechnology, Human Genome, 2.1 Biological and endogenous factors, Animals, Cardiomegaly, Genetic Loci, Genome-Wide Association Study, Humans, electrocardiogram, genetic association study, heart failure, left ventricular hypertrophy, QRS, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundMyocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death.ObjectivesThis meta-analysis sought to gain insights into the genetic determinants of myocardial mass.MethodsWe carried out a genome-wide association meta-analysis of 4 QRS traits in up to 73,518 individuals of European ancestry, followed by extensive biological and functional assessment.ResultsWe identified 52 genomic loci, of which 32 are novel, that are reliably associated with 1 or more QRS phenotypes at p < 1 × 10(-8). These loci are enriched in regions of open chromatin, histone modifications, and transcription factor binding, suggesting that they represent regions of the genome that are actively transcribed in the human heart. Pathway analyses provided evidence that these loci play a role in cardiac hypertrophy. We further highlighted 67 candidate genes at the identified loci that are preferentially expressed in cardiac tissue and associated with cardiac abnormalities in Drosophila melanogaster and Mus musculus. We validated the regulatory function of a novel variant in the SCN5A/SCN10A locus in vitro and in vivo.ConclusionsTaken together, our findings provide new insights into genes and biological pathways controlling myocardial mass and may help identify novel therapeutic targets.

Published
2016

36. Impact of genetic variants on the upstream efficacy of renin-angiotensin system inhibitors for the prevention of atrial fibrillation

Author

Roberts, Jason D, Dewland, Thomas A, Glidden, David V, Hoffmann, Thomas J, Arking, Dan E, Chen, Lin Y, Psaty, Bruce M, Olgin, Jeffrey E, Alonso, Alvaro, Heckbert, Susan R, and Marcus, Gregory M

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Heart Disease, Prevention, Clinical Research, Hypertension, Genetics, Atherosclerosis, Cardiovascular, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being, Aged, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Atrial Fibrillation, Female, Genetic Variation, Genome-Wide Association Study, Humans, Male, Pharmacogenomic Testing, Polymorphism, Single Nucleotide, Primary Prevention, Proportional Hazards Models, Renin-Angiotensin System, Treatment Outcome, United States, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundRenin-angiotensin system (RAS) inhibition via angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers may reduce the risk of developing atrial fibrillation (AF) in certain populations, but the evidence is conflicting. Recent genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with AF, potentially identifying clinically relevant subtypes of the disease. We sought to investigate the impact of carrier status of 9 AF-associated SNPs on the efficacy of RAS inhibition for the primary prevention of AF.MethodsWe performed SNP-RAS inhibitor interaction testing with unadjusted and adjusted Cox proportional hazards models using a discovery (Cardiovascular Health Study) and a replication (Atherosclerosis Risk in Communities) cohort. Additive genetic models were used for the SNP analyses, and 2-tailed P values

Published
2016

37. Gene-gene Interaction Analyses for Atrial Fibrillation

Author

Lin, Honghuang, Mueller-Nurasyid, Martina, Smith, Albert V, Arking, Dan E, Barnard, John, Bartz, Traci M, Lunetta, Kathryn L, Lohman, Kurt, Kleber, Marcus E, Lubitz, Steven A, Geelhoed, Bastiaan, Trompet, Stella, Niemeijer, Maartje N, Kacprowski, Tim, Chasman, Daniel I, Klarin, Derek, Sinner, Moritz F, Waldenberger, Melanie, Meitinger, Thomas, Harris, Tamara B, Launer, Lenore J, Soliman, Elsayed Z, Chen, Lin Y, Smith, Jonathan D, Van Wagoner, David R, Rotter, Jerome I, Psaty, Bruce M, Xie, Zhijun, Hendricks, Audrey E, Ding, Jingzhong, Delgado, Graciela E, Verweij, Niek, van der Harst, Pim, Macfarlane, Peter W, Ford, Ian, Hofman, Albert, Uitterlinden, André, Heeringa, Jan, Franco, Oscar H, Kors, Jan A, Weiss, Stefan, Völzke, Henry, Rose, Lynda M, Natarajan, Pradeep, Kathiresan, Sekar, Kääb, Stefan, Gudnason, Vilmundur, Alonso, Alvaro, Chung, Mina K, Heckbert, Susan R, Benjamin, Emelia J, Liu, Yongmei, März, Winfried, Rienstra, Michiel, Jukema, J Wouter, Stricker, Bruno H, Dörr, Marcus, Albert, Christine M, and Ellinor, Patrick T

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Heart Disease, Human Genome, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Aged, Atrial Fibrillation, Cohort Studies, Epistasis, Genetic, Female, Genetic Association Studies, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Male, Membrane Transport Proteins, Middle Aged, Multivariate Analysis, Muscle Proteins, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Potassium Channels
Abstract

Atrial fibrillation (AF) is a heritable disease that affects more than thirty million individuals worldwide. Extensive efforts have been devoted to the study of genetic determinants of AF. The objective of our study is to examine the effect of gene-gene interaction on AF susceptibility. We performed a large-scale association analysis of gene-gene interactions with AF in 8,173 AF cases, and 65,237 AF-free referents collected from 15 studies for discovery. We examined putative interactions between genome-wide SNPs and 17 known AF-related SNPs. The top interactions were then tested for association in an independent cohort for replication, which included more than 2,363 AF cases and 114,746 AF-free referents. One interaction, between rs7164883 at the HCN4 locus and rs4980345 at the SLC28A1 locus, was found to be significantly associated with AF in the discovery cohorts (interaction OR = 1.44, 95% CI: 1.27-1.65, P = 4.3 × 10-8). Eight additional gene-gene interactions were also marginally significant (P

Published
2016

38. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, F. B., Niles, J. L., Jayne, D. R. W., Merkel, P. A., Bruchfeld, A., Yue, H., Schall, T. J., Bekker, P., Peh, C. A., Chakera, A., Cooper, B., Kurtkoti, J., Langguth, D., Levidiotis, V., Luxton, G., Mount, P., Mudge, D., Noble, E., Phoon, R., Ranganathan, D., Ritchie, A., Ryan, J., Suranyi, M., Rosenkranz, A., Lhotta, K., Kronbichler, A., Demoulin, N., Bovy, C., Hellemans, R., Hougardy, J., Sprangers, B., Wissing, K., Pagnoux, C., Barbour, S., Brachemi, S., Cournoyer, S., Girard, L., Laurin, L., Liang, P., Philibert, D., Walsh, M., Tesar, V., Becvar, R., Horak, P., Rychlik, I., Szpirt, W., Dieperink, H., Gregersen, J., Ivarsen, P., Krarup, E., Lyngsoe, C., Rigothier, C., Augusto, J., Belot, A., Chauveau, D., Cornec, D., Jourde-Chiche, N., Ficheux, M., Karras, A., Klein, A., Maurier, F., Mesbah, R., Moranne, O., Neel, A., Quemeneur, T., Saadoun, D., Terrier, B., Zaoui, P., Schaier, M., Benck, U., Bergner, R., Busch, M., Floege, J., Grundmann, F., Haller, H., Haubitz, M., Hellmich, B., Henes, J., Hohenstein, B., Hugo, C., Iking-Konert, C., Arndt, F., Kubacki, T., Kotter, I., Lamprecht, P., Lindner, T., Halbritter, J., Mehling, H., Schonermarck, U., Venhoff, N., Vielhauer, V., Witzke, O., Szombati, I., Szucs, G., Garibotto, G., Alberici, F., Brunetta, E., Dagna, L., De Vita, S., Emmi, G., Gabrielli, A., Manenti, L., Pieruzzi, F., Roccatello, D., Salvarani, C., Dobashi, H., Atsumi, T., Fujimoto, S., Hagino, N., Ihata, A., Kaname, S., Kaneko, Y., Katagiri, A., Katayama, M., Kirino, Y., Kitagawa, K., Komatsuda, A., Kono, H., Kurasawa, T., Matsumura, R., Mimura, T., Morinobu, A., Murakawa, Y., Naniwa, T., Nanki, T., Ogawa, N., Oshima, H., Sada, K., Sugiyama, E., Takeuchi, T., Taki, H., Tamura, N., Tsukamoto, T., Yamagata, K., Yamamura, M., van Daele, P., Rutgers, A., Teng, Y., Walker, R., Chua, I., Collins, M., Rabindranath, K., de Zoysa, J., Svensson, M., Grevbo, B., Kalstad, S., Little, M., Clarkson, M., Molloy, E., Pamplona, I. A., Anton, J., Lucia, V. B., Ciggaran, S., Cid, M. C., Encarnacion, M. D., Oliveras, X. F., Soler, M. J., Rusinol, H. M., Praga, M., Porras, L. Q., Segarra, A., Segelmark, M., Soveri, I., Thomaidi, E., Westman, K., Neumann, T., Burnier, M., Daikeler, T., Dudler, J., Hauser, T., Seeger, H., Vogt, B., Jayne, D., Burton, J., Al Jayyousi, R., Amin, T., Andrews, J., Baines, L., Brogan, P., Dasgupta, B., Doulton, T., Flossmann, O., Griffin, S., Harper, J., Harper, L., Kidder, D., Klocke, R., Lanyon, P., Luqmani, R., Mclaren, J., Makanjuola, D., Mccann, L., Nandagudi, A., Selvan, S., O'Riordan, E., Patel, M., Patel, R., Pusey, C., Rajakariar, R., Robson, J., Robson, M., Salama, A., Smyth, L., Sznajd, J., Taylor, J., Merkel, P., Sreih, A., Belilos, E., Bomback, A., Carlin, J., Chen Lin, Y. C., Derebail, V., Dragoi, S., Dua, A., Forbess, L., Geetha, D., Gipson, P., Gohh, R., Greenwood, G. T., Hugenberg, S., Jimenez, R., Kaskas, M., Kermani, T., Kivitz, A., Koening, C., Langford, C., Marder, G., Mohamed, A., Monach, P., Neyra, N., Niemer, G., Niles, J., Obi, R., Owens, C., Parks, D., Podoll, A., Rovin, B., Sam, R., Shergy, W., Silva, A., Specks, U., Spiera, R., Springer, J., Striebich, C., Swarup, A., Thakar, S., Tiliakos, A., Tsai, Y., Waguespack, D., Wasko, M. C., Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, and Wasko, M

Subjects
avacopan, Clinical Research, renal recovery, Nephrology, low eGFR, complement 5a receptor, complement, ANCA-associated vasculiti
Abstract

INTRODUCTION: In the 330-patient ADVOCATE trial of avacopan for the treatment of antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, in which 81% of patients had renal involvement, estimated glomerular filtration rate (eGFR) increased on average 7.3 ml/min per 1.73 m(2) in the avacopan group and 4.1 ml/min per 1.73 m(2) in the prednisone group (P = 0.029) at week 52. This new analysis examines the results in the patient subgroup with severe renal insufficiency at enrollment into the trial, i.e., eGFR ≤20 ml/min per 1.73 m(2). METHODS: eGFR was determined at baseline and over the course of the trial. Changes in eGFR were compared between the 2 treatment groups. RESULTS: In ADVOCATE, 27 of 166 patients (16%) in the avacopan group and 23 of 164 patients (14%) in the prednisone group had a baseline eGFR ≤20 ml/min per 1.73 m(2). At week 52, eGFR increased on average 16.1 and 7.7 ml/min per 1.73 m(2) in the avacopan and prednisone groups, respectively (P = 0.003). The last eGFR value measured during the 52-week treatment period was ≥2-fold higher than baseline in 41% of patients in the avacopan group compared to 13% in the prednisone group (P = 0.030). More patients in the avacopan group versus prednisone group had increases in eGFR above 20, 30, and 45 ml/min per 1.73 m(2), respectively. Serious adverse events occurred in 13 of 27 patients (48%) in the avacopan group and 16 of 23 patients (70%) in the prednisone group. CONCLUSION: Among patients with baseline eGFR ≤20 ml/min per 1.73 m(2) in the ADVOCATE trial, eGFR improved more in the avacopan group than in the prednisone group.

Published
2023

43. Renal Recovery for Patients with ANCA-Associated Vasculitis and Low eGFR in the ADVOCATE Trial of Avacopan

Author

Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., Wasko M. C., Cortazar, F, Niles, J, Jayne, D, Merkel, P, Bruchfeld, A, Yue, H, Schall, T, Bekker, P, Peh, C, Chakera, A, Cooper, B, Kurtkoti, J, Langguth, D, Levidiotis, V, Luxton, G, Mount, P, Mudge, D, Noble, E, Phoon, R, Ranganathan, D, Ritchie, A, Ryan, J, Suranyi, M, Rosenkranz, A, Lhotta, K, Kronbichler, A, Demoulin, N, Bovy, C, Hellemans, R, Hougardy, J, Sprangers, B, Wissing, K, Pagnoux, C, Barbour, S, Brachemi, S, Cournoyer, S, Girard, L, Laurin, L, Liang, P, Philibert, D, Walsh, M, Tesar, V, Becvar, R, Horak, P, Rychlik, I, Szpirt, W, Dieperink, H, Gregersen, J, Ivarsen, P, Krarup, E, Lyngsoe, C, Rigothier, C, Augusto, J, Belot, A, Chauveau, D, Cornec, D, Jourde-Chiche, N, Ficheux, M, Karras, A, Klein, A, Maurier, F, Mesbah, R, Moranne, O, Neel, A, Quemeneur, T, Saadoun, D, Terrier, B, Zaoui, P, Schaier, M, Benck, U, Bergner, R, Busch, M, Floege, J, Grundmann, F, Haller, H, Haubitz, M, Hellmich, B, Henes, J, Hohenstein, B, Hugo, C, Iking-Konert, C, Arndt, F, Kubacki, T, Kotter, I, Lamprecht, P, Lindner, T, Halbritter, J, Mehling, H, Schonermarck, U, Venhoff, N, Vielhauer, V, Witzke, O, Szombati, I, Szucs, G, Garibotto, G, Alberici, F, Brunetta, E, Dagna, L, De Vita, S, Emmi, G, Gabrielli, A, Manenti, L, Pieruzzi, F, Roccatello, D, Salvarani, C, Dobashi, H, Atsumi, T, Fujimoto, S, Hagino, N, Ihata, A, Kaname, S, Kaneko, Y, Katagiri, A, Katayama, M, Kirino, Y, Kitagawa, K, Komatsuda, A, Kono, H, Kurasawa, T, Matsumura, R, Mimura, T, Morinobu, A, Murakawa, Y, Naniwa, T, Nanki, T, Ogawa, N, Oshima, H, Sada, K, Sugiyama, E, Takeuchi, T, Taki, H, Tamura, N, Tsukamoto, T, Yamagata, K, Yamamura, M, van Daele, P, Rutgers, A, Teng, Y, Walker, R, Chua, I, Collins, M, Rabindranath, K, de Zoysa, J, Svensson, M, Grevbo, B, Kalstad, S, Little, M, Clarkson, M, Molloy, E, Pamplona, I, Anton, J, Lucia, V, Ciggaran, S, Cid, M, Encarnacion, M, Oliveras, X, Soler, M, Rusinol, H, Praga, M, Porras, L, Segarra, A, Segelmark, M, Soveri, I, Thomaidi, E, Westman, K, Neumann, T, Burnier, M, Daikeler, T, Dudler, J, Hauser, T, Seeger, H, Vogt, B, Burton, J, Al Jayyousi, R, Amin, T, Andrews, J, Baines, L, Brogan, P, Dasgupta, B, Doulton, T, Flossmann, O, Griffin, S, Harper, J, Harper, L, Kidder, D, Klocke, R, Lanyon, P, Luqmani, R, Mclaren, J, Makanjuola, D, Mccann, L, Nandagudi, A, Selvan, S, O'Riordan, E, Patel, M, Patel, R, Pusey, C, Rajakariar, R, Robson, J, Robson, M, Salama, A, Smyth, L, Sznajd, J, Taylor, J, Sreih, A, Belilos, E, Bomback, A, Carlin, J, Chen Lin, Y, Derebail, V, Dragoi, S, Dua, A, Forbess, L, Geetha, D, Gipson, P, Gohh, R, Greenwood, G, Hugenberg, S, Jimenez, R, Kaskas, M, Kermani, T, Kivitz, A, Koening, C, Langford, C, Marder, G, Mohamed, A, Monach, P, Neyra, N, Niemer, G, Obi, R, Owens, C, Parks, D, Podoll, A, Rovin, B, Sam, R, Shergy, W, Silva, A, Specks, U, Spiera, R, Springer, J, Striebich, C, Swarup, A, Thakar, S, Tiliakos, A, Tsai, Y, Waguespack, D, Wasko, M, Cortazar F. B., Niles J. L., Jayne D. R. W., Merkel P. A., Bruchfeld A., Yue H., Schall T. J., Bekker P., Peh C. A., Chakera A., Cooper B., Kurtkoti J., Langguth D., Levidiotis V., Luxton G., Mount P., Mudge D., Noble E., Phoon R., Ranganathan D., Ritchie A., Ryan J., Suranyi M., Rosenkranz A., Lhotta K., Kronbichler A., Demoulin N., Bovy C., Hellemans R., Hougardy J., Sprangers B., Wissing K., Pagnoux C., Barbour S., Brachemi S., Cournoyer S., Girard L., Laurin L., Liang P., Philibert D., Walsh M., Tesar V., Becvar R., Horak P., Rychlik I., Szpirt W., Dieperink H., Gregersen J., Ivarsen P., Krarup E., Lyngsoe C., Rigothier C., Augusto J., Belot A., Chauveau D., Cornec D., Jourde-Chiche N., Ficheux M., Karras A., Klein A., Maurier F., Mesbah R., Moranne O., Neel A., Quemeneur T., Saadoun D., Terrier B., Zaoui P., Schaier M., Benck U., Bergner R., Busch M., Floege J., Grundmann F., Haller H., Haubitz M., Hellmich B., Henes J., Hohenstein B., Hugo C., Iking-Konert C., Arndt F., Kubacki T., Kotter I., Lamprecht P., Lindner T., Halbritter J., Mehling H., Schonermarck U., Venhoff N., Vielhauer V., Witzke O., Szombati I., Szucs G., Garibotto G., Alberici F., Brunetta E., Dagna L., De Vita S., Emmi G., Gabrielli A., Manenti L., Pieruzzi F., Roccatello D., Salvarani C., Dobashi H., Atsumi T., Fujimoto S., Hagino N., Ihata A., Kaname S., Kaneko Y., Katagiri A., Katayama M., Kirino Y., Kitagawa K., Komatsuda A., Kono H., Kurasawa T., Matsumura R., Mimura T., Morinobu A., Murakawa Y., Naniwa T., Nanki T., Ogawa N., Oshima H., Sada K., Sugiyama E., Takeuchi T., Taki H., Tamura N., Tsukamoto T., Yamagata K., Yamamura M., van Daele P., Rutgers A., Teng Y., Walker R., Chua I., Collins M., Rabindranath K., de Zoysa J., Svensson M., Grevbo B., Kalstad S., Little M., Clarkson M., Molloy E., Pamplona I. A., Anton J., Lucia V. B., Ciggaran S., Cid M. C., Encarnacion M. D., Oliveras X. F., Soler M. J., Rusinol H. M., Praga M., Porras L. Q., Segarra A., Segelmark M., Soveri I., Thomaidi E., Westman K., Neumann T., Burnier M., Daikeler T., Dudler J., Hauser T., Seeger H., Vogt B., Jayne D., Burton J., Al Jayyousi R., Amin T., Andrews J., Baines L., Brogan P., Dasgupta B., Doulton T., Flossmann O., Griffin S., Harper J., Harper L., Kidder D., Klocke R., Lanyon P., Luqmani R., McLaren J., Makanjuola D., McCann L., Nandagudi A., Selvan S., O'Riordan E., Patel M., Patel R., Pusey C., Rajakariar R., Robson J., Robson M., Salama A., Smyth L., Sznajd J., Taylor J., Merkel P., Sreih A., Belilos E., Bomback A., Carlin J., Chen Lin Y. C., Derebail V., Dragoi S., Dua A., Forbess L., Geetha D., Gipson P., Gohh R., Greenwood G. T., Hugenberg S., Jimenez R., Kaskas M., Kermani T., Kivitz A., Koening C., Langford C., Marder G., Mohamed A., Monach P., Neyra N., Niemer G., Niles J., Obi R., Owens C., Parks D., Podoll A., Rovin B., Sam R., Shergy W., Silva A., Specks U., Spiera R., Springer J., Striebich C., Swarup A., Thakar S., Tiliakos A., Tsai Y., Waguespack D., and Wasko M. C.

Abstract

Introduction: In the 330-patient ADVOCATE trial of avacopan for the treatment of antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis, in which 81% of patients had renal involvement, estimated glomerular filtration rate (eGFR) increased on average 7.3 ml/min per 1.73 m2 in the avacopan group and 4.1 ml/min per 1.73 m2 in the prednisone group (P = 0.029) at week 52. This new analysis examines the results in the patient subgroup with severe renal insufficiency at enrollment into the trial, i.e., eGFR ≤20 ml/min per 1.73 m2. Methods: eGFR was determined at baseline and over the course of the trial. Changes in eGFR were compared between the 2 treatment groups. Results: In ADVOCATE, 27 of 166 patients (16%) in the avacopan group and 23 of 164 patients (14%) in the prednisone group had a baseline eGFR ≤20 ml/min per 1.73 m2. At week 52, eGFR increased on average 16.1 and 7.7 ml/min per 1.73 m2 in the avacopan and prednisone groups, respectively (P = 0.003). The last eGFR value measured during the 52-week treatment period was ≥2-fold higher than baseline in 41% of patients in the avacopan group compared to 13% in the prednisone group (P = 0.030). More patients in the avacopan group versus prednisone group had increases in eGFR above 20, 30, and 45 ml/min per 1.73 m2, respectively. Serious adverse events occurred in 13 of 27 patients (48%) in the avacopan group and 16 of 23 patients (70%) in the prednisone group. Conclusion: Among patients with baseline eGFR ≤20 ml/min per 1.73 m2 in the ADVOCATE trial, eGFR improved more in the avacopan group than in the prednisone group.

Published
2023

44. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society

Author

January, Craig T., Wann, L. Samuel, Calkins, Hugh, Chen, Lin Y., Cigarroa, Joaquin E., Cleveland, Joseph C., Jr., Ellinor, Patrick T., Ezekowitz, Michael D., Field, Michael E., Furie, Karen L., Heidenreich, Paul A., Murray, Katherine T., Shea, Julie B., Tracy, Cynthia M., and Yancy, Clyde W.

Published
2019
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49. A Common SCN5A Variant Is Associated with PR Interval and Atrial Fibrillation Among African Americans

Author

ILKHANOFF, LEONARD, ARKING, DAN E, LEMAITRE, ROZENN N, ALONSO, ALVARO, CHEN, LIN Y, DURDA, PETER, HESSELSON, STEPHANIE E, KERR, KATHLEEN F, MAGNANI, JARED W, MARCUS, GREGORY M, SCHNABEL, RENATE B, SMITH, J GUSTAV, SOLIMAN, ELSAYED Z, REINER, ALEXANDER P, SOTOODEHNIA, NONA, and Investigators, on behalf of the Candidate‐Gene Association Resource Consortium and the Cardiac Arrest Blood Study

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Research, Atherosclerosis, Cardiovascular, Heart Disease, Good Health and Well Being, Adult, Black or African American, Aged, Aged, 80 and over, Atrial Fibrillation, Case-Control Studies, Cohort Studies, Death, Sudden, Cardiac, Female, Genetic Variation, Humans, Male, Middle Aged, NAV1.5 Voltage-Gated Sodium Channel, Prospective Studies, Risk Factors, Single-Blind Method, atrial fibrillation, electrocardiogram, genetics, PR interval, sudden death, Candidate-Gene Association Resource (CARE) Consortium and the Cardiac Arrest Blood Study (CABS) Investigators, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

ObjectiveWe examined the association of rs7626962 (S1103Y) or rs7629265, a variant in high linkage disequilibrium with S1103Y (r(2) = 0.87 - 1), with sudden cardiac death (SCD) and atrial fibrillation (AF) among African Americans.BackgroundThe SCN5A missense variant S1103Y has been associated with SCD among African Americans in small case-control studies, but larger population-based studies are needed to validate these findings. The association of this variant with AF has not been fully explored.MethodsUsing genotyping data on over 7,000 African Americans from 5 cohorts (Atherosclerosis Risk in Communities [ARIC], Cleveland Family Study [CFS], Jackson Heart Study [JHS], Multi-Ethnic Study of Atherosclerosis [MESA], Cardiovascular Health Study [CHS]), we examined the association of rs7629265 with electrocardiographic PR, QRS, and QT intervals, and with incident AF and SCD. We examined association of S1103Y (rs7626962) with SCD using a population-based case-control study of SCD Cardiac Arrest Blood Study (CABS).ResultsMeta-analyses across 5 cohorts demonstrated that rs7629265 was significantly associated with PR duration (β = -4.1 milliseconds; P = 2.2×10(-6) ), but not significantly associated with QRS or QT intervals. In meta-analyses of prospectively followed ARIC and CHS participants (n = 3,656), rs7629265 was associated with increased AF risk (n = 299 AF cases; HR = 1.74, P = 1.9 × 10(-4) ). By contrast, rs7629265 was not significantly associated with SCD risk in ARIC (n = 83 SCD cases; P = 0.30) or CHS (n = 54 SCD cases; P = 0.47). Similarly, S1103Y was not significantly associated with SCD risk in CABS (n = 225 SCD cases; P = 0.29).ConclusionThe common SCN5A variant, rs7629265, is associated with increased AF risk and shorter PR interval among African Americans. In contrast to prior reports, we found no evidence of association of rs7629265 or rs7626962 (S1103Y) with SCD risk in the general population.

Published
2014

50. Novel Genetic Markers Associate With Atrial Fibrillation Risk in Europeans and Japanese

Author

Lubitz, Steven A, Lunetta, Kathryn L, Lin, Honghuang, Arking, Dan E, Trompet, Stella, Li, Guo, Krijthe, Bouwe P, Chasman, Daniel I, Barnard, John, Kleber, Marcus E, Dörr, Marcus, Ozaki, Kouichi, Smith, Albert V, Müller-Nurasyid, Martina, Walter, Stefan, Agarwal, Sunil K, Bis, Joshua C, Brody, Jennifer A, Chen, Lin Y, Everett, Brendan M, Ford, Ian, Franco, Oscar H, Harris, Tamara B, Hofman, Albert, Kääb, Stefan, Mahida, Saagar, Kathiresan, Sekar, Kubo, Michiaki, Launer, Lenore J, Macfarlane, Peter W, Magnani, Jared W, McKnight, Barbara, McManus, David D, Peters, Annette, Psaty, Bruce M, Rose, Lynda M, Rotter, Jerome I, Silbernagel, Guenther, Smith, Jonathan D, Sotoodehnia, Nona, Stott, David J, Taylor, Kent D, Tomaschitz, Andreas, Tsunoda, Tatsuhiko, Uitterlinden, Andre G, Van Wagoner, David R, Völker, Uwe, Völzke, Henry, Murabito, Joanne M, Sinner, Moritz F, Gudnason, Vilmundur, Felix, Stephan B, März, Winfried, Chung, Mina, Albert, Christine M, Stricker, Bruno H, Tanaka, Toshihiro, Heckbert, Susan R, Jukema, J Wouter, Alonso, Alvaro, Benjamin, Emelia J, and Ellinor, Patrick T

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Genetics, Heart Disease, Cardiovascular, Clinical Research, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Adult, Aged, Aged, 80 and over, Asian People, Atrial Fibrillation, Chromosome Mapping, Chromosomes, Human, Pair 4, Europe, Female, Genetic Markers, Genetic Predisposition to Disease, Homeodomain Proteins, Humans, Japan, Male, Middle Aged, Polymorphism, Single Nucleotide, Transcription Factors, White People, atrial fibrillation, atrial flutter, genetic, prognosis, risk, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

ObjectivesThis study sought to identify nonredundant atrial fibrillation (AF) genetic susceptibility signals and examine their cumulative relations with AF risk.BackgroundAF-associated loci span broad genomic regions that may contain multiple susceptibility signals. Whether multiple signals exist at AF loci has not been systematically explored.MethodsWe performed association testing conditioned on the most significant, independently associated genetic markers at 9 established AF loci using 2 complementary techniques in 64,683 individuals of European ancestry (3,869 incident and 3,302 prevalent AF cases). Genetic risk scores were created and tested for association with AF in Europeans and an independent sample of 11,309 individuals of Japanese ancestry (7,916 prevalent AF cases).ResultsWe observed at least 4 distinct AF susceptibility signals on chromosome 4q25 upstream of PITX2, but not at the remaining 8 AF loci. A multilocus score comprised 12 genetic markers demonstrated an estimated 5-fold gradient in AF risk. We observed a similar spectrum of risk associated with these markers in Japanese. Regions containing AF signals on chromosome 4q25 displayed a greater degree of evolutionary conservation than the remainder of the locus, suggesting that they may tag regulatory elements.ConclusionsThe chromosome 4q25 AF locus is architecturally complex and harbors at least 4 AF susceptibility signals in individuals of European ancestry. Similar polygenic AF susceptibility exists between Europeans and Japanese. Future work is necessary to identify causal variants, determine mechanisms by which associated loci predispose to AF, and explore whether AF susceptibility signals classify individuals at risk for AF and related morbidity.

Published
2014

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