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2. Lifestyle habits associated with cardiac conduction disease.

Author

Frimodt-Møller, Emilie K, Soliman, Elsayed Z, Kizer, Jorge R, Vittinghoff, Eric, Psaty, Bruce M, Biering-Sørensen, Tor, Gottdiener, John S, and Marcus, Gregory M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Aging, Nutrition, Prevention, Heart Disease, Cardiovascular, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Humans, Male, Female, Aged, Cohort Studies, Cardiac Conduction System Disease, Bundle-Branch Block, Electrocardiography, Risk Factors, Habits, Conduction disease, Atrioventricular block, Bundle branch block, Lifestyle habits, Physical activity, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

AimsCardiac conduction disease can lead to syncope, heart failure, and death. The only available therapy is pacemaker implantation, with no established prevention strategies. Research to identify modifiable risk factors has been scant.Methods and resultsData from the Cardiovascular Health Study, a population-based cohort study of adults ≥ 65 years with annual 12-lead electrocardiograms obtained over 10 years, were utilized to examine relationships between baseline characteristics, including lifestyle habits, and conduction disease. Of 5050 participants (mean age 73 ± 6 years; 52% women), prevalent conduction disease included 257 with first-degree atrioventricular block, 99 with left anterior fascicular block, 9 with left posterior fascicular block, 193 with right bundle branch block (BBB), 76 with left BBB, and 102 with intraventricular block at baseline. After multivariable adjustment, older age, male sex, a larger body mass index, hypertension, and coronary heart disease were associated with a higher prevalence of conduction disease, whereas White race and more physical activity were associated with a lower prevalence. Over a median follow-up on 7 (interquartile range 1-9) years, 1036 developed incident conduction disease. Older age, male sex, a larger BMI, and diabetes were each associated with incident conduction disease. Of lifestyle habits, more physical activity (hazard ratio 0.91, 95% confidence interval 0.84-0.98, P = 0.017) was associated with a reduced risk, while smoking and alcohol did not exhibit a significant association.ConclusionWhile some difficult to control comorbidities were associated with conduction disease as expected, a readily modifiable lifestyle factor, physical activity, was associated with a lower risk.

Published
2023

3. Genetic architecture of spatial electrical biomarkers for cardiac arrhythmia and relationship with cardiovascular disease.

Author

Young, William J, Haessler, Jeffrey, Benjamins, Jan-Walter, Repetto, Linda, Yao, Jie, Isaacs, Aaron, Harper, Andrew R, Ramirez, Julia, Garnier, Sophie, van Duijvenboden, Stefan, Baldassari, Antoine R, Concas, Maria Pina, Duong, ThuyVy, Foco, Luisa, Isaksen, Jonas L, Mei, Hao, Noordam, Raymond, Nursyifa, Casia, Richmond, Anne, Santolalla, Meddly L, Sitlani, Colleen M, Soroush, Negin, Thériault, Sébastien, Trompet, Stella, Aeschbacher, Stefanie, Ahmadizar, Fariba, Alonso, Alvaro, Brody, Jennifer A, Campbell, Archie, Correa, Adolfo, Darbar, Dawood, De Luca, Antonio, Deleuze, Jean-François, Ellervik, Christina, Fuchsberger, Christian, Goel, Anuj, Grace, Christopher, Guo, Xiuqing, Hansen, Torben, Heckbert, Susan R, Jackson, Rebecca D, Kors, Jan A, Lima-Costa, Maria Fernanda, Linneberg, Allan, Macfarlane, Peter W, Morrison, Alanna C, Navarro, Pau, Porteous, David J, Pramstaller, Peter P, Reiner, Alexander P, Risch, Lorenz, Schotten, Ulrich, Shen, Xia, Sinagra, Gianfranco, Soliman, Elsayed Z, Stoll, Monika, Tarazona-Santos, Eduardo, Tinker, Andrew, Trajanoska, Katerina, Villard, Eric, Warren, Helen R, Whitsel, Eric A, Wiggins, Kerri L, Arking, Dan E, Avery, Christy L, Conen, David, Girotto, Giorgia, Grarup, Niels, Hayward, Caroline, Jukema, J Wouter, Mook-Kanamori, Dennis O, Olesen, Morten Salling, Padmanabhan, Sandosh, Psaty, Bruce M, Pattaro, Cristian, Ribeiro, Antonio Luiz P, Rotter, Jerome I, Stricker, Bruno H, van der Harst, Pim, van Duijn, Cornelia M, Verweij, Niek, Wilson, James G, Orini, Michele, Charron, Philippe, Watkins, Hugh, Kooperberg, Charles, Lin, Henry J, Wilson, James F, Kanters, Jørgen K, Sotoodehnia, Nona, Mifsud, Borbala, Lambiase, Pier D, Tereshchenko, Larisa G, and Munroe, Patricia B

Subjects
Humans, Cardiovascular Diseases, Electrocardiography, Risk Factors, Arrhythmias, Cardiac, Atrioventricular Block, Genome-Wide Association Study, Biomarkers, Human Genome, Cardiovascular, Genetics, Heart Disease
Abstract

The 3-dimensional spatial and 2-dimensional frontal QRS-T angles are measures derived from the vectorcardiogram. They are independent risk predictors for arrhythmia, but the underlying biology is unknown. Using multi-ancestry genome-wide association studies we identify 61 (58 previously unreported) loci for the spatial QRS-T angle (N = 118,780) and 11 for the frontal QRS-T angle (N = 159,715). Seven out of the 61 spatial QRS-T angle loci have not been reported for other electrocardiographic measures. Enrichments are observed in pathways related to cardiac and vascular development, muscle contraction, and hypertrophy. Pairwise genome-wide association studies with classical ECG traits identify shared genetic influences with PR interval and QRS duration. Phenome-wide scanning indicate associations with atrial fibrillation, atrioventricular block and arterial embolism and genetically determined QRS-T angle measures are associated with fascicular and bundle branch block (and also atrioventricular block for the frontal QRS-T angle). We identify potential biology involved in the QRS-T angle and their genetic relationships with cardiovascular traits and diseases, may inform future research and risk prediction.

Published
2023

4. Contributors

Author

Ackerman, Michael J., primary, Adedinsewo, Demilade A., additional, Akbilgic, Oguz, additional, Al-Falahi, Zaidon, additional, Alkhatib, Deya, additional, Alkhouli, Mohamad, additional, Awerbach, Jordan D., additional, Axelrod, David M., additional, Baker, G. Hamilton, additional, Bashir, Mohamad, additional, Bond, Raymond, additional, Bos, J. Martijn, additional, Brisk, Robert, additional, Brown, Sherry-Ann, additional, Butler, Liam, additional, C. Chang, Anthony, additional, Camara, Oscar, additional, Chou, Timothy, additional, Davis, Matthew, additional, Dearani, Joseph A., additional, Dorraki, Mohsen, additional, Doukky, Rami, additional, Druz, Regina, additional, Ehwerhemuepha, Louis, additional, Ernst, Zachary, additional, Feaster, William, additional, Feeny, Albert K., additional, Fernandez-Campos, Beatriz A., additional, Fisher, Michael, additional, Flores, Mona G., additional, Franklin, Wayne J., additional, Frederickson, Abby, additional, Gaffar, Sharib, additional, Gates, Darren, additional, Gearhart, Addison, additional, Gerke, Sara, additional, Gomez, Javier, additional, Goto, Shinichi, additional, Grutter, Giorgia, additional, Hall, E. Kevin, additional, Jacobs, Jeffrey P., additional, Jefferies, John L., additional, Jegatheeswaran, Anusha, additional, Jenkins, Kathy, additional, Jone, Pei-Ni, additional, Kouzehkonan, Vahid Ghodrati, additional, Kumar, S. Ram, additional, Lai, Wyman, additional, Laussen, Peter C., additional, Lei, Howard, additional, Leta, Ruben, additional, Liao, Zhibin, additional, Limon, Alfonso, additional, Lopez-Jimenez, Francisco, additional, Lopuszko, Aleksandra, additional, Maher, Kevin, additional, Marano, Rachel, additional, Mattia, Donald, additional, McEneaney, David, additional, McMahon, Colin J., additional, Mesana, Thierry, additional, Moras, Patrizio, additional, Moreno, Tatiana, additional, Moustafa, Abdel Hakim, additional, Nafee, Tarek, additional, Nag, Nitish, additional, Nahar, Jai, additional, Nguyen, Hoang H., additional, Olajide, Olufemi, additional, Overman, David M., additional, Paul Finn, J., additional, Ramirez, Jessily P., additional, Rayan, David, additional, Recto, Mitch, additional, Reddy, Charitha D., additional, Sengupta, Partho P., additional, Shamavu, Ketemwabi Y., additional, Silversides, Candice K., additional, Soliman, Elsayed Z., additional, St Louis, James D., additional, Sun, Louise Y., additional, Tan, Sven, additional, Tandon, Animesh, additional, Tcheng, James E., additional, Toscano, Alessandra, additional, Tozzi, Alberto Eugenio, additional, Tran, Tu Hao, additional, Trivedi, Bhavya, additional, Tsang, Wendy, additional, Tseng, Andrew S., additional, van den Hengel, Anton, additional, Verjans, Johan W., additional, and Young, Krista, additional

Published
2024
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9. Prevalence of frequent premature ventricular contractions and nonsustained ventricular tachycardia in older women screened for atrial fibrillation in the Women’s Health Initiative

Author

Gomez, Sofia E., Larson, Joseph, Hlatky, Mark A., Rodriguez, Fatima, Wheeler, Matthew, Greenland, Philip, LaMonte, Michael, Froelicher, Victor, Stefanick, Marcia L., Wallace, Robert, Kooperberg, Charles, Tinker, Lesley F., Schoenberg, Jenny, Soliman, Elsayed Z., Vitolins, Mara Z., Saquib, Nazmus, Nuño, Tomas, Haring, Bernhard, and Perez, Marco V.

Published
2024
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12. Monogenic and Polygenic Contributions to QTc Prolongation in the Population.

Author

Nauffal, Victor, Morrill, Valerie N, Jurgens, Sean J, Choi, Seung Hoan, Hall, Amelia W, Weng, Lu-Chen, Halford, Jennifer L, Austin-Tse, Christina, Haggerty, Christopher M, Harris, Stephanie L, Wong, Eugene K, Alonso, Alvaro, Arking, Dan E, Benjamin, Emelia J, Boerwinkle, Eric, Min, Yuan-I, Correa, Adolfo, Fornwalt, Brandon K, Heckbert, Susan R, National Heart, Lung, and Blood Institute Trans-Omics for Precision Medicine (TOPMed) Consortium, Kooperberg, Charles, Lin, Henry J, J F Loos, Ruth, Rice, Kenneth M, Gupta, Namrata, Blackwell, Thomas W, Mitchell, Braxton D, Morrison, Alanna C, Psaty, Bruce M, Post, Wendy S, Redline, Susan, Rehm, Heidi L, Rich, Stephen S, Rotter, Jerome I, Soliman, Elsayed Z, Sotoodehnia, Nona, Lunetta, Kathryn L, Ellinor, Patrick T, Lubitz, Steven A, and TOPMed Investigators

Subjects
National Heart, Lung, and Blood Institute Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Investigators, Humans, Long QT Syndrome, Electrocardiography, Heterozygote, Multifactorial Inheritance, Genome-Wide Association Study, Whole Genome Sequencing, QT interval, long QT syndrome, monogenic, polygenic, sudden cardiac death, Human Genome, Heart Disease, Prevention, Cardiovascular, Genetics, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

BackgroundRare sequence variation in genes underlying cardiac repolarization and common polygenic variation influence QT interval duration. However, current clinical genetic testing of individuals with unexplained QT prolongation is restricted to examination of monogenic rare variants. The recent emergence of large-scale biorepositories with sequence data enables examination of the joint contribution of rare and common variations to the QT interval in the population.MethodsWe performed a genome-wide association study of the QTc in 84 630 UK Biobank participants and created a polygenic risk score (PRS). Among 26 976 participants with whole-genome sequencing and ECG data in the TOPMed (Trans-Omics for Precision Medicine) program, we identified 160 carriers of putative pathogenic rare variants in 10 genes known to be associated with the QT interval. We examined QTc associations with the PRS and with rare variants in TOPMed.ResultsFifty-four independent loci were identified by genome-wide association study in the UK Biobank. Twenty-one loci were novel, of which 12 were replicated in TOPMed. The PRS composed of 1 110 494 common variants was significantly associated with the QTc in TOPMed (ΔQTc/decile of PRS=1.4 ms [95% CI, 1.3 to 1.5]; P=1.1×10-196). Carriers of putative pathogenic rare variants had longer QTc than noncarriers (ΔQTc=10.9 ms [95% CI, 7.4 to 14.4]). Of individuals with QTc>480 ms, 23.7% carried either a monogenic rare variant or had a PRS in the top decile (3.4% monogenic, 21% top decile of PRS).ConclusionsQTc duration in the population is influenced by both rare variants in genes underlying cardiac repolarization and polygenic risk, with a sizeable contribution from polygenic risk. Comprehensive assessment of the genetic determinants of QTc prolongation includes incorporation of both polygenic and monogenic risk.

Published
2022

14. Endophenotype effect sizes support variant pathogenicity in monogenic disease susceptibility genes

Author

Halford, Jennifer L, Morrill, Valerie N, Choi, Seung Hoan, Jurgens, Sean J, Melloni, Giorgio, Marston, Nicholas A, Weng, Lu-Chen, Nauffal, Victor, Hall, Amelia W, Gunn, Sophia, Austin-Tse, Christina A, Pirruccello, James P, Khurshid, Shaan, Rehm, Heidi L, Benjamin, Emelia J, Boerwinkle, Eric, Brody, Jennifer A, Correa, Adolfo, Fornwalt, Brandon K, Gupta, Namrata, Haggerty, Christopher M, Harris, Stephanie, Heckbert, Susan R, Hong, Charles C, Kooperberg, Charles, Lin, Henry J, Loos, Ruth JF, Mitchell, Braxton D, Morrison, Alanna C, Post, Wendy, Psaty, Bruce M, Redline, Susan, Rice, Kenneth M, Rich, Stephen S, Rotter, Jerome I, Schnatz, Peter F, Soliman, Elsayed Z, Sotoodehnia, Nona, Wong, Eugene K, Sabatine, Marc S, Ruff, Christian T, Lunetta, Kathryn L, Ellinor, Patrick T, and Lubitz, Steven A

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Good Health and Well Being, Disease Susceptibility, Endophenotypes, Humans, Long QT Syndrome, Virulence, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium
Abstract

Accurate and efficient classification of variant pathogenicity is critical for research and clinical care. Using data from three large studies, we demonstrate that population-based associations between rare variants and quantitative endophenotypes for three monogenic diseases (low-density-lipoprotein cholesterol for familial hypercholesterolemia, electrocardiographic QTc interval for long QT syndrome, and glycosylated hemoglobin for maturity-onset diabetes of the young) provide evidence for variant pathogenicity. Effect sizes are associated with pathogenic ClinVar assertions (P

Published
2022

17. An Adaptive QRS Detection Algorithm for Ultra-Long-Term ECG Recordings

Author

Malik, John, Soliman, Elsayed Z, and Wu, Hau-Tieng

Subjects
Electrical Engineering and Systems Science - Signal Processing, Statistics - Applications
Abstract

Background: Accurate detection of QRS complexes during mobile, ultra-long-term ECG monitoring is challenged by instances of high heart rate, dramatic and persistent changes in signal amplitude, and intermittent deformations in signal quality that arise due to subject motion, background noise, and misplacement of the ECG electrodes. Purpose: We propose a revised QRS detection algorithm which addresses the above-mentioned challenges. Methods and Results: Our proposed algorithm is based on a state-of-the-art algorithm after applying two key modifications. The first modification is implementing local estimates for the amplitude of the signal. The second modification is a mechanism by which the algorithm becomes adaptive to changes in heart rate. We validated our proposed algorithm against the state-of-the-art algorithm using short-term ECG recordings from eleven annotated databases available at Physionet, as well as four ultra-long-term (14-day) ECG recordings which were visually annotated at a central ECG core laboratory. On the database of ultra-long-term ECG recordings, our proposed algorithm showed a sensitivity of 99.90% and a positive predictive value of 99.73%. Meanwhile, the state-of-the-art QRS detection algorithm achieved a sensitivity of 99.30% and a positive predictive value of 99.68% on the same database. The numerical efficiency of our new algorithm was evident, as a 14-day recording sampled at 200 Hz was analyzed in approximately 157 seconds. Conclusions: We developed a new QRS detection algorithm. The efficiency and accuracy of our algorithm makes it a good fit for mobile health applications, ultra-long-term and pathological ECG recordings, and the batch processing of large ECG databases.

Published
2020

18. Rare Coding Variants Associated With Electrocardiographic Intervals Identify Monogenic Arrhythmia Susceptibility Genes: A Multi-Ancestry Analysis.

Author

Choi, Seung Hoan, Jurgens, Sean J, Haggerty, Christopher M, Hall, Amelia W, Halford, Jennifer L, Morrill, Valerie N, Weng, Lu-Chen, Lagerman, Braxton, Mirshahi, Tooraj, Pettinger, Mary, Guo, Xiuqing, Lin, Henry J, Alonso, Alvaro, Soliman, Elsayed Z, Kornej, Jelena, Lin, Honghuang, Moscati, Arden, Nadkarni, Girish N, Brody, Jennifer A, Wiggins, Kerri L, Cade, Brian E, Lee, Jiwon, Austin-Tse, Christina, Blackwell, Tom, Chaffin, Mark D, Lee, Christina J-Y, Rehm, Heidi L, Roselli, Carolina, Regeneron Genetics Center, Redline, Susan, Mitchell, Braxton D, Sotoodehnia, Nona, Psaty, Bruce M, Heckbert, Susan R, Loos, Ruth JF, Vasan, Ramachandran S, Benjamin, Emelia J, Correa, Adolfo, Boerwinkle, Eric, Arking, Dan E, Rotter, Jerome I, Rich, Stephen S, Whitsel, Eric A, Perez, Marco, Kooperberg, Charles, Fornwalt, Brandon K, Lunetta, Kathryn L, Ellinor, Patrick T, Lubitz, Steven A, and NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium

Subjects
Regeneron Genetics Center, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, Humans, Long QT Syndrome, Death, Sudden, Cardiac, Genetic Predisposition to Disease, Electrocardiography, Heterozygote, Female, Male, Genetic Variation, Exome Sequencing, death, sudden, cardiac, epidemiology, genetics, genome, population, Clinical Research, Cardiovascular, Genetics, Heart Disease, Human Genome, Biotechnology, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, death, sudden, cardiac
Abstract

BackgroundAlterations in electrocardiographic (ECG) intervals are well-known markers for arrhythmia and sudden cardiac death (SCD) risk. While the genetics of arrhythmia syndromes have been studied, relations between electrocardiographic intervals and rare genetic variation at a population level are poorly understood.MethodsUsing a discovery sample of 29 000 individuals with whole-genome sequencing from Trans-Omics in Precision Medicine and replication in nearly 100 000 with whole-exome sequencing from the UK Biobank and MyCode, we examined associations between low-frequency and rare coding variants with 5 routinely measured electrocardiographic traits (RR, P-wave, PR, and QRS intervals and corrected QT interval).ResultsWe found that rare variants associated with population-based electrocardiographic intervals identify established monogenic SCD genes (KCNQ1, KCNH2, and SCN5A), a controversial monogenic SCD gene (KCNE1), and novel genes (PAM and MFGE8) involved in cardiac conduction. Loss-of-function and pathogenic SCN5A variants, carried by 0.1% of individuals, were associated with a nearly 6-fold increased odds of the first-degree atrioventricular block (P=8.4×10-5). Similar variants in KCNQ1 and KCNH2 (0.2% of individuals) were associated with a 23-fold increased odds of marked corrected QT interval prolongation (P=4×10-25), a marker of SCD risk. Incomplete penetrance of such deleterious variation was common as over 70% of carriers had normal electrocardiographic intervals.ConclusionsOur findings indicate that large-scale high-depth sequence data and electrocardiographic analysis identifies monogenic arrhythmia susceptibility genes and rare variants with large effects. Known pathogenic variation in conventional arrhythmia and SCD genes exhibited incomplete penetrance and accounted for only a small fraction of marked electrocardiographic interval prolongation.

Published
2021

19. Comparison of the Relation of Carotid Intima-Media Thickness With Incident Heart Failure With Reduced Versus Preserved Ejection Fraction (from the Multi-Ethnic Study of Atherosclerosis [MESA])

Author

Aladin, Amer I, Soliman, Elsayed Z, Kitzman, Dalane W, Dardari, Zeina, Rasool, Shereen H, Yeboah, Joseph, Budoff, Matthew J, Psaty, Bruce M, Ouyang, Pamela, Polak, Joseph F, Blumenthal, Roger S, McEvoy, John W, Gandhi, Sanjay K, and Herrington, David M

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Heart Disease, Aging, Atherosclerosis, Cardiovascular, Clinical Research, Aged, Carotid Artery Diseases, Carotid Intima-Media Thickness, Female, Heart Failure, Humans, Incidence, Male, Middle Aged, Proportional Hazards Models, Stroke Volume, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

Increased carotid intima-media thickness (cIMT) is associated with heart failure (HF) in previous studies, but it is not known whether the association of cIMT differs between HF with reduced (HFrEF) versus preserved ejection fraction (HFpEF). We studied 6699 participants (mean age 62 ± 10 years, 47% male, and 38% white) from the Multi-Ethnic Study of Atherosclerosis (MESA) with baseline cIMT measurements. We classified HF events as HFrEF (EF

Published
2021

22. ISE/ISHNE Expert Consensus Statement on ECG Diagnosis of Left Ventricular Hypertrophy: The Change of the Paradigm. The joint paper of the International Society of Electrocardiology and the International Society for Holter Monitoring and Noninvasive Electrocardiology

Author

Bacharova, Ljuba, Chevalier, Philippe, Gorenek, Bulent, Jons, Christian, Li, Yi-Gang, Locati, Emanuela T., Maanja, Maren, Pérez-Riera, Andrés Ricardo, Platonov, Pyotr G., Ribeiro, Antonio Luiz P., Schocken, Douglas, Soliman, Elsayed Z., Svehlikova, Jana, Tereshchenko, Larisa G., Ugander, Martin, Varma, Niraj, Zaklyazminskaya, Elena, and Ikeda, Takanori

Published
2023
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29. Multi-Ethnic Genome-Wide Association Study of Decomposed Cardioelectric Phenotypes Illustrates Strategies to Identify and Characterize Evidence of Shared Genetic Effects for Complex Traits

Author

Baldassari, Antoine R, Sitlani, Colleen M, Highland, Heather M, Arking, Dan E, Buyske, Steve, Darbar, Dawood, Gondalia, Rahul, Graff, Misa, Guo, Xiuqing, Heckbert, Susan R, Hindorff, Lucia A, Hodonsky, Chani J, Ida Chen, Yii-Der, Kaplan, Robert C, Peters, Ulrike, Post, Wendy, Reiner, Alex P, Rotter, Jerome I, Shohet, Ralph V, Seyerle, Amanda A, Sotoodehnia, Nona, Tao, Ran, Taylor, Kent D, Wojcik, Genevieve L, Yao, Jie, Kenny, Eimear E, Lin, Henry J, Soliman, Elsayed Z, Whitsel, Eric A, North, Kari E, Kooperberg, Charles, and Avery, Christy L

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Genetics, Clinical Research, Human Genome, Black or African American, CD36 Antigens, Cardiovascular Diseases, Electrocardiography, Gene Frequency, Genetic Loci, Genome-Wide Association Study, Genotype, Hispanic or Latino, Homeodomain Proteins, Humans, Membrane Glycoproteins, Molecular Chaperones, Phenotype, Polymorphism, Single Nucleotide, Transcription Factors, White People, cardiovascular diseases, electrophysiology, epidemiology, genome-wide association study, population, Medical Biotechnology, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundWe examined how expanding electrocardiographic trait genome-wide association studies to include ancestrally diverse populations, prioritize more precise phenotypic measures, and evaluate evidence for shared genetic effects enabled the detection and characterization of loci.MethodsWe decomposed 10 seconds, 12-lead electrocardiograms from 34 668 multi-ethnic participants (15% Black; 30% Hispanic/Latino) into 6 contiguous, physiologically distinct (P wave, PR segment, QRS interval, ST segment, T wave, and TP segment) and 2 composite, conventional (PR interval and QT interval) interval scale traits and conducted multivariable-adjusted, trait-specific univariate genome-wide association studies using 1000-G imputed single-nucleotide polymorphisms. Evidence of shared genetic effects was evaluated by aggregating meta-analyzed univariate results across the 6 continuous electrocardiographic traits using the combined phenotype adaptive sum of powered scores test.ResultsWe identified 6 novels (CD36, PITX2, EMB, ZNF592, YPEL2, and BC043580) and 87 known loci (adaptive sum of powered score test P

Published
2020

30. Associations between QT interval subcomponents, HIV serostatus, and inflammation

Author

Wu, Katherine C, Bhondoekhan, Fiona, Haberlen, Sabina A, Ashikaga, Hiroshi, Brown, Todd T, Budoff, Matthew J, D'Souza, Gypsyamber, Magnani, Jared W, Kingsley, Lawrence A, Palella, Frank J, Margolick, Joseph B, Martínez‐Maza, Otoniel, Altekruse, Sean F, Soliman, Elsayed Z, and Post, Wendy S

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, HIV/AIDS, Prevention, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Adult, Aged, Biomarkers, Electrocardiography, HIV Infections, Humans, Inflammation, Long QT Syndrome, Longitudinal Studies, Male, Middle Aged, Prospective Studies, Risk Factors, arrhythmias, electrocardiography, HIV, inflammation, QT interval, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundThe total QT interval comprises both ventricular depolarization and repolarization currents. Understanding how HIV serostatus and other risk factors influence specific QT interval subcomponents could improve our mechanistic understanding of arrhythmias.MethodsTwelve-lead electrocardiograms (ECGs) were acquired in 774 HIV-infected (HIV+) and 652 HIV-uninfected (HIV-) men from the Multicenter AIDS Cohort Study. Individual QT subcomponent intervals were analyzed: R-onset to R-peak, R-peak to R-end, JT segment, T-onset to T-peak, and T-peak to T-end. Using multivariable linear regressions, we investigated associations between HIV serostatus and covariates, including serum concentrations of inflammatory biomarkers such as interleukin-6 (IL-6), and each QT subcomponent.ResultsAfter adjustment for demographics and risk factors, HIV+ versus HIV- men differed only in repolarization phase durations with longer T-onset to T-peak by 2.3 ms (95% CI 0-4.5, p

Published
2020

38. Cardiac Biomarkers and Risk of Atrial Fibrillation in Chronic Kidney Disease: The CRIC Study

Author

Lamprea‐Montealegre, Julio A, Zelnick, Leila R, Shlipak, Michael G, Floyd, James S, Anderson, Amanda H, He, Jiang, Christenson, Rob, Seliger, Stephen L, Soliman, Elsayed Z, Deo, Rajat, Ky, Bonnie, Feldman, Harold I, Kusek, John W, deFilippi, Christopher R, Wolf, Myles S, Shafi, Tariq, Go, Alan S, Bansal, Nisha, Appel, Lawrence J, Lash, James P, Rao, Panduranga S, Rahman, Mahboob, and Townsend, Raymond R

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Clinical Research, Cardiovascular, Heart Disease, Aetiology, Detection, screening and diagnosis, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Good Health and Well Being, Adult, Aged, Atrial Fibrillation, Biomarkers, Female, Humans, Male, Middle Aged, Prospective Studies, Renal Insufficiency, Chronic, Risk Assessment, Young Adult, atrial fibrillation, biomarker, chronic kidney disease, CRIC Study Investigators, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Abstract

Background We tested associations of cardiac biomarkers of myocardial stretch, injury, inflammation, and fibrosis with the risk of incident atrial fibrillation (AF) in a prospective study of chronic kidney disease patients. Methods and Results The study sample was 3053 participants with chronic kidney disease in the multicenter CRIC (Chronic Renal Insufficiency Cohort) study who were not identified as having AF at baseline. Cardiac biomarkers, measured at baseline, were NT-proBNP (N-terminal pro-B-type natriuretic peptide), high-sensitivity troponin T, galectin-3, growth differentiation factor-15, and soluble ST-2. Incident AF ("AF event") was defined as a hospitalization for AF. During a median follow-up of 8 years, 279 (9%) participants developed a new AF event. In adjusted models, higher baseline log-transformed NT-proBNP (N-terminal pro-B-type natriuretic peptide) was associated with incident AF (adjusted hazard ratio [HR] per SD higher concentration: 2.11; 95% CI, 1.75, 2.55), as was log-high-sensitivity troponin T (HR 1.42; 95% CI, 1.20, 1.68). These associations showed a dose-response relationship in categorical analyses. Although log-soluble ST-2 was associated with AF risk in continuous models (HR per SD higher concentration 1.35; 95% CI, 1.16, 1.58), this association was not consistent in categorical analyses. Log-galectin-3 (HR 1.05; 95% CI, 0.91, 1.22) and log-growth differentiation factor-15 (HR 1.16; 95% CI, 0.96, 1.40) were not significantly associated with incident AF. Conclusions We found strong associations between higher NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity troponin T concentrations, and the risk of incident AF in a large cohort of participants with chronic kidney disease. Increased atrial myocardial stretch and myocardial cell injury may be implicated in the high burden of AF in patients with chronic kidney disease.

Published
2019

39. Predictors of electrocardiographic QT interval prolongation in men with HIV

Author

Wu, Katherine C, Zhang, Long, Haberlen, Sabina A, Ashikaga, Hiroshi, Brown, Todd T, Budoff, Matthew J, D'Souza, Gypsyamber, Kingsley, Lawrence A, Palella, Frank J, Margolick, Joseph B, Martínez-Maza, Otoniel, Soliman, Elsayed Z, and Post, Wendy S

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Heart Disease, Cardiovascular, HIV/AIDS, Clinical Research, Prevention, Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Adult, Anti-Retroviral Agents, B-Cell Activating Factor, Biomarkers, Correlation of Data, Death, Sudden, Cardiac, Electrocardiography, HIV Infections, Humans, Intercellular Adhesion Molecule-1, Interleukin-6, Long QT Syndrome, Male, Middle Aged, Risk Assessment, Risk Factors, Serologic Tests, United States, cardiac risk factors and prevention, electrocardiography, inflammatory markers, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

ObjectiveHIV-infected (HIV+) individuals may be at increased risk for sudden arrhythmic cardiac death. Some studies have reported an association between HIV infection and prolongation of the electrocardiographic QT interval, a measure of ventricular repolarisation, which could potentiate ventricular arrhythmias. We aimed to assess whether HIV+ men have longer QT intervals than HIV-uninfected (HIV-) men and to determine factors associated with QT duration.MethodsWe performed resting 12-lead ECGs in 774 HIV+ and 652 HIV- men in the Multicenter AIDS Cohort Study (MACS). We used multivariable linear and logistic regression analyses to assess associations between HIV serostatus and Framingham corrected QT interval (QTc), after accounting for potential confounders. We also determined associations among QTc interval and HIV-related factors in HIV+ men. In a subgroup of participants, levels of serum markers of inflammation were also assessed.ResultsAfter adjusting for demographics and risk factors, QTc was 4.0 ms longer in HIV+ than HIV- men (p

Published
2019

40. GWAS of QRS duration identifies new loci specific to Hispanic/Latino populations

Author

Swenson, Brenton R, Louie, Tin, Lin, Henry J, Méndez-Giráldez, Raúl, Below, Jennifer E, Laurie, Cathy C, Kerr, Kathleen F, Highland, Heather, Thornton, Timothy A, Ryckman, Kelli K, Kooperberg, Charles, Soliman, Elsayed Z, Seyerle, Amanda A, Guo, Xiuqing, Taylor, Kent D, Yao, Jie, Heckbert, Susan R, Darbar, Dawood, Petty, Lauren E, McKnight, Barbara, Cheng, Susan, Bello, Natalie A, Whitsel, Eric A, Hanis, Craig L, Nalls, Mike A, Evans, Daniel S, Rotter, Jerome I, Sofer, Tamar, Avery, Christy L, and Sotoodehnia, Nona

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Cardiovascular, Human Genome, Heart Disease, Good Health and Well Being, Electrocardiography, Genetic Loci, Genome-Wide Association Study, Hispanic or Latino, Humans, Middle Aged, Molecular Sequence Annotation, Phenotype, Polymorphism, Single Nucleotide, General Science & Technology
Abstract

BackgroundThe electrocardiographically quantified QRS duration measures ventricular depolarization and conduction. QRS prolongation has been associated with poor heart failure prognosis and cardiovascular mortality, including sudden death. While previous genome-wide association studies (GWAS) have identified 32 QRS SNPs across 26 loci among European, African, and Asian-descent populations, the genetics of QRS among Hispanics/Latinos has not been previously explored.MethodsWe performed a GWAS of QRS duration among Hispanic/Latino ancestry populations (n = 15,124) from four studies using 1000 Genomes imputed genotype data (adjusted for age, sex, global ancestry, clinical and study-specific covariates). Study-specific results were combined using fixed-effects, inverse variance-weighted meta-analysis.ResultsWe identified six loci associated with QRS (P

Published
2019

41. 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

43. Genome-wide analyses identify SCN5A as a susceptibility locus for premature atrial contraction frequency

Author

Thériault, Sébastien, Imboden, Medea, Biggs, Mary L., Austin, Thomas R., Aeschbacher, Stefanie, Schaffner, Emmanuel, Brody, Jennifer A., Bartz, Traci M., Risch, Martin, Grossmann, Kirsten, Lin, Henry J., Soliman, Elsayed Z., Post, Wendy S., Risch, Lorenz, Krieger, Jose E., Pereira, Alexandre C., Heckbert, Susan R., Sotoodehnia, Nona, Probst-Hensch, Nicole M., and Conen, David

Published
2022
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47. Genetic analyses of the electrocardiographic QT interval and its components identify additional loci and pathways

Author

Young, William J., Lahrouchi, Najim, Isaacs, Aaron, Duong, ThuyVy, Foco, Luisa, Ahmed, Farah, Brody, Jennifer A., Salman, Reem, Noordam, Raymond, Benjamins, Jan-Walter, Haessler, Jeffrey, Lyytikäinen, Leo-Pekka, Repetto, Linda, Concas, Maria Pina, van den Berg, Marten E., Weiss, Stefan, Baldassari, Antoine R., Bartz, Traci M., Cook, James P., Evans, Daniel S., Freudling, Rebecca, Hines, Oliver, Isaksen, Jonas L., Lin, Honghuang, Mei, Hao, Moscati, Arden, Müller-Nurasyid, Martina, Nursyifa, Casia, Qian, Yong, Richmond, Anne, Roselli, Carolina, Ryan, Kathleen A., Tarazona-Santos, Eduardo, Thériault, Sébastien, van Duijvenboden, Stefan, Warren, Helen R., Yao, Jie, Raza, Dania, Aeschbacher, Stefanie, Ahlberg, Gustav, Alonso, Alvaro, Andreasen, Laura, Bis, Joshua C., Boerwinkle, Eric, Campbell, Archie, Catamo, Eulalia, Cocca, Massimiliano, Cutler, Michael J., Darbar, Dawood, De Grandi, Alessandro, De Luca, Antonio, Ding, Jun, Ellervik, Christina, Ellinor, Patrick T., Felix, Stephan B., Froguel, Philippe, Fuchsberger, Christian, Gögele, Martin, Graff, Claus, Graff, Mariaelisa, Guo, Xiuqing, Hansen, Torben, Heckbert, Susan R., Huang, Paul L., Huikuri, Heikki V., Hutri-Kähönen, Nina, Ikram, M. Arfan, Jackson, Rebecca D., Junttila, Juhani, Kavousi, Maryam, Kors, Jan A., Leal, Thiago P., Lemaitre, Rozenn N., Lin, Henry J., Lind, Lars, Linneberg, Allan, Liu, Simin, MacFarlane, Peter W., Mangino, Massimo, Meitinger, Thomas, Mezzavilla, Massimo, Mishra, Pashupati P., Mitchell, Rebecca N., Mononen, Nina, Montasser, May E., Morrison, Alanna C., Nauck, Matthias, Nauffal, Victor, Navarro, Pau, Nikus, Kjell, Pare, Guillaume, Patton, Kristen K., Pelliccione, Giulia, Pittman, Alan, Porteous, David J., Pramstaller, Peter P., Preuss, Michael H., Raitakari, Olli T., Reiner, Alexander P., Ribeiro, Antonio Luiz P., Rice, Kenneth M., Risch, Lorenz, Schlessinger, David, Schotten, Ulrich, Schurmann, Claudia, Shen, Xia, Shoemaker, M. Benjamin, Sinagra, Gianfranco, Sinner, Moritz F., Soliman, Elsayed Z., Stoll, Monika, Strauch, Konstantin, Tarasov, Kirill, Taylor, Kent D., Tinker, Andrew, Trompet, Stella, Uitterlinden, André, Völker, Uwe, Völzke, Henry, Waldenberger, Melanie, Weng, Lu-Chen, Whitsel, Eric A., Wilson, James G., Avery, Christy L., Conen, David, Correa, Adolfo, Cucca, Francesco, Dörr, Marcus, Gharib, Sina A., Girotto, Giorgia, Grarup, Niels, Hayward, Caroline, Jamshidi, Yalda, Järvelin, Marjo-Riitta, Jukema, J. Wouter, Kääb, Stefan, Kähönen, Mika, Kanters, Jørgen K., Kooperberg, Charles, Lehtimäki, Terho, Lima-Costa, Maria Fernanda, Liu, Yongmei, Loos, Ruth J. F., Lubitz, Steven A., Mook-Kanamori, Dennis O., Morris, Andrew P., O’Connell, Jeffrey R., Olesen, Morten Salling, Orini, Michele, Padmanabhan, Sandosh, Pattaro, Cristian, Peters, Annette, Psaty, Bruce M., Rotter, Jerome I., Stricker, Bruno, van der Harst, Pim, van Duijn, Cornelia M., Verweij, Niek, Wilson, James F., Arking, Dan E., Ramirez, Julia, Lambiase, Pier D., Sotoodehnia, Nona, Mifsud, Borbala, Newton-Cheh, Christopher, and Munroe, Patricia B.

Published
2022
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48. Publisher Correction: Endophenotype effect sizes support variant pathogenicity in monogenic disease susceptibility genes

Author

Halford, Jennifer L., Morrill, Valerie N., Choi, Seung Hoan, Jurgens, Sean J., Melloni, Giorgio, Marston, Nicholas A., Weng, Lu-Chen, Nauffal, Victor, Hall, Amelia W., Gunn, Sophia, Austin-Tse, Christina A., Pirruccello, James P., Khurshid, Shaan, Rehm, Heidi L., Benjamin, Emelia J., Boerwinkle, Eric, Brody, Jennifer A., Correa, Adolfo, Fornwalt, Brandon K., Gupta, Namrata, Haggerty, Christopher M., Harris, Stephanie, Heckbert, Susan R., Hong, Charles C., Kooperberg, Charles, Lin, Henry J., Loos, Ruth J. F., Mitchell, Braxton D., Morrison, Alanna C., Post, Wendy, Psaty, Bruce M., Redline, Susan, Rice, Kenneth M., Rich, Stephen S., Rotter, Jerome I., Schnatz, Peter F., Soliman, Elsayed Z., Sotoodehnia, Nona, Wong, Eugene K., Sabatine, Marc S., Ruff, Christian T., Lunetta, Kathryn L., Ellinor, Patrick T., and Lubitz, Steven A.

Published
2022
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50. Prediction of Incident Heart Failure in CKD: The CRIC Study

Author

Appel, Lawrence J., Chen, Jing, Cohen, Debbie, Feldman, Harold I., Go, Alan S., Lash, James P., Nelson, Robert G., Rahman, Mahboob, Rao, Panduranga S., Shah, Vallabh O., Unruh, Mark L., Zelnick, Leila R., Shlipak, Michael G., Soliman, Elsayed Z., Anderson, Amanda, Christenson, Robert, Kansal, Mayank, Deo, Rajat, He, Jiang, Jaar, Bernard G., Weir, Matthew R., Rao, Panduranga, Cohen, Debbie L., Cohen, Jordana B., Go, Alan, and Bansal, Nisha

Published
2022
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