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974 results on '"Okin, Peter M."'

1. Abstract 10863: Left Ventricular Apical Injury Augments Stroke Likelihood in Patients With Systolic Dysfunction and No Left Ventricular Thrombus - Multiparametric Tissue Characterization and Strain Assessment via Cardiac Magnetic Resonance

Author

Kagan, Ruth, Villar, Pablo, Tak, Katherine, Jain, Raina, Rivadeneira, Maria, Agoglia, Hannah, Kim, Jiwon, Okin, Peter M, Devereux, Richard B, Segal, Alan Z, Merkler, Alexander E, Kamel, Hooman, and Weinsaft, Jonathan W

Published
2022
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4. 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

21. Evidence of Heterogeneity by Race/Ethnicity in Genetic Determinants of QT Interval

Author

Seyerle, Amanda A., Young, Alicia M., Jeff, Janina M., Melton, Phillip E., Jorgensen, Neal W., Lin, Yi, Carty, Cara L., Deelman, Ewa, Heckbert, Susan R., Hindorff, Lucia A., Jackson, Rebecca D., Martin, Lisa W., Okin, Peter M., Perez, Marco V., Psaty, Bruce M., Soliman, Elsayed Z., Whitsel, Eric A., North, Kari E., Laston, Sandra, Kooperberg, Charles, and Avery, Christy L.

Published
2014

22. Assessment of the 12-Lead Electrocardiogram as a Screening Test for Detection of Cardiovascular Disease in Healthy General Populations of Young People (12–25 Years of Age): A Scientific Statement From the American Heart Association and the American College of Cardiology

Author

Maron, Barry J., Friedman, Richard A., Kligfield, Paul, Levine, Benjamin D., Viskin, Sami, Chaitman, Bernard R., Okin, Peter M., Saul, J. Philip, Salberg, Lisa, Van Hare, George F., Soliman, Elsayed Z., Chen, Jersey, Matherne, G. Paul, Bolling, Steven F., Mitten, Matthew J., Caplan, Arthur, Balady, Gary J., and Thompson, Paul D.

Published
2014
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24. Enlargement and Hypertrophy

Author

Macfarlane, Peter W., Okin, Peter M., Lawrie, T. D. Veitch, Milliken, John A., Macfarlane, Peter W., editor, van Oosterom, A., editor, Pahlm, Olle, editor, Kligfield, Paul, editor, Janse, Michiel, editor, and Camm, John, editor

Published
2010
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32. Development of systolic dysfunction unrelated to myocardial infarction in treated hypertensive patients with left ventricular hypertrophy. The LIFE Study

Author

Chinali, Marcello, primary, Aurigemma, Gerard P., additional, Gerdts, Eva, additional, Wachtell, Kristian, additional, Okin, Peter M., additional, Muthiah, Anujan, additional, Kjeldsen, Sverre E., additional, Julius, Stevo, additional, de Simone, Giovanni, additional, and Devereux, Richard B., additional

Published
2022
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35. Left Atrial Systolic Force in Hypertensive Patients with Left Ventricular Hypertrophy:A Predictor of Incident Atrial Fibrillation. The LIFE Study

Author

Gerholt, Lotte, Bang, Casper N., Gerdts, Eva, Larstorp, Anne Cecilie, Kjeldsen, Sverre E., Julius, Stevo, Wachtell, Kristian, Okin, Peter M., and Devereux, Richard B.

Abstract

It remains unknown whether left atrial systolic force (LASF), a measure of left atrial function, can be used as a predictor of new-onset atrial fibrillation (NOAF). Furthermore, the effect of the treatment with atenolol and losartan on LASF is unclear. A total of 758 patients without atrial fibrillation at baseline were enrolled from the Losartan Intervention For Endpoint (LIFE) reduction in hypertension echocardiography sub-study. Participants of the LIFE study were randomized to either atenolol-or losartan-based treatment. The mean follow-up was 59 months. LASF was calculated using the average mitral orifice area and mitral peak. The velocity was obtained by Doppler echocardiography. At baseline, 25% of patients had a LASF ≤ 10.3 kdyn. Compared to other quartiles, this quartile had a higher proportion of men, lower heart rate, body mass index, and age. After controlling for these variables, patients in the first quartile had a lower stroke volume compared to other quartiles. New-onset AF occurred in 29 (8.1/1,000 patient-years of follow-up) patients. In multivariable Cox regression analyses with backward elimination, increasing LASF was associated with a lower risk of NOAF (hazard ratio [HR] = 0.90 [95% confidence interval 0.85-0.96], p = 0.001). Integrated discrimination improvement was 0.054 (p = 0.004) and there was a borderline significant net reclassification improvement of 19.2% (p = 0.075). Over time LASF decreased more in the atenolol-based than the losartan-based treatment group ( < 0.001). Low LASF was associated with a higher risk of new-onset AF. Losartan-based treatment was associated with better preservation of LASF compared to atenolol-based treatment.

Published
2022

37. Atrial fibrillation onset before heart failure or vice versa: what is worst? A nationwide register study.

Author

Pallisgaard, Jannik, Greve, Anders M, Lock-Hansen, Morten, Thune, Jens Jakob, Fosboel, Emil Loldrup, Devereux, Richard B, Okin, Peter M, Gislason, Gunnar H, Torp-Pedersen, Christian, and Bang, Casper N

Abstract

Aims: Atrial fibrillation (AF) and heart failure (HF) often coexist. However, whether AF onset before HF or vice versa is associated with the worst outcome remains unclear. A consensus of large studies can guide future research and preventive strategies to better target high-risk patients.Methods and Results: We included all Danish cases with the coexistence of AF and HF (2005-17) using nationwide registries. Patients were divided into three separate groups (i) AF before HF, (ii) HF before AF, or (iii) AF and HF diagnosed concurrently (±30 days). Adjusting landmark Cox analyses (index date was the time of the latter diagnosis of AF or HF) were used for evaluating the association of the three groups with a composite outcome of ischaemic stroke or death. Among a total of 49 042 patients included, 40% had AF before HF, 27% had HF before AF, and 33% had AF and HF diagnosed concurrently. The composite endpoint accrued more often in patients with HF before AF compared to the two other groups (<0.001), and this remained significant in the adjusted analyses with hazard ratios (95% confidence intervals) of 1.26 (1.22-1.30) compared to AF before HF. Finally, antihypertensive treatment, oral anticoagulants, amiodarone, statins, and AF ablation were associated with a lower hazard ratio of the composite endpoint (all < 0.001).Conclusions: In this large Danish national cohort, diagnosis of HF before AF was associated with an increased absolute risk of death compared to AF before HF and AF and HF diagnosed concurrently. Antihypertensive treatment, oral anticoagulants, amiodarone, statins, and AF ablation may improve prognosis. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Heart rate is associated with red blood cell fatty acid concentration: The Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study

Author

Ebbesson, Sven O.E., Devereux, Richard B., Cole, Shelley, Ebbesson, Lars O.E., Fabsitz, Richard R., Haack, Karin, Harris, William S., Howard, Wm. James, Laston, Sandra, Lopez-Alvarenga, Juan Carlos, MacCluer, Jean W., Okin, Peter M., Tejero, M. Elizabeth, Voruganti, V. Saroja, Wenger, Charlotte R., Howard, Barbara V., and Comuzzie, Anthony G.

Published
2010
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