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dc.creatorCauwenberghs, N. (Nicholas)-
dc.creatorRavassa, S. (Susana)-
dc.creatorThijs, L. (Lutgarde)-
dc.creatorHaddad, F. (Francois)-
dc.creatorYang, W.Y. (Wen Yi)-
dc.creatorWei, F.F. (Fang Fei)-
dc.creatorLópez, B. (Begoña)-
dc.creatorGonzalez, A. (Arantxa)-
dc.creatorDiez, J. (Javier)-
dc.creatorStaessen, J.A. (Jan A.)-
dc.creatorKuznetsova, T. (Tatiana)-
dc.date.accessioned2022-03-11T13:44:50Z-
dc.date.available2022-03-11T13:44:50Z-
dc.date.issued2019-
dc.identifier.citationCauwenberghs, N. (Nicholas); Ravassa, S. (Susana); Thijs, L. (Lutgarde); et al. "Circulating biomarkers predicting longitudinal changes in left ventricular structure and function in a general population". Journal of the American Heart Association. 8 (2), 2019, e010430es
dc.identifier.issn2047-9980-
dc.identifier.urihttps://hdl.handle.net/10171/63151-
dc.description.abstractBackground Serial imaging studies in the general population remain important to evaluate the usefulness of pathophysiologically relevant biomarkers in predicting progression of left ventricular (LV) remodeling and dysfunction. Here, we assessed in a general population whether these circulating biomarkers at baseline predict longitudinal changes in LV structure and function. Methods and Results In 592 participants (mean age, 50.8 years; 51.4% women; 40.5% hypertensive), we derived echocardiographic indexes reflecting LV structure and function at baseline and after 4.7 years. At baseline, we measured alkaline phosphatase, markers of collagen turnover (procollagen type I, C‐terminal telopeptide, matrix metalloproteinase‐1) and high‐sensitivity cardiac troponin T. We regressed longitudinal changes in LV indexes on baseline biomarker levels and reported standardized effect sizes as a fraction of the standard deviation of LV change. After full adjustment, a decline in LV longitudinal strain (−14.2%) and increase in E/e′ ratio over time (+18.9%; P≤0.019) was associated with higher alkaline phosphatase activity at baseline. Furthermore, longitudinal strain decreased with higher levels of collagen I production and degradation at baseline (procollagen type I, −14.2%; C‐terminal telopeptide, −16.4%; P≤0.029). An increase in E/e′ ratio over time was borderline associated with lower matrix metalloproteinase‐1 (+9.8%) and lower matrix metalloproteinase‐1/tissue inhibitor of metalloproteinase‐1 ratio (+11.9%; P≤0.041). Higher high‐sensitivity cardiac troponin T levels at baseline correlated significantly with an increase in relative wall thickness (+23.1%) and LV mass index (+18.3%) during follow‐up (P≤0.035). Conclusions We identified a set of biomarkers predicting adverse changes in LV structure and function over time. Circulating biomarkers reflecting LV stiffness, injury, and collagen composition might improve the identification of subjects at risk for subclinical cardiac maladaptation.es_ES
dc.description.sponsorshipThe Studies Coordinating Centre received support from the European Union (HEALTH-F7-305507 HOMAGE), the European Research Council (ERC Advanced Grant-2011-294713- EPLORE, PoC 713601-uPROPHET) and the Fonds voor Wetenschappelijk Onderzoek Vlaanderen (G.0880.13, G.0881.13, G0C5319N, ERA-CVD JTC2017-046, 11Z0916N).es_ES
dc.language.isoenges_ES
dc.publisherOvid Technologies (Wolters Kluwer Health)es_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectCardiac biomarkerses_ES
dc.subjectCardiac dysfunctiones_ES
dc.subjectPhosphatasees_ES
dc.subjectPopulation studieses_ES
dc.subjectRemodelinges_ES
dc.titleCirculating biomarkers predicting longitudinal changes in left ventricular structure and function in a general populationes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.description.noteThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.es_ES
dc.identifier.doi10.1161/jaha.118.010430-
dadun.citation.number2es_ES
dadun.citation.publicationNameJournal of the American Heart Associationes_ES
dadun.citation.startingPagee010430es_ES
dadun.citation.volume8es_ES

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