دورية أكاديمية
Pathophysiological pathways in patients with heart failure and atrial fibrillation.
| العنوان: | Pathophysiological pathways in patients with heart failure and atrial fibrillation. |
|---|---|
| المؤلفون: | Santema BT; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Arita VA; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Sama IE; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Kloosterman M; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., van den Berg MP; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Nienhuis HLA; Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Van Gelder IC; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., van der Meer P; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Zannad F; Department of Cardiology, INSERM, Centre d'Investigations Cliniques Plurithé matique 1433, INSERM U1116, Université de Lorraine, CHRU de Nancy, F-CRIN INI-CRCT, Nancy, France., Metra M; Department of Medical and Surgical Specialties, Institute of Cardiology, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy., Ter Maaten JM; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Cleland JG; Department of Cardiology, National Heart & Lung Institute, Royal Brompton & Harefield Hospitals, Imperial College, London, UK.; Department of Cardiology, Robertson Institute of Biostatistics and Clinical Trials Unit, University of Glasgow, Glasgow, UK., Ng LL; Department of Cardiovascular Sciences, University of Leicester, Leicester, UK.; Department of Cardiology, NIHR Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, UK., Anker SD; Department of Cardiology (CVK) and Berlin Institute of Health Center for Regenerative Therapies (BCRT), German Centre for Cardiovascular Research (DZHK) Partner Site Berlin, Charité Universitätsmedizin Berlin, Berlin, Germany., Lang CC; Division of Molecular and Clinical Medicine, School of Medicine Centre for Cardiovascular and Lung Biology, Ninewells Hospital & Medical School, University of Dundee, Dundee, UK., Samani NJ; Department of Cardiovascular Sciences, University of Leicester, Leicester, UK.; Department of Cardiology, NIHR Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, UK., Dickstein K; Department of Cardiology, University of Bergen, Bergen, Norway.; Department of Cardiology, Stavanger University Hospital, Stavanger, Norway., Filippatos G; Department of Cardiology, National and Kapodistrian University of Athens, Attikon University Hospital, Athens, Greece., van Veldhuisen DJ; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Lam CSP; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.; Department of Cardiology, National Heart Centre Singapore and Duke-National University of Singapore, Singapore, Singapore., Rienstra M; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands., Voors AA; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. |
| المصدر: | Cardiovascular research [Cardiovasc Res] 2022 Aug 24; Vol. 118 (11), pp. 2478-2487. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Oxford Journals Country of Publication: England NLM ID: 0077427 Publication Model: Print Cited Medium: Internet ISSN: 1755-3245 (Electronic) Linking ISSN: 00086363 NLM ISO Abbreviation: Cardiovasc Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2008- : Oxford : Oxford Journals Original Publication: London, British Medical Assn. |
| مواضيع طبية MeSH: | Atrial Fibrillation*/complications , Atrial Fibrillation*/diagnosis , Atrial Fibrillation*/epidemiology , Heart Failure* , Somatomedins*, Biomarkers ; Female ; Humans ; Prognosis |
| مستخلص: | Aims: Atrial fibrillation (AF) and heart failure (HF) are two growing epidemics that frequently co-exist. We aimed to gain insights into the underlying pathophysiological pathways in HF patients with AF by comparing circulating biomarkers using pathway overrepresentation analyses. Methods and Results: From a panel of 92 biomarkers from different pathophysiological domains available in 1620 patients with HF, we first tested which biomarkers were dysregulated in patients with HF and AF (n = 648) compared with patients in sinus rhythm (n = 972). Secondly, pathway overrepresentation analyses were performed to identify biological pathways linked to higher plasma concentrations of biomarkers in patients who had HF and AF. Findings were validated in an independent HF cohort (n = 1219, 38% with AF). Patient with AF and HF were older, less often women, and less often had a history of coronary artery disease compared with those in sinus rhythm. In the index cohort, 24 biomarkers were up-regulated in patients with AF and HF. In the validation cohort, eight biomarkers were up-regulated, which all overlapped with the 24 biomarkers found in the index cohort. The strongest up-regulated biomarkers in patients with AF were spondin-1 (fold change 1.18, P = 1.33 × 10-12), insulin-like growth factor-binding protein-1 (fold change 1.32, P = 1.08 × 10-8), and insulin-like growth factor-binding protein-7 (fold change 1.33, P = 1.35 × 10-18). Pathway overrepresentation analyses revealed that the presence of AF was associated with activation amyloid-beta metabolic processes, amyloid-beta formation, and amyloid precursor protein catabolic processes with a remarkable consistency observed in the validation cohort. Conclusion: In two independent cohorts of patients with HF, the presence of AF was associated with activation of three pathways related to amyloid-beta. These hypothesis-generating results warrant confirmation in future studies. Competing Interests: Conflict of interest: A.A.V. and/or his institution received grants and/or consultancy reimbursements from Amgen, AstraZeneca, Bayer AG, Boehringer, Cytokinetics, Merck, Myokardia, Novartis, Roche, and Novo Nordisk. B.T.S. received funding from the Dutch Heart Foundation (2019T094). I.C.V.G. reports support from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch heart Foundation (CVON 2014-9 and CVON 2018-28) and support from Medtronic to the institution. F.Z. reports personal fees from Amgen, Applied Therapeutics, AstraZeneca, Bayer, Boehringer, Boston Scientific, Cardior, Cardiorenal, Cereno pharmaceutical, Cirius, CVCT, CVRx, Janssen, Novartis, Merck, and Vifor Fresenius. P.v.d.M. received consultancy fees and/or grants from Novartis, Servier, Vifor, Pharma, Astra Zeneca, Pfizer, and Ionis. C.S.P.L. is supported by a Clinician Scientist Award from the National Medical Research Council of Singapore; has received research support from Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, and Vifor Pharma; has served as consultant or on the Advisory Board/Steering Committee/Executive Committee for Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, Vifor Pharma, Novartis, Amgen, Merck, Janssen Research & Development LLC, Menarini, Boehringer Ingelheim, Novo Nordisk, Abbott Diagnostics, Corvia, Stealth BioTherapeutics, JanaCare, Biofourmis, Darma, Applied Therapeutics, MyoKardia, Cytokinetics, WebMD Global LLC, Radcliffe Group Ltd and Corpus; and serves as co-founder and non-executive director of eKo.ai. G.F. is committee member in trials and/or registries sponsored by Medtronic, Novartis, BI, Vifor, Servier, outside the submitted work. S.D.A. reports receiving fees from Abbott Vascular, Bayer, Boehringer Ingelheim, Cardiac Dimension, Impulse Dynamics, Novartis, Servier, and Vifor Pharma, and grant support from Abbott Vascular and Vifor Pharma. V.A.A. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant (754425). None of the funders had any role in the trial design, the collection or analysis of the data, or the writing of the manuscript. All other authors declare no conflict of interest. (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.) |
| التعليقات: | Comment in: Cardiovasc Res. 2022 Jul 05;:. (PMID: 35788838) |
| References: | Lancet. 1977 Jan 1;1(8001):27-8. (PMID: 63661) Stroke. 1997 Feb;28(2):316-21. (PMID: 9040682) J Am Coll Cardiol. 2016 Dec 6;68(22):2395-2407. (PMID: 27908343) Alzheimers Dement. 2014 Jan;10(1):45-52. (PMID: 23535033) Front Physiol. 2018 Oct 09;9:1383. (PMID: 30356673) Eur J Heart Fail. 2020 May;22(5):821-833. (PMID: 32243695) J Card Fail. 2017 Jan;23(1):20-28. (PMID: 27317843) Am J Cardiol. 2003 Mar 20;91(6A):2D-8D. (PMID: 12670636) Eur Heart J. 2018 Nov 14;39(43):3867-3875. (PMID: 30137304) Clin Res Cardiol. 2020 Mar;109(3):331-338. (PMID: 31263996) Eur J Heart Fail. 2020 Mar;22(3):519-527. (PMID: 31919934) Circulation. 2017 Apr 18;135(16):1547-1563. (PMID: 28416525) Eur Heart J. 2014 Aug 21;35(32):2140-5. (PMID: 24970336) J Am Coll Cardiol. 2016 Nov 15;68(20):2217-2228. (PMID: 27855811) PLoS One. 2014 Apr 22;9(4):e95192. (PMID: 24755770) JACC Heart Fail. 2016 Nov;4(11):860-869. (PMID: 27744089) Curr Heart Fail Rep. 2019 Dec;16(6):285-303. (PMID: 31782077) Bioinformatics. 2009 Apr 15;25(8):1091-3. (PMID: 19237447) J Am Coll Cardiol. 2016 Sep 6;68(10):1014-20. (PMID: 27585505) JACC Heart Fail. 2017 Feb;5(2):92-98. (PMID: 28017355) J Alzheimers Dis. 2010;19(1):311-23. (PMID: 20061647) J Am Heart Assoc. 2013 Apr 22;2(2):e000098. (PMID: 23608605) Eur Heart J. 2019 Apr 21;40(16):1287-1293. (PMID: 30753432) Nucleic Acids Res. 2019 Jan 8;47(D1):D506-D515. (PMID: 30395287) J Alzheimers Dis. 2018;62(1):61-72. (PMID: 29439352) Lancet. 2014 Dec 20;384(9961):2235-43. (PMID: 25193873) J Gerontol A Biol Sci Med Sci. 2014 May;69(5):609-15. (PMID: 24077599) Genome Res. 2003 Nov;13(11):2498-504. (PMID: 14597658) Eur Heart J. 2018 Aug 21;39(32):2987-2996. (PMID: 29401239) Circulation. 2019 Jan 22;139(4):431-443. (PMID: 30586695) Amyloid. 2015;22(3):147-55. (PMID: 25997105) JACC Heart Fail. 2020 Mar;8(3):234-242. (PMID: 32035890) Circ Arrhythm Electrophysiol. 2020 Feb;13(2):e007607. (PMID: 31941368) J Am Coll Cardiol. 2018 Sep 4;72(10):1081-1090. (PMID: 30165978) Nat Rev Neurol. 2017 Sep 29;13(10):612-623. (PMID: 28960209) Circulation. 2002 Oct 15;106(16):2091-7. (PMID: 12379579) Proc Natl Acad Sci U S A. 2004 Feb 24;101(8):2548-53. (PMID: 14983046) Circulation. 2009 Sep 29;120(13):1203-12. (PMID: 19752327) Eur Heart J. 2017 Jun 21;38(24):1883-1890. (PMID: 28329163) N Engl J Med. 2018 Sep 13;379(11):1007-1016. (PMID: 30145929) Circ Heart Fail. 2018 Oct;11(10):e005133. (PMID: 30354399) JAMA Cardiol. 2019 May 1;4(5):466-472. (PMID: 30878017) Europace. 2016 Oct;18(10):1455-1490. (PMID: 27402624) Eur J Heart Fail. 2016 Jun;18(6):716-26. (PMID: 27126231) |
| فهرسة مساهمة: | Keywords: Amyloid-beta; Atrial fibrillation; Heart failure; Pathway analysis |
| المشرفين على المادة: | 0 (Biomarkers) 0 (Somatomedins) |
| تواريخ الأحداث: | Date Created: 20211023 Date Completed: 20220826 Latest Revision: 20221104 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC9400416 |
| DOI: | 10.1093/cvr/cvab331 |
| PMID: | 34687289 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1755-3245 |
|---|---|
| DOI: | 10.1093/cvr/cvab331 |