Left atrial disease and left atrial reverse remodelling across different stages of heart failure development and progression: a new target for prevention and treatment
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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The left atrium is a dynamic chamber with peculiar characteristics. Stressors and disease mechanisms may deeply modify its structure and function, leading to left atrial remodelling and disease. Left atrial disease is a predictor of poor outcomes. It may be a consequence of left ventricular systolic and diastolic dysfunction and neurohormonal and inflammatory activation and/or actively contribute to the progression and clinical course of heart failure through multiple mechanisms such as left ventricular filling and development of atrial fibrillation and subsequent embolic events. There is growing evidence that therapy may improve left atrial function and reverse left atrial remodelling. Whether this translates into changes in patient's prognosis is still unknown. In this review we report current data about changes in left atrial size and function across different stages of development and progression of heart failure. At each stage, drug therapies, lifestyle interventions and procedures have been associated with improvement in left atrial structure and function, namely a reduction in left atrial volume and/or an improvement in left atrial strain function, a process that can be defined as left atrial reverse remodelling and, in some cases, this has been associated with improvement in clinical outcomes. Further evidence is still needed mainly with respect of the possible role of left atrial reverse remodelling as an independent mechanism affecting the patient's clinical course and as regards better standardization of clinically meaningful changes in left atrial measurements. Summarizing current evidence, this review may be the basis for further studies.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | European Journal of Heart Failure |
| Vol/bind | 24 |
| Sider (fra-til) | 959–975 |
| ISSN | 1388-9842 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
T.B.S.: Steering Committee of the Amgen financed GALACTIC‐HF trial and the Boston Scientific financed LUX‐Dx TRENDS, Chief investigator of the Sanofi Pasteur financed NUDGEFLU trial, the DANFLU‐1 & DANFLU‐2 trials; research grants: Sanofi Pasteur & GE Healthcare; advisory boards: Sanofi Pasteur, Amgen & GSK; and speaker honoraria: Novartis, Sanofi Pasteur, GSK & Bayer. S.D.S. received research grants from Actelion, Alnylam, Amgen, AstraZeneca, Bellerophon, Bayer, BMS, Celladon, Cytokinetics, Eidos, Gilead, GSK, Ionis, Lilly, Mesoblast, MyoKardia, NIH/NHLBI, Neurotronik, Novartis, NovoNordisk, Respicardia, Sanofi Pasteur, Theracos, US2.AI and has consulted for Abbott, Action, Akros, Alnylam, Amgen, Arena, AstraZeneca, Bayer, Boehringer Ingelheim, BMS, Cardior, Cardurion, Corvia, Cytokinetics, Daiichi‐Sankyo, GSK, Lilly, Merck, Myokardia, Novartis, Roche, Theracos, Quantum Genomics, Cardurion, Janssen, Cardiac Dimensions, Tenaya, Sanofi‐Pasteur, Dinaqor, Tremeau, CellProThera, Moderna, American Regent, Sarepta, Lexicon, Anacardio, Akros, Puretech Health. M.M received personal fees of minimal amounts in the last 3 years from Actelion, Amgen, Livanova, Servier and Vifor pharma as member of Executive or Data Monitoring Committees of sponsored clinical trials and from AstraZeneca, Abbott Vascular, Bayer, Boehringer Ingelheim and Edwards Therapeutics for participation in advisory boards and/or speeches at sponsored meetings. All other authors have nothing to disclose. Conflict of interest:
Funding Information:
Open Access Funding provided by Università degli Studi di Brescia within the CRUI-CARE Agreement. Conflict of interest: T.B.S.: Steering Committee of the Amgen financed GALACTIC-HF trial and the Boston Scientific financed LUX-Dx TRENDS, Chief investigator of the Sanofi Pasteur financed NUDGEFLU trial, the DANFLU-1 & DANFLU-2 trials; research grants: Sanofi Pasteur & GE Healthcare; advisory boards: Sanofi Pasteur, Amgen & GSK; and speaker honoraria: Novartis, Sanofi Pasteur, GSK & Bayer. S.D.S. received research grants from Actelion, Alnylam, Amgen, AstraZeneca, Bellerophon, Bayer, BMS, Celladon, Cytokinetics, Eidos, Gilead, GSK, Ionis, Lilly, Mesoblast, MyoKardia, NIH/NHLBI, Neurotronik, Novartis, NovoNordisk, Respicardia, Sanofi Pasteur, Theracos, US2.AI and has consulted for Abbott, Action, Akros, Alnylam, Amgen, Arena, AstraZeneca, Bayer, Boehringer Ingelheim, BMS, Cardior, Cardurion, Corvia, Cytokinetics, Daiichi-Sankyo, GSK, Lilly, Merck, Myokardia, Novartis, Roche, Theracos, Quantum Genomics, Cardurion, Janssen, Cardiac Dimensions, Tenaya, Sanofi-Pasteur, Dinaqor, Tremeau, CellProThera, Moderna, American Regent, Sarepta, Lexicon, Anacardio, Akros, Puretech Health. M.M received personal fees of minimal amounts in the last 3 years from Actelion, Amgen, Livanova, Servier and Vifor pharma as member of Executive or Data Monitoring Committees of sponsored clinical trials and from AstraZeneca, Abbott Vascular, Bayer, Boehringer Ingelheim and Edwards Therapeutics for participation in advisory boards and/or speeches at sponsored meetings. All other authors have nothing to disclose.
Publisher Copyright:
© 2022 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.
ID: 313052064