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CVD imposes a heterogeneous spectrum of cardiac remodelling, depending on the insult nature, that is, pressure or volume overload, ischaemia, arrhythmias, infection, pathogenic gene variant, or cardiotoxicity. Moreover, the progression of CVD-induced remodelling is influenced by sex, age, genetic background and comorbidities, impacting patients' outcomes and prognosis. Cardiac reverse remodelling (RR) is defined as any normative improvement in cardiac geometry and function, driven by therapeutic interventions and rarely occurring spontaneously. While RR is the outcome desired for most CVD treatments, they often only slow\/halt its progression or modify risk factors, calling for novel and more timely RR approaches. Interventions triggering RR depend on the myocardial insult and include drugs (renin\u2013angiotensin\u2013aldosterone system inhibitors, beta-blockers, diuretics and sodium\u2013glucose cotransporter 2 inhibitors), devices (cardiac resynchronization therapy, ventricular assist devices), surgeries (valve replacement, coronary artery bypass graft), or physiological responses (deconditioning, postpartum). Subsequently, cardiac RR is inferred from the degree of normalization of left ventricular mass, ejection fraction and end-diastolic\/end-systolic volumes, whose extent often correlates with patients' prognosis. However, strategies aimed at achieving sustained cardiac improvement, predictive models assessing the extent of RR, or even clinical endpoints that allow for distinguishing complete from incomplete RR or adverse remodelling objectively, remain limited and controversial. This scientific statement aims to define RR, clarify its underlying (patho)physiologic mechanisms and address (non)pharmacological options and promising strategies to promote RR, focusing on the left heart. We highlight the predictors of the extent of RR and review the prognostic significance\/impact of incomplete RR\/adverse remodelling. Lastly, we present an overview of RR animal models and potential future strategies under pre-clinical evaluation.<\/jats:p>","DOI":"10.1002\/ejhf.3264","type":"journal-article","created":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T02:19:56Z","timestamp":1717553996000},"page":"1454-1479","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Mechanisms of Myocardial Reverse Remodelling and Its Clinical Significance: A Scientific Statement of the ESC Working Group on Myocardial Function"],"prefix":"10.1093","volume":"26","author":[{"given":"In\u00eas","family":"Falc\u00e3o-Pires","sequence":"first","affiliation":[{"name":"UnIC@RISE, Department of Surgery and Physiology, Faculty of Medicine of the University of Porto , Porto ,","place":["Portugal"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana Filipa","family":"Ferreira","sequence":"additional","affiliation":[{"name":"UnIC@RISE, Department of 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Ruhr University Bochum , Bochum ,","place":["Germany"]},{"name":"HCEMM-SU Cardiovascular Comorbidities Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University , Budapest ,","place":["Hungary"]},{"name":"Department of Physiology, Cardiovascular Research Institute Maastricht University Maastricht , Maastricht ,","place":["the Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda W.","family":"Van Laake","sequence":"additional","affiliation":[{"name":"Division Heart and Lungs, Department of Cardiology and Regenerative Medicine Center, University Medical Center Utrecht , Utrecht ,","place":["The Netherlands"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank","family":"Lezoualc'h","sequence":"additional","affiliation":[{"name":"Institut des Maladies M\u00e9taboliques et Cardiovasculaires, Inserm, Universit\u00e9 Paul Sabatier, UMR 1297-I2MC , Toulouse 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