TY - JOUR
T1 - Mechanisms of myocardial reverse remodelling and its clinical significance
T2 - A scientific statement of the ESC Working Group on Myocardial Function
AU - Falcão-Pires, Inês
AU - Ferreira, Ana Filipa
AU - Trindade, Fábio
AU - Bertrand, Luc
AU - Ciccarelli, Michele
AU - Visco, Valeria
AU - Dawson, Dana
AU - Hamdani, Nazha
AU - Van Laake, Linda W.
AU - Lezoualc'h, Frank
AU - Linke, Wolfgang A.
AU - Lunde, Ida G.
AU - Rainer, Peter P.
AU - Abdellatif, Mahmoud
AU - Van der Velden, Jolanda
AU - Cosentino, Nicola
AU - Paldino, Alessia
AU - Pompilio, Giulio
AU - Zacchigna, Serena
AU - Heymans, Stephane
AU - Thum, Thomas
AU - Tocchetti, Carlo Gabriele
N1 - Publisher Copyright:
© 2024 European Society of Cardiology.
PY - 2024/7
Y1 - 2024/7
N2 - Cardiovascular disease (CVD) is the leading cause of morbimortality in Europe and worldwide. 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–angiotensin–aldosterone system inhibitors, beta-blockers, diuretics and sodium–glucose 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.
AB - Cardiovascular disease (CVD) is the leading cause of morbimortality in Europe and worldwide. 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–angiotensin–aldosterone system inhibitors, beta-blockers, diuretics and sodium–glucose 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.
KW - Adverse remodelling
KW - Heart failure
KW - Myocardial remodelling
KW - Physiologic remodelling
KW - Reverse remodelling
UR - http://www.scopus.com/inward/record.url?scp=85195206149&partnerID=8YFLogxK
U2 - 10.1002/ejhf.3264
DO - 10.1002/ejhf.3264
M3 - Review article
AN - SCOPUS:85195206149
SN - 1388-9842
VL - 26
SP - 1454
EP - 1479
JO - European Journal of Heart Failure
JF - European Journal of Heart Failure
IS - 7
ER -