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Aortic stenosis (AS) imposes a chronic, progressive pressure overload on the left ventricle. The myocardium responds through a sequence of mechanical and biological processes that initially preserve wall stress and cardiac output but eventually become maladaptive, leading to fibrosis, loss of contractile reserve and clinical heart failure. Integrating myocardial fibrosis assessment and staging frameworks into clinical decision-making may support earlier valve replacement, even before conventional triggers such as symptoms or reduced ejection fraction, to prevent irreversible myocardial damage in patients with severe/significant AS. Advances in imaging biomarkers - including cardiac magnetic resonance-derived late gadolinium enhancement, extracellular volume quantification and strain analysis - allow for more personalized risk stratification and may help identify which patients with asymptomatic severe AS stand to benefit most from earlier intervention. Beyond the valve procedure itself, adjunctive pharmacological strategies, such as antifibrotic therapies, renin-angiotensin system blockade, neprilysin inhibition and metabolic modulators, are being explored to address persistent fibrotic and metabolic remodelling that valve replacement alone cannot reverse. Equally important is the optimal treatment of concomitant cardiovascular comorbidities such as hypertension, coronary artery disease and atrial fibrillation, which may aggravate myocardial remodelling and blunt the benefits of valve replacement if left untreated.