These pathophysiologic alterations can blunt the haemodynamic benefits of valve replacement and sustain neurohormonal activation, thereby maintaining high natriuretic peptide levels.17 Comorbidities like AF, renal dysfunction, and pulmonary hypertension may further exacerbate myocardial load.18,19 In contrast, patients who exhibit postprocedural NT-proBNP decline may represent a subgroup with more favourable myocardial substrate and greater capacity for reverse remodeling.5,6. Here, NPPB is linked to pulmonary hypertension.