Effect of renin-angiotensin system inhibition on left ventricular mass regression after transcatheter aortic valve replacement: a randomised controlled trial.

Abstract

Residual left ventricular (LV) hypertrophy and incomplete reverse remodelling after transcatheter aortic valve replacement (TAVR) are associated with adverse outcomes. Whether renin-angiotensin system inhibitors (RASi) promote reverse remodelling in patients with heart failure and LV ejection fraction (LVEF) ≥40% following TAVR remains uncertain. In this multicentre, prospective, randomised, open-label, blinded-endpoint trial, patients aged ≥60 years with symptomatic severe aortic stenosis, LVEF ≥40% and successful TAVR were randomly assigned (1:1) to standard care alone or standard care plus RASi (ACE inhibitor, angiotensin II receptor blocker or angiotensin receptor-neprilysin inhibitor). The primary endpoint was change in LV mass index (LVMI) at 12 months. Secondary endpoints included changes in LV volumes, LVEF, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and functional status. A total of 200 patients were randomised; 194 were included in the modified intention-to-treat analysis (RASi n=95; control n=99). At 12 months, RASi therapy was associated with a greater reduction in LVMI compared with control (adjusted mean difference -12.77 g/m², 95% CI -24.73 to -0.81; p=0.036). Consistent improvements were observed in LV end-diastolic and end-systolic volumes. Functional status (New York Heart Association class) improved modestly in the RASi group. No significant differences were observed in LVEF or NT-proBNP. In patients with heart failure and LVEF ≥40% following TAVR, RAS inhibition led to enhanced reverse LV remodelling over 12 months, reflected by greater regression of LV mass and volumes. These findings support the potential role for RASi in modifying post-TAVR myocardial remodelling, although larger trials are required to determine whether these structural benefits translate into improved clinical outcomes. ChiCTR2100042266.