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RAS inhibitor use after TAVI linked to lower mortality in severe aortic stenosis

RAS inhibitor use after TAVI linked to lower mortality in severe aortic stenosis
Photo by Navy Medicine / Unsplash
Key Takeaway
Consider that RAS inhibitor use after TAVI may be associated with lower mortality, but evidence is observational.

This systematic review and meta-analysis of observational data included 36,015 patients with severe aortic stenosis undergoing transcatheter aortic valve implantation (TAVI). The study compared outcomes for patients who used renin-angiotensin system (RAS) inhibitors after TAVI versus those who did not.

The primary outcome was all-cause mortality. RAS inhibitor use was associated with lower odds of all-cause mortality (OR 0.74, 95% CI 0.70-0.78). Secondary outcomes showed lower odds for cardiovascular mortality (OR 0.62, 95% CI 0.55-0.72), cerebrovascular events (OR 0.59, 95% CI 0.47-0.74), and heart failure hospitalization (OR 0.84, 95% CI 0.77-0.92). No clear association was observed for myocardial infarction (OR 0.95, 95% CI 0.59-1.53).

Safety and tolerability data were not reported. Key limitations include the observational nature of the data, potential for residual confounding, and limited statistical power for specific cardiovascular outcomes. The authors note that randomized controlled trials are needed to clarify clinical utility.

Practice relevance is restrained; the association does not imply causation. These findings may inform hypothesis generation but should not change clinical practice without further evidence.

Study Details

Study typeRct
Sample sizen = 36,015
EvidenceLevel 2
PublishedMay 2026
View Original Abstract ↓
Background: Aortic stenosis (AS) carries a high mortality risk if left untreated. Transcatheter aortic valve implantation (TAVI) has emerged as a primary treatment modality for many patients with severe AS. Observational data suggest that renin-angiotensin system (RAS) inhibitor use following TAVI are associated with lower risk, but with divergent reported effects and limited statistical power for specific cardiovascular outcome. This study aimed to assess the association between RAS inhibitor use and clinical outcomes after TAVI. Methods: A systematic literature search was conducted in EMBASE and PubMed. Eligible studies included those reporting on RAS inhibitor use in TAVI populations. The primary outcome was all-cause mortality. Secondary outcomes included cardiovascular mortality, myocardial infarction (MI), cerebrovascular events, and heart failure (HF) hospitalization. Results: Nine observational studies including 36,015 patients were included. RAS inhibitor use was associated with lower odds of all-cause mortality (OR 0.74, 95% CI 0.70?0.78), cardiovascular mortality (OR 0.62, 95% CI 0.55?0.72), cerebrovascular events (OR 0.59, 95% CI 0.47?0.74), and HF hospitalization (OR 0.84, 95% CI 0.77?0.92). No clear association was observed for MI (OR 0.95, 95% CI 0.59?1.53). Conclusions: RAS inhibitor use was associated with favorable clinical outcomes following TAVI. However, these findings are based on observational data, which are subject to residual confounding. Randomized controlled trials are needed to clarify the clinical utility of RAS inhibitors in this setting.
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