Key result
High plasma renin activity (PRA-S) was an independent predictor of all-cause death in patients with HFpEF (HR 2.14; 95% CI 1.20-3.82; p=0.010), regardless of RAAS inhibitor treatment.
Why the study?
Although RAAS-inhibiting drugs induce compensatory renin up-regulation, PRA exhibits large variability in HFrEF, and its response to RAASi and prognostic effect in HFpEF remained unclear.
Is high plasma renin activity (PRA-S) associated with increased risk of all-cause death in patients with HFpEF?
Cohort (n=150)
No
Is high plasma renin activity (PRA-S) associated with increased risk of all-cause death in patients with HFpEF?
High plasma renin activity is an independent predictor of all-cause mortality in patients with HFpEF, regardless of RAAS inhibitor treatment.
High PRA-S may aid mortality risk stratification in HFpEF; leaves open whether renin-targeted therapies improve outcomes.
Drugs which interact with the renin angiotensin aldosterone system (RAAS) aim to reduce the negative effects of angiotensin (Ang) II. Treatment with these drugs anticipate a compensatory up-regulation of renin; however, it has been shown that there is a large variability in circulating plasma renin (PRA), even in patients with optimal medical therapy in patients with heart failure (HF) with reduced ejection fraction (HFrEF). Our aim was to measure plasma renin activity (PRA-S), its response to RAAS inhibitor (RAASi) therapies and its effects on outcome in patients with HF with preserved ejection fraction (HFpEF). For this purpose, 150 HFpEF patients were included into a prospective single-center registry. Equilibrium (eq) angiotensin metabolites were measured from serum samples using mass spectroscopy. PRA-S (eqAng I + eqAng II) was calculated and compared in respect to the primary endpoint defined as all-cause death. PRA-S in patients with RAASi therapy was not significantly higher than in patients without RAASi (p = 0.262). Even after adjusting for confounding factors, PRA-S remained predictive for all-cause death in the multivariable model with a hazard ratio of 2.14 (95%CI 1.20–3.82, p = 0.010). We conclude that high PRA-S is associated with poor prognosis in patients with HFpEF, regardless of RAASi treatment, which could ultimately result in hyperactivated RAAS and consecutive negative effects on the cardiovascular and renal system, leading to poor outcome in patients with HFpEF.
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Binder et al. (2021) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) (n=150). Plasma renin activity (PRA-S) was evaluated on All-cause death (HR 2.14, 95% CI 1.20-3.82, p=0.010). High plasma renin activity (PRA-S) was an independent predictor of all-cause death in patients with HFpEF (HR 2.14; 95% CI 1.20-3.82; p=0.010), regardless of RAAS inhibitor treatment.
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