Key result
Baseline plasma renin concentration shows no association with all-cause mortality in stable HFrEF.
Why the study?
Single renin measurements provide limited additional prognostic value in HFrEF, and whether assessing renin trajectories overcomes these weaknesses had not been reported.
Do baseline active plasma renin concentrations or 1-year renin trajectories predict all-cause mortality and unplanned heart failure hospitalizations in patients with stable HFrEF on contemporary guideline-directed medical therapy?
Cohort (n=505)
No
Do baseline active plasma renin concentrations or 1-year renin trajectories predict all-cause mortality and unplanned heart failure hospitalizations in patients with stable HFrEF on contemporary guideline-directed medical therapy?
Neither single baseline measurements nor 1-year longitudinal trajectories of active plasma renin concentration provide meaningful prognostic value for mortality or heart failure hospitalization in stable HFrEF patients treated with contemporary guideline-directed medical therapy.
Baseline renin lacks prognostic value in stable HFrEF; leaves open whether trajectories add utility under contemporary GDMT.
Introduction. The renin-angiotensin system (RAS) is the main target of neurohumoral therapy in heart failure with reduced ejection fraction (HFrEF) effectively reducing mortality. Reasonably, renin might serve as a biomarker for risk prediction and therapy response. Renin indeed bears some additional value to clinical risk models, albeit the effect is not pronounced. Whether assessing renin trajectories can overcome the weaknesses of single renin measurements has not been reported. Methods. A total of 505 patients with stable HFrEF were enrolled prospectively and followed through routine clinical visits. Active plasma renin concentration was documented up to 5 years. Changes in renin were analyzed throughout the disease course, and survival was compared for different renin trajectories within the first year. Results. Baseline renin levels were not related to all-cause mortality (crude HR for an increase of 100 μiE/ml: 1.01 (95% CI: 0.99–1.02), [Formula: see text]) but associated with unplanned HF hospitalizations (crude HR: 1.01 (95% CI: 1.00-1.02), [Formula: see text]). Renin increased during the disease course from baseline to 1-year and 2-year FUP (122.7 vs. 185.6 μIU/ml, [Formula: see text], and 122.7 vs. 258.5 μIU/ml, [Formula: see text]). Both survival and unplanned HF hospitalization rates were comparable for different renin trajectories at 1-year FUP ([Formula: see text], [Formula: see text]). Conclusions. Intriguingly, renin is not a good biomarker to indicate prognosis in HF, while renin trajectories over a 1-year period do not have an additional value. Rapid physiologic plasma renin variations, but also opposing effects of angiotensinogen-derived metabolites under presence of RAS blockade, might obscure the predictive ability of renin.
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Han et al. (2023) conducted a cohort in Stable heart failure with reduced ejection fraction (HFrEF) (n=505). Active plasma renin concentration (baseline and 1-year trajectories) vs. Normal renin levels (≤46 μIU/ml) or different 1-year renin trajectories was evaluated on All-cause mortality (HR 1.01, 95% CI 0.99-1.02, p=0.414). Baseline active plasma renin concentration was not associated with all-cause mortality (crude HR per 100 μiE/ml increase 1.01, 95% CI 0.99-1.02, p=0.414) in stable HFrEF patients.
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