Key result
Loop diuretic deprescribing proves safe in very old HF patients, yielding similar hospitalization and mortality rates.
Why the study?
Deprescribing loop diuretics in older adults with heart failure has been suggested as a safe strategy, but clear evidence and identification of the best-suited patient phenotype remain lacking.
Does deprescribing loop diuretics increase HF hospitalizations or mortality in very old patients with heart failure?
Cohort (n=114)
No
Does deprescribing loop diuretics increase HF hospitalizations or mortality in very old patients with heart failure?
Deprescribing loop diuretics in very old patients with heart failure and low congestion appears safe without increasing mortality or HF hospitalizations.
May support deprescribing in selected low-congestion very old HF patients; leaves open confirmation by RCTs.
Introduction Managing loop diuretics (LD) in very old patients with heart failure (HF) is challenging. While they are crucial for reducing congestion during acute decompensation, their overtitration in the chronic phase can lead to adverse effects such as dehydration, electrolyte imbalances, hypotension, and falls. In older adults, deprescribing LD has been suggested as a safe strategy to improve quality of life without worsening outcomes, but clear evidence remains lacking. Purpose To identify the phenotype of very old patients with HF best suited for safe diuretic deprescribing. Methods This retrospective study included very old (>80 years) patients with HF and on LD discharged from our Geriatrics Unit between 2020 and 2024 (T0) who had at least two follow-up visits (T1 and T2) at our cardio-geriatric clinic. Patients underwent a Comprehensive Geriatric Assessment, blood tests, NYHA classification for dyspnea, and assessment of congestion through POCUS. HF-related hospitalizations at 6 months from T1 and all-cause mortality at 12 months were recorded. Multivariate logistic regression models were used to identify determinants of diuretic deprescribing. Kaplan-Meier curves and Cox regression survival analysis were used to assess the time to first HF hospitalization and all-cause mortality. Results The study population had a mean age of 87.2 (SD 5.7) years, a median diuretic burden of 33.5 mg, and NYHA class 2. Of 114 patients, 24 underwent deprescribing at T1. No significant differences in frailty, disability, or comorbidity burden were found between the deprescribed group and controls. Both groups had similar dyspnea severity and HF-related hospitalizations between T0 and T1. The deprescribed group tended to have lower NTproBNP levels (p=0.098) and less congestion on POCUS, with a smaller inferior vena cava diameter (p=0.008), a lower degree of pleural effusion (p=0.022), and fewer B-lines (p=0.078). Additionally, the deprescribed group had higher LD doses (p=0.003) at T1 and more frequent use of ACEi/ARBs (p=0.021). Multivariate logistic regression found that ACEi/ARB use was most strongly associated with deprescribing, with a non-significant trend [OR 4.01 (95% CI: 0.95–16.98, p=0.060)]. At T2, patients who underwent deprescribing did not experience worsening dyspnea or increases in diuretic doses compared to controls. All-cause mortality (22.2% vs. 16.7%, p=0.553) and HF re-hospitalizations (14.4% vs. 8.3%, p=0.421) were similar between the groups, and survival curves did not differ significantly (Figure 1). Conclusions In very old patients on ACEi/ARB and higher diuretic burden, combined with lower biochemical and ultrasound congestion, LD deprescribing seems to be a safe strategy that does not increase the risk of hospitalization for HF or mortality. Our pilot study supports LD deprescribing to combat clinical inertia, reduce drug costs, and potentially improve the quality of life in very elderly patients.
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Mazzarone et al. (2025) conducted a cohort in Heart failure (n=114). Deprescribing loop diuretics vs. Continuation of loop diuretics (controls) was evaluated on All-cause mortality at 12 months (p=0.553). Deprescribing loop diuretics in very old patients with heart failure was associated with similar rates of all-cause mortality (22.2% vs. 16.7%, p=0.553) compared to controls.
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