Key result
High-dose furosemide cuts major clinical events ~50% vs. low-dose in acute HFrEF.
Why the study?
HFrEF and HFpEF have distinct hemodynamic characteristics in acute heart failure, prompting evaluation of the differential response to aggressive diuresis between these groups.
Does a high-dose intravenous furosemide strategy improve diuresis and clinical outcomes without worsening renal function compared to a low-dose strategy in patients with acute heart failure, and does this effect differ between HFrEF and HFpEF?
RCT (n=300)
Double-blind
1:1:1:1
Does a high-dose intravenous furosemide strategy improve diuresis and clinical outcomes without worsening renal function compared to a low-dose strategy in patients with acute heart failure, and does this effect differ between HFrEF and HFpEF?
Effect estimate: HR 0.50 (95% CI 0.27-0.93)
Absolute Event Rate: 24% vs 45%
p-value: p=0.03
May support high-dose furosemide in acute HFrEF; hypothesis-generating and requires randomized confirmation before practice change.
Background: HFrEF and HFpEF had distinct hemodynamic characteristics in the setting of acute heart failure (AHF). The objective of our study is to evaluate the differential response to aggressive diuresis in Heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Methods: Patients in DOSE trial with left ventricular ejection fraction (LVEF) measurement were included (n=300), and classified into HFrEF (n=193) and HFpEF (n=107). Effect of high-dose versus low-dose furosemide strategy was compared separately in HFrEF and HFpEF. Results: High-dose strategy significantly increased change in creatinine and cystatin C at 72 hours in HFpEF (treatment difference: 0.16; 95% confidence interval [CI]: 0.02-0.30 mg/dl; P=0.03 for creatinine, and treatment difference: 0.26; 95% CI: 0.09-0.43 mg/dl; P=0.003 for cystatin C) but not in HFrEF (treatment difference: -0.05, 95% CI: -0.14-0.03 mg/dl; P=0.24 for creatinine, and treatment difference: -0.06, 95% CI: -0.15-0.02 mg/dl; P=0.15 for cystatin C) (P for interaction<0.01 for both). There were significantly more net fluid loss, weight loss, and congestion-free patients at 72 hours in high-dose group in HFrEF, but not in HFpEF. Compared with low-dose group, high-dose group had a significantly lower risk of composite clinical outcome of death, total hospitalizations and unscheduled visits due to heart failure (hazard ratio [HR]: 0.50, 95% CI: 0.27-0.93; P=0.03) in HFrEF, but a comparable risk (HR: 0.99, 95% CI: 0.48-0.23; P=0.98) in HFpEF. Conclusions: AHF on the basis of HFrEF and HFpEF responded differently to aggressive diuresis. Future trials should be designed separately for HFrEF and HFpEF.
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Liu et al. (2020) conducted an RCT in Acute heart failure with reduced and preserved ejection fraction (n=300). High-dose furosemide vs. Low-dose furosemide (daily intravenous dose equal to daily oral dose) was evaluated on Composite clinical outcome of death, total hospitalizations and unscheduled visits due to heart failure in HFrEF (HR 0.50, 95% CI 0.27-0.93, p=0.03). High-dose furosemide reduced the risk of the composite clinical outcome of death, hospitalizations, and unscheduled visits by 50% (HR 0.50) compared to low-dose furosemide in patients with acute heart failure and reduced ejection fraction.
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