Treatment of acute heart failure (AHF) is focused on alleviation of congestion, volume overload, and shortening of hospital stay [1,2]. Most of the decongestion is achieved early after admission and decreased in the following days. 25% Of patients have residual signs of congestion at discharge [3]. A rigorous and quick diuretic response is associated with improved outcomes. However, it has been proven difficult to assess the treatment effect of diuretics by evaluating congestion status after start of therapy [4-7].
An Heart Failure Association ESC consensus paper has proposed to study spot urinary sodium and/or diuresis very early after initiation of diuretics, and to intensify or expand (loop) diuretic treatment if natriuresis or diuresis are insufficient [8]. This single-center prospective study aimed to investigate the clinical importance of urinary sodium excretion in AHF patients.
The diagnosis of AHF was based on the ESC heart failure guidelines [1] and enrolled patients (n=175, mean age was 71±14 years, 44% were female) presented with signs and symptoms of congestion, requiring intravenous diuretic therapy. Patients received intravenous vasodilators when systolic blood pressure was >110 mmHg at admission and all patients received bumetanide as the preferred loop diuretic (dose was determined by the treating physician). Urinary volume and urinary sodium were measured from urine collected in the following time frames: 0-6h, 6-24h, 24-48h, 48-72h, and 72-96h after diuretic initiation. The variable of interest was urinary sodium excretion in the first 6 hours after diuretic initiation (urinary sodium concentration x urinary volume over 6h).
The primary clinical endpoint was all-cause mortality after admission. Secondary endpoints included HF rehospitalization after discharge and a combined endpoint of first occurrence of all-cause mortality and/or HF rehospitalization. The median follow-up was 257 (152-427) days.
This prospective study in patients with AHF showed that low urinary sodium excretion during the first 6h after diuretic initiation was associated with lower urine volume in the first 24h, and with all-cause mortality.
1. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, Falk V, González-Juanatey JR, Harjola VP, Jankowska EA, Jessup M, Linde C, Nihoyannopoulos P, Parissis JT, Pieske B, Riley JP, Rosano GM, Ruilope LM, Ruschitzka F, Rutten FH, van der Meer P. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail 2016;18:891–975.
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6. Verbrugge FH, Dupont M, Steels P, Grieten L, Swennen Q, TangWH, Mullens W. The kidney in congestive heart failure: ‘are natriuresis, sodium, and diuretics really the good, the bad and the ugly?’. Eur J Heart Fail 2014;16:133–142.
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8. Mullens W, Damman K, Harjola VP, Mebazaa A, Brunner-La Rocca HP,Martens P, Testani JM, Tang WH, Orso F, Rossignol P, Metra M, Filippatos G, Seferovic PM, Ruschitzka F, Coats AJ. The use of diuretics in heart failure with congestion – a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail 2019;21:137–155.
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