Abstract

Dr. Trullas et al. commented on the practical use of diuretics in patients with acute and chronic heart failure, a position statement on behalf of the Heart Failure Association (HFA).1 They advocate to use thiazides early on during the treatment of acute heart failure. In addition, Dr. Escobar et al. proposed to use urinary potassium to guide thiazide usage. We do agree that diuretic and natriuretic response to a diuretic administered should always be interpreted in light of the dose and type of the diuretic agent, the degree of volume overload, body composition, and underlying renal function. In addition, while assessment of renal function is generally performed by measuring serum creatinine as a rather poor surrogate for glomerular filtration rate, this only represents part of the nephron's function. Alterations in tubular sodium handling with increased proximal sodium reabsorption in heart failure are at least equally important in understanding while interpreting the response to a diuretic agent. As such, the measurement of urinary sodium content has recently experienced a renewed interest as an indicator for diuretic response.2 As acknowledged by the authors, the statements on thiazide usage are not supported by any randomized clinical trial at this moment. Currently, there is a study ongoing comparing Metolazone Versus Chlorothiazide for Acute Decompensated Heart Failure With Diuretic Resistance (NCT03574857). In addition, data on guiding of diuretic therapy based upon urinary potassium excretion are extremely sparse. Aside from dosing issues that are not easy to overcome in daily clinical practice, observational data underscore the frequent occurrence of hypokalaemia, and propensity-matched observational data indicate thiazides to be independent predictors of a higher risk for all-cause mortality.3 Given the relative safety of high-dose loop diuretics in the Diuretic Optimal Strategy Evaluation in Acute Heart Failure (DOSE-AHF) trial, the Cardio-Renal Study Group of the HFA therefore opted to prefer initial intensification of the loop diuretic dose before adding a thiazide diuretic in case of insufficient natriuretic response.1, 4 Kazory and Costanzo question the treatment algorithm, where ultrafiltration is positioned very late in the treatment cascade. The authors point to possible benefits with ultrafiltration and advocate an earlier rather than late usage of ultrafiltration. It is important to note that this position statement was primarily focused on the use of diuretics, not ultrafiltration. Even though the authors suggest favourable effects of ultrafiltration, there is no definite proof on the additive value of ultrafiltration at any timepoint in the treatment of acute heart failure. Therefore this treatment remains reserved for patients who do not respond to conventional and combination diuretic therapy, as also reflected in the European Society of Cardiology heart failure guidelines.5 If anything, trials like CARRESS-HF have shown that with a proper, elaborate, diuretic treatment algorithm, as proposed in the consensus paper, most patients will respond favourably to conventional diuretic therapy.6 This avoids the need for invasive treatment with ultrafiltration, with inherent vascular complications, without resulting in substantial improved outcomes. Therefore, rather than positioning ultrafiltration early in some patients, we postulate that especially early assessment of diuretic response and subsequent adaptation of diuretic therapy will be the way to move forward in the majority of patients with acute heart failure.

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