Trace element equilibrium in acute heart failure and the effect of empagliflozin
Abstract
Sodium–glucose cotransporter 2 inhibitors (SGLT2i) have shown to be potent therapeutic agents in heart failure (HF) irrespective of ejection fraction, improving cardiometabolic features and reducing risk of hospitalization for HF.1 Favourable effects of SGLT2i on outcome have been explained by altering glucose metabolism, enhancing diuresis and stimulating erythropoiesis, and are presumed to arise (partly) through alterations in renal blood flow and glomerular filtration rate (GFR).1,2 Yet, subsequent disruption in electrolyte equilibrium due to direct changes in filtrate composition is a frequently feared side-effect.3 While clinical data have shown minimal or inconclusive impact on most plasma electrolytes, other than a slight increase in plasma magnesium concentration,3 limited research has been performed in the acute phase of HF concerning the effect of SGLT2i on plasma trace elements. Trace elements are important for optimal cardiac function, but up to 50% of patients with HF present with single or multiple deficiencies, adversely and independently affecting prognosis.4 Therefore, we aimed to elucidate the effect of empagliflozin on plasma calcium (Ca), copper (Cu), iron (Fe), selenium (Se) and zinc (Zn) levels in patients with acute HF. We included 79 patients (≥18 years old) from the randomized, double-blind, placebo-controlled, multicentre pilot study on the effects of empagliflozin on clinical outcomes in patients with acute decompensated HF (EMPA-RESPONSE-AHF).…
How strong is the evidence?
Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design. Reported size: 79 participants or records.
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