Tackling myocardial oxidative stress with empagliflozin: are we big enough to fight heart failure with preserved ejection fraction?
Abstract
This editorial refers to ‘Empagliflozin improves endothelial and cardiomyocyte function in human heart failure with preserved ejection fraction via reduced pro-inflammatory-oxidative pathways and protein kinase Gα oxidation’, by D. Kolijn et al., pp. 495–507. Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome characterized by impaired left ventricular (LV) relaxation, elevated LV filling pressures, fluid retention, and microvascular dysfunction. Described as the ‘single largest unmet need in cardiovascular medicine’, HFpEF represents ∼65% of new HF diagnoses and associates with a poor prognosis.1 Established treatments (i.e. RAAS inhibitors) for heart failure with reduced ejection fraction (HFrEF) are not effective in HFpEF, as shown by several randomized trials such as the CHARM‐Preserved, PEP‐CHF, I‐PRESERVE, TOPCAT, and the recent PARAGON-HF.2 The overall lack of available therapies, coupled with the alarming prevalence of comorbidities (obesity, hypertension, diabetes, and ageing), calls for understanding the mechanistic basis underlying HFpEF. Over the last few years, sodium-glucose cotransporter-2 inhibitors (SGLT2i) have shown a consistent and rather striking effect in reducing HF hospitalization (hHF) and cardiovascular mortality in patients with type 2 diabetes (T2D). A recent meta‐analysis including 34 322 patients from the EMPA‐REG OUTCOME, CANVAS, and DECLARE‐TIMI 58 trials showed that SGLT‐2i reduced the risk of hHF by 23%, with a…
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: 34 participants or records.
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