{"id":"7653002b0db9","type":"article","url":"https://hartvaat.nl/2021/10/01/sglt2-remmers-en-hf-hospitalisatie-en-hartfunctie-systematische-review/","title":"SGLT2-remmers en HF-hospitalisatie en hartfunctie: systematische review","title_en":"Sodium-glucose cotransporter 2 inhibitor effects on heart failure hospitalization and cardiac function: systematic review.","category":"hartfalen","category_label":"Hartfalen","professions":["cardioloog","internist"],"tags":["acuut-hartfalen","canagliflozine","dapagliflozine","empagliflozine","hfref"],"journal":"ESC heart failure","doi":"10.1002/ehf2.13483","source_url":"https://doi.org/10.1002/ehf2.13483","authors":["Roy Rasalam","John J Atherton","Gary Deed","Michael Molloy-Bland","Neale Cohen","Andrew Sindone"],"significance":6,"published":"2021-10-01","source_date":"2021-10-01","image":"","kennis":[],"congress":"","summary_en":"This systematic review evaluated the effects of SGLT2 inhibitors on heart failure hospitalization and cardiac function parameters, consolidating the mechanistic and clinical evidence for SGLT2 inhibitor cardioprotection.","created":"2026-07-03T10:29:24Z","updated":"2026-07-03T13:28:32Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Systematische review naar het effect van SGLT2-remmers op HF-hospitalisatie en hartfunctie.","abstract_original":"AIMS: To systematically review randomized controlled trials assessing effects of sodium-glucose cotransporter 2 inhibitors (SGLT2is) on hospitalization for heart failure (HHF) and cardiac structure/function and explore randomized controlled trial (RCT)-derived evidence for SGLT2i efficacy mechanisms in heart failure (HF). METHODS AND RESULTS: Systematic searches of Medline and Embase were performed. In seven trials [3730-17 160 patients; low risk of bias (RoB)], SGLT2is significantly reduced the relative risk of HHF by 27-39% vs. placebo, including in two studies in patients with HF with reduced ejection fraction with or without type-2 diabetes mellitus (T2DM). Improvements in conventional cardiovascular risk factors, including glycaemic levels, cannot account for these effects. Five trials (56-105 patients; low RoB) assessed the effects of 6-12 months of SGLT2i treatment on left ventricular structure/function; four reported significant improvements vs. placebo, and one did not. Five trials (low RoB) assessed SGLT2i treatment effects on serum N-terminal pro B-type natriuretic peptide levels; significant reductions vs. placebo were reported after 8-12 months (two studies; 3730-4744 patients) but not ≤12 weeks (three studies; 80-263 patients). Limited available RCT-derived evidence suggests various possible cardioprotective SGLT2i mechanisms, including improved haemodynamics (natriuresis and reduced interstitial fluid without blood volume contraction/neurohormonal activation) and vascular function, enhanced erythropoiesis, reduced tissue sodium and epicardial fat/inflammation, decreased sympathetic tone, and beneficial changes in cellular energetics. CONCLUSIONS: Sodium-glucose cotransporter 2 inhibitors reduce HHF regardless of T2DM status, and reversal of adverse left ventricular remodelling likely contributes to this efficacy. Hypothesis-driven mechanistic trials remain sparse, although numerous trials are planned or ongoing."}