{"id":"2ac6c487c7e5","type":"article","url":"https://hartvaat.nl/2026/10/07/dapagliflozin-verbetert-ecg-markers-van-ventriculaire-repolarisatie-bij-hartfale/","title":"Dapagliflozin verbetert ECG-markers van ventriculaire repolarisatie bij hartfalen — prospectief cohort","title_en":"Dapagliflozin and ventricular repolarization across heart failure phenotypes.","category":"hartfalen","category_label":"Hartfalen","professions":["cardioloog","internist"],"tags":[],"journal":"Current medical research and opinion","doi":"10.1080/03007995.2026.2741494","source_url":"https://doi.org/10.1080/03007995.2026.2741494","authors":["Gülüzar Traş","Fuat Polat","Melike Saday Bozkurt","İsmail Altıntaş"],"significance":4,"published":"2026-10-15","source_date":"2026-10-07","image":"","kennis":["https://hartvaat.nl/kennis/hartfalen/icd-bij-hartfalen/","https://hartvaat.nl/kennis/hartfalen/wat-is-hartfalen/"],"congress":"","summary_en":"In a prospective, non-randomized cohort of 700 patients with type 2 diabetes, dapagliflozin significantly improved electrocardiographic markers of ventricular repolarization over three months compared to standard antidiabetic therapy. The greatest improvements were observed in HFrEF (QTc reduction of 14.3 ms), followed by HFpEF and those without heart failure. As these findings rely on surrogate ECG parameters rather than clinical arrhythmic outcomes, randomized controlled trials are needed to confirm any potential antiarrhythmic benefit.","created":"2026-10-08T01:21:22Z","updated":"2026-10-08T01:21:22Z","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":"Een prospectief, niet-gerandomiseerd cohortonderzoek onder 700 patiënten met type 2-diabetes toont dat dapagliflozin na drie maanden leidt tot significante verbeteringen van ECG-markers van ventriculaire repolarisatie vergeleken met bestaande antidiabetische therapie. Het effect was het sterkst bij HFrEF (QTc-reductie van 14,3 ms), gevolgd door HFpEF en patiënten zonder hartfalen. Omdat het gaat om surrogaatparameters en niet om klinische hartritmestoornissen, zijn gerandomiseerde trials nodig om de klinische relevantie te bevestigen.","abstract_original":"BACKGROUND: Type 2 diabetes mellitus (T2DM) is associated with abnormal ventricular repolarization and increased arrhythmic risk. Sodium-glucose cotransporter-2 (SGLT-2) inhibitors may exert electrophysiological effects beyond glycemic control. We investigated changes in electrocardiographic (ECG) markers of ventricular repolarization after dapagliflozin initiation in SGLT-2 inhibitor-naïve patients with T2DM according to heart failure (HF) phenotype. METHODS: In this prospective, non-randomized, controlled observational study, 700 patients with T2DM were enrolled between June 2023 and February 2026. Patients initiating dapagliflozin (n = 350) were classified as HFrEF (LVEF <50%, n = 87), HFpEF (LVEF ≥50% with HF, n = 93), or no HF (LVEF ≥50% without HF, n = 170); 350 controls continued pre-existing antidiabetic therapy. Twelve-lead ECG and echocardiography were performed at baseline and 3 months. Prespecified endpoints included QT, QTc, QT dispersion, Tp-e, Tp-e/QT, and Tp-e/QTc. Inverse probability of treatment weighting and Holm-Bonferroni correction were applied. RESULTS: Dapagliflozin was associated with greater reductions in all prespecified ECG parameters than controls (all between-group p <0.001; Cohen's d = 0.48-1.08), with consistent findings after IPTW. Reductions were greatest in HFrEF (QTc = -14.3 ms; Tp-e = -9.1 ms), followed by HFpEF (-11.2 and -7.4 ms) and no HF (-7.6 and -3.8 ms); all between-subgroup comparisons p <0.001. HFrEF independently predicted greater QTc reduction (β = -4.8 ms vs no HF, p < 0.001). Change in Tp-e correlated weakly with HbA1c change (r = -0.145, p = 0.037). LVEF increased in HFrEF (+3.2%) and HFpEF (+0.9%). CONCLUSIONS: Dapagliflozin initiation was associated with reductions in multiple ECG markers of ventricular repolarization, with the greatest changes observed in HFrEF. These findings concern surrogate ECG measures and do not establish a reduction in clinical arrhythmic events. Confirmation in prospective randomized trials is warranted."}