{"id":"72be967268e8","type":"article","url":"https://hartvaat.nl/2020/09/21/dapagliflozine-op-lv-hypertrofie-bij-diabetes-type-2-dapa-lvh-gerandomiseerde-tr/","title":"Dapagliflozine op LV-hypertrofie bij diabetes type 2: DAPA-LVH gerandomiseerde trial","title_en":"A randomized controlled trial of dapagliflozin on left ventricular hypertrophy in people with type two diabetes: the DAPA-LVH trial.","category":"preventie","category_label":"Preventie","professions":["cardioloog","internist"],"tags":["dapa-hf","dapagliflozine","diabetes-type-2","emperor-trials"],"journal":"European heart journal","doi":"10.1093/eurheartj/ehaa419","source_url":"https://doi.org/10.1093/eurheartj/ehaa419","authors":["Alexander J M Brown","Stephen Gandy","Rory McCrimmon","John Graeme Houston","Allan D Struthers","Chim C Lang"],"significance":7,"published":"2020-09-21","source_date":"2020-09-21","image":"","kennis":["https://hartvaat.nl/kennis/preventie/preventie-bij-diabetes/","https://hartvaat.nl/kennis/cardiometabool/diabetes-en-cardiovasculair-risico/"],"congress":"","summary_en":"The DAPA-LVH trial demonstrated that dapagliflozin significantly regresses left ventricular hypertrophy in patients with type 2 diabetes, providing the first randomized evidence that SGLT2 inhibitors have direct structural cardiac benefits beyond hemodynamic effects.","created":"2026-07-03T10:28:46Z","updated":"2026-07-03T13:27:55Z","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":"DAPA-LVH trial die aantoonde dat dapagliflozine LV-hypertrofie vermindert bij diabetes type 2. Structureel cardioprotectief effect van SGLT2-remming.","abstract_original":"AIM: We tested the hypothesis that dapagliflozin may regress left ventricular hypertrophy (LVH) in people with type 2 diabetes (T2D). METHODS AND RESULTS: We randomly assigned 66 people (mean age 67 ± 7 years, 38 males) with T2D, LVH, and controlled blood pressure (BP) to receive dapagliflozin 10 mg once daily or placebo for 12 months. Primary endpoint was change in absolute left ventricular mass (LVM), assessed by cardiac magnetic resonance imaging. In the intention-to-treat analysis, dapagliflozin significantly reduced LVM compared with placebo with an absolute mean change of -2.82g [95% confidence interval (CI): -5.13 to -0.51, P = 0.018]. Additional sensitivity analysis adjusting for baseline LVM, baseline BP, weight, and systolic BP change showed the LVM change to remain statistically significant (mean change -2.92g; 95% CI: -5.45 to -0.38, P = 0.025). Dapagliflozin significantly reduced pre-specified secondary endpoints including ambulatory 24-h systolic BP (P = 0.012), nocturnal systolic BP (P = 0.017), body weight (P < 0.001), visceral adipose tissue (VAT) (P < 0.001), subcutaneous adipose tissue (SCAT) (P = 0.001), insulin resistance, Homeostatic Model Assessment of Insulin Resistance (P = 0.017), and high-sensitivity C-reactive protein (hsCRP) (P = 0.049). CONCLUSION: Dapagliflozin treatment significantly reduced LVM in people with T2D and LVH. This reduction in LVM was accompanied by reductions in systolic BP, body weight, visceral and SCAT, insulin resistance, and hsCRP. The regression of LVM suggests dapagliflozin can initiate reverse remodelling and changes in left ventricular structure that may partly contribute to the cardio-protective effects of dapagliflozin. CLINICALTRIALS.GOV IDENTIFIER: NCT02956811."}