Dapagliflozin, Inflammation, and Left Ventricular Remodeling in Patients with Type 2 Diabetes and Left Ventricular Hypertrophy
Background and Aim
Sodium-glucose co-transporter 2 (SGLT2) inhibitors like dapagliflozin have shown benefits in heart failure (HF) by reversing remodelling, but the mechanisms behind these benefits are not fully understood. Inflammation is thought to contribute to HF, and there is evidence suggesting that SGLT2 inhibitors may reduce inflammation, although clinical data is limited. This study aimed to investigate whether dapagliflozin’s effects on cardiac remodelling in individuals with type 2 diabetes (T2D) and left ventricular hypertrophy (LVH) were associated with its impact on inflammation.
Methods
The study involved 60 patients with T2D and LVH without symptomatic HF who participated in the DAPA-LVH trial. They were randomly assigned to receive dapagliflozin 10 mg daily or a placebo for 12 months and underwent cardiac magnetic resonance imaging (CMR) at the beginning and end of the treatment period. Inflammatory markers such as C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin 6 (IL-6), interleukin 10 (IL-10), and neutrophil-to-lymphocyte ratio (NLR) were measured in plasma samples. The primary analysis aimed to investigate the effect of dapagliflozin on inflammation and assess the relationships between changes in inflammatory markers and LV mass and global longitudinal strain (GLS), as well as the potential modulation of dapagliflozin’s effect on LV mass and GLS by baseline levels of inflammation.
Results
After 12 months of treatment, dapagliflozin significantly reduced CRP compared to the placebo. There were no significant statistical changes in other inflammatory markers. Modest correlations were observed between improvements in GLS and reduced inflammation at 12 months.
Conclusions
Dapagliflozin led to a significant reduction in CRP compared to the placebo. Correlations were found between reductions in inflammatory markers, including IL-1β, and improvements in global longitudinal strain. Reductions in systemic inflammation may contribute to the cardiovascular benefits of dapagliflozin.
PMID: 38997620 | DOI: 10.1186/s12872-024-04022-7
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