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Dapagliflozin, inflammation and left ventricular remodelling in patients with type 2 diabetes and left ventricular
Adel Dihoum1, Alexander Jm Brown1, Rory J McCrimmon2
1Division of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Ninewells Hospital and Medical School, Dundee, Scotland, UK.
Insights
Sodium-glucose co-transporter 2 (SGLT2) inhibitors like dapagliflozin reduce C-reactive protein (CRP) in patients with type 2 diabetes and left ventricular hypertrophy. These reductions in inflammation correlate with improved global longitudinal strain, suggesting a role in cardiovascular benefits.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Sodium-glucose co-transporter 2 (SGLT2) inhibitors demonstrate cardiovascular benefits in heart failure (HF), but underlying mechanisms, particularly anti-inflammatory effects, require clinical validation.
- Inflammation is a key factor in HF pathophysiology, and SGLT2 inhibitors show potential for mitigating inflammatory processes.
Purpose of the Study:
- To investigate if dapagliflozin improves cardiac remodelling in type 2 diabetes (T2D) patients with left ventricular hypertrophy (LVH) by reducing inflammation.
- To assess the association between changes in inflammatory markers and cardiac remodelling metrics (LV mass, global longitudinal strain) following dapagliflozin treatment.
Main Methods:
- Sixty patients with T2D and LVH (without symptomatic HF) from the DAPA-LVH trial were randomized to dapagliflozin (10 mg/day) or placebo for 12 months.
- Plasma levels of C-reactive protein (CRP), TNF-α, IL-1β, IL-6, IL-10, and neutrophil-to-lymphocyte ratio (NLR) were measured. Cardiac magnetic resonance imaging (CMR) assessed LV mass and global longitudinal strain (GLS) at baseline and end of treatment.
Main Results:
- Dapagliflozin significantly reduced CRP levels compared to placebo after 12 months (p=0.026).
- No significant changes were observed in other inflammatory markers (TNF-α, IL-1β, IL-6, IL-10, NLR).
- Modest correlations were found between improvements in GLS and reduced levels of NLR, IL-1β, and TNF-α.
Conclusions:
- Dapagliflozin significantly reduced CRP levels in patients with T2D and LVH.
- Improvements in global longitudinal strain were correlated with reductions in certain inflammatory markers, suggesting a potential role for systemic inflammation reduction in dapagliflozin's cardiovascular benefits.
Background And Aims:
Sodium-glucose co-transporter 2 (SGLT2) inhibitors have beneficial effects in heart failure (HF), including reverse remodelling, but the mechanisms by which these benefits are conferred are unclear. Inflammation is implicated in the pathophysiology of heart failure (HF) and there are some pre-clinical data suggesting that SGLT2 inhibitors may reduce inflammation. There is however a lack of clinical data. The aim of our study was to investigate whether improvements in cardiac remodelling caused by dapagliflozin in individuals with type 2 diabetes (T2D) and left ventricular hypertrophy (LVH) were associated with its effects on inflammation.
Methods:
We measured C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin 6 (IL-6), and interleukin 10 (IL-10) and neutrophil-to-lymphocyte ratio (NLR) in plasma samples of 60 patients with T2D and left ventricular hypertrophy (LVH) but without symptomatic HF from the DAPA-LVH trial in which participants were randomised dapagliflozin 10 mg daily or placebo for 12 months and underwent cardiac magnetic resonance imaging (CMR) at baseline and end of treatment. The primary analysis was to investigate the effect of dapagliflozin on inflammation and to assess the relationships between changes in inflammatory markers and LV mass and global longitudinal strain (GLS) and whether the effect of dapagliflozin on LV mass and GLS was modulated by baseline levels of inflammation.
Results:
Following 12 months of treatment dapagliflozin significantly reduced CRP compared to placebo (mean difference of -1.96; 95% CI -3.68 to -0.24, p = 0.026). There were no significant statistical changes in other inflammatory markers. There were modest correlations between improvements in GLS and reduced inflammation (NLR (r = 0.311), IL-1β (r = 0.246), TNF-α (r = 0.230)) at 12 months.
Conclusions:
Dapagliflozin caused a significant reduction in CRP compared to placebo. There were correlations between reductions in inflammatory markers including IL-1β and improvements in global longitudinal strain (but not reduced LV mass). Reductions in systemic inflammation might play a contributory role in the cardiovascular benefits of dapagliflozin.
Trial Registration:
Clinicaltrials.gov NCT02956811 (06/11/2016).
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