Key result
Dapagliflozin is linked to ~137% higher IL-10 at one year post-PCI in AMI and T2DM.
Why the study?
The effects of SGLT2 inhibitors on inflammatory biomarkers in AMI patients after PCI with comorbid T2DM remain poorly characterized.
Does dapagliflozin improve inflammatory biomarkers and cardiac function in patients with acute myocardial infarction and type 2 diabetes after percutaneous coronary intervention?
Cohort (n=56)
No
Does dapagliflozin improve inflammatory biomarkers and cardiac function in patients with acute myocardial infarction and type 2 diabetes after percutaneous coronary intervention?
Absolute Event Rate: 3.22% vs 1.36%
p-value: p=0.001
Dapagliflozin may exert anti-inflammatory effects post-AMI in patients with T2DM, as evidenced by significantly elevated IL-10 levels at 1 year.
Background Acute myocardial infarction (AMI) triggers a robust inflammatory response that contributes to adverse ventricular remodeling. Sodium-glucose cotransporter-2 (SGLT2) inhibitors have demonstrated anti-inflammatory properties beyond glycemic control, but their effects on inflammatory biomarkers in AMI patients after percutaneous coronary intervention (PCI) with comorbid type 2 diabetes mellitus (T2DM) remain poorly characterized. Patients with comorbid type 2 diabetes mellitus (T2DM) are at particularly high risk due to amplified inflammation, coronary microvascular dysfunction, and elevated restenosis rates following PCI. Methods This single-center, prospective exploratory observational cohort study enrolled 60 AMI patients with comorbid T2DM after successful PCI at Baoji Central Hospital between January 2023 and June 2025 (Ethics: BZYL2022-26-1). No single primary endpoint was pre-specified because of the exploratory design. Patients were categorized into dapagliflozin ( n = 41) and control ( n = 19) groups based on clinical treatment decisions; 4 patients (all control) were excluded, yielding 56 for analysis. Three inflammatory biomarkers (IL-10, TNF-α, MMP-9), cardiac function parameters (LVEF, SV, LVEDD, LVESD), and metabolic indices were assessed at baseline, 1 month, 6 months, and 1 year. Bonferroni correction (α′ = 0.0167) and propensity score matching (PSM) were applied. Results The principal exploratory finding was significantly elevated IL-10 at 1 year in the dapagliflozin group vs. controls (3.22 ± 3.51 vs. 1.36 ± 0.67 pg/mL, P = 0.001), surviving Bonferroni correction (α′ = 0.0167). MMP-9 declined in both groups (dapagliflozin: -66.2%, P < 0.001; control: -48.7%), consistent with natural post-AMI decline, with no significant between-group difference at 1 year ( P = 0.323). Within the dapagliflozin group, LDL-C decreased by 20.8% ( P < 0.001) and LVESD by 8.8% ( P = 0.002). After PSM (14 pairs), IL-10 between-group differences remained significant ( P = 0.028). Conclusions In this exploratory study, dapagliflozin was associated with significantly elevated IL-10 at 1 year—the only inflammatory biomarker showing a significant between-group difference surviving Bonferroni correction and PSM. MMP-9 declined in both groups, consistent with natural post-AMI inflammation, without significant between-group difference. These hypothesis-generating findings are consistent with a possible anti-inflammatory effect of dapagliflozin post-AMI and warrant confirmation in larger randomized trials.
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Feng et al. (2026) conducted a cohort in Acute myocardial infarction with comorbid type 2 diabetes mellitus (n=56). Dapagliflozin vs. Control was evaluated on IL-10 levels at 1 year (p=0.001). Dapagliflozin exposure was associated with significantly elevated IL-10 at 1 year compared to controls (3.22 vs. 1.36 pg/mL, P=0.001) in patients with AMI and T2DM after PCI.
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