Abstract
BACKGROUND: As a novel oral anti-hyperglycemic agent, sodium-glucose cotransporter 2 inhibitors (SGLT2-i) have been demonstrated to improve cardiovascular outcomes in acute myocardial infarction (AMI) patients with type 2 diabetes mellitus (T2DM). However, the mechanism responsible for the beneficial effects remains unclear. Recently, extensive studies have demonstrated a close relationship between elevated fasting triglyceride-glucose (TyG) index and the risk of AMI. Additionally, research has identified that SGLT2-i can reduce the TyG index in T2DM patients. However, it remains ambiguous whether the benefit of SGLT2-i in patients with AMI and T2DM is due to an improvement in the TyG index. Consequently, we aimed to assess the impact of SGLT2-i on the TyG index in AMI patients with T2DM. METHODS: A retrospective and cross-sectional study was conducted on 180 AMI patients with T2DM admitted to the chest pain center of the Second Affiliated Hospital of Anhui Medical University from January 2020 to January 2023. Based on the hypoglycemic regimens administered after admission, the patients were categorized into a control group (79 cases treated with sulfonylureas, α-glycosidase inhibitors, metformin, etc.) and a SGLT2-i group (101 cases administered with dapagliflozin or empagliflozin). Propensity score matching (PSM) was adopted to balance the baseline characteristics of patients and minimize selection bias to confirm the robustness of the results. After PSM, control group remained 32 patients, and SGLT2-i group remained 37 patients. All patients underwent regular follow-up after discharge, and comparisons were made between the two groups in terms of clinical indicators and major adverse cardiovascular events (MACEs) in 1 year. Univariate and Multivariate Cox regression analysis was performed to identify the predictors of MACE. RESULTS: Significant differences were observed between the two groups in terms of various parameters before PSM, included age, proportion of insulin use, Gensini score, serum creatinine (Cr), total cholesterol (TC), and cardiac troponin I (cTnI). After PSM, there were no statistically significant differences in baseline clinical indicators and laboratory tests. The median follow-up period was 11 months in both cohorts. The comparison of follow-up results between the two groups after matching confirmed statistically significant differences in triglyceride (TG) reduction index reduction, left ventricular end-diastolic diameter (LVDD) reduction, and white blood cell (WBC) reduction in the SGLT2-i group (all P<0.05). Additionally, a higher incidence of MACEs was observed in the control group (P=0.01). Univariate analysis showed that usage of SGLT2-i, Cr, low-density lipoprotein cholesterol (LDL-C), TyG index at baseline, and changes of TyG index (TyG at follow-up minus TyG at baseline) were associated with the risk of MACE. However, multivariate analysis showed only usage of SGLT2-i was associated with the risk of MACE [hazard ratio (HR) =0.077; 95% confidence interval (CI): 0.009-0.682; P=0.02]. CONCLUSIONS: In AMI patients with T2DM, the use of SGLT2-i was associated with a lower risk of MACE and an improvement of TyG index during 11 months follow-up. Our findings offer new insights into the cardio-protective mechanisms of SGLT2-i in the context of AMI.