Search

• Multicenter international registry with T2DM patients and AMI undergoing PCI. • SGLT2-I users exhibited significantly lower creatinine values at 72 h after PCI. • The rate of CI-AKI was significantly lower in SGLT2-I compared to non-SGLT2-I users. • SGLT2-I were identified as an independent predictor of reduced rate of CI-AKI. To analyze the association between chronic SGLT2-I treatment and development of contrast-induced acute kidney injury (CI-AKI) in diabetic patients with acute myocardial infarction (AMI) undergoing PCI. Multicenter international registry of consecutive patients with type 2 diabetes mellitus (T2DM) and AMI undergoing PCI between 2018 and 2021. The study population was stratified by the presence of chronic kidney disease (CKD) and anti-diabetic therapy at admission (SGLT2-I versus non-SGLT2-I users). The study population consisted of 646 patients: 111 SGLT2-I users [28 (25.2%) with CKD] and 535 non-SGLT2-I users [221 (41.3%) with CKD]. The median age was 70 [61–79] years. SGLT2-I users exhibited significantly lower creatinine values at 72 h after PCI, both in the non-CKD and CKD stratum. The overall rate of CI-AKI was 76 (11.8%), significantly lower in SGLT2-I users compared to non-SGLT2-I patients (5.4% vs 13.1%, p = 0.022). This finding was also confirmed in patients without CKD (p = 0.040). In the CKD cohort, SGLT2-I users maintained significantly lower creatinine values at discharge. The use of SGLT2-I was an independent predictor of reduced rate of CI-AKI (OR 0.356; 95%CI 0.134–0.943, p = 0.038). In T2DM patients with AMI, the use of SGLT2-I was associated with a lower risk of CI-AKI, mostly in patients without CKD. [ABSTRACT FROM AUTHOR]

A hyperglycemic state, also in non-diabetic subjects, may be associated with acute coronary syndrome (ACS). Aim of this review is to describe the pathophysiologic association between ACS and hyperglycemic state, the protective mechanisms of a tight glycaemic control in ACS on CV outcomes, and the supporting clinical evidence. Several mechanisms may be responsible of a poor CV outcome in subjects with hyperglycemia during ACS. Endothelial NAPDH oxidase-2 (NOX2) activation in response to high glucose alters the balance between Raf/MAPK-dependent vasoconstriction and PI3K/Akt-dependent vasodilation in favour of constriction. Hyperglycaemia induces an overproduction of superoxide by the mitochondrial electron transport chain through different molecular mechanisms. Moreover, hyperglycaemia increases the size of the infarct by causing myocardial cell death through apoptosis and reducing the collateral blood flow. High FFA concentrations lead to toxicity mechanisms in acutely ischemic myocardium. On the other hand, a tight glycaemic control in ACS exerts a cardioprotective action by anti-inflammatory and anti-apoptotic mechanisms, anti-oxidative stress, endothelium protection, FFA reduction, anti-glucotoxic effect, IR and cardiac fuel metabolisms improvement, heart stem cells protection and reduced activation of adrenergic system. Unfortunately, the clinical studies supporting the above pathophysiological background are few and sometimes controversial, more likely due the risk of hypoglycemia linked to the insulin therapy generally used during ACS. Intriguingly, GLP-1 RA and SGLT2i, demonstrated highly effective in the cardiovascular prevention in high-risk subjects without the risk of hypoglycemia, might keep this cardioprotective effect even in acute conditions such as ASC. [ABSTRACT FROM AUTHOR]