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Patients with type 2 diabetes mellitus are at an increased risk of cardiovascular disease and microvascular and macrovascular complications. Although multiple classes of antidiabetic drugs are currently available, cardiovascular complications of diabetes still cause considerable morbidity and premature cardiovascular mortality in diabetic patients. The development of new drugs represented a conceptual breakthrough in the treatment of patients with type 2 diabetes mellitus. In addition to improving glycemic homeostasis, these new treatments have consistently demonstrated relevant cardiovascular and renal benefits due to their multiple pleiotropic effects. The aim of this review is to analyze the direct and indirect mechanisms by which glucagon-like peptide 1 receptor agonists favorably impact cardiovascular outcome and report current indications for their implementation in clinical practice based on national and international guidelines.

Sodium-glucose cotransporter 2 inhibitors (SGLT2-i), initially developed as glucose-lowering agents for the treatment of type 2 diabetes, based on significant clinical benefits shown in patients with heart failure, have recently been included among the first-line drugs for the treatment of heart failure with reduced ejection fraction. International guidelines recommend SGLT2-i use in association with neuro-hormonal modulators (renin-angiotensin blockers, beta-blockers, and aldosterone antagonists). Although SGLT2-i are well tolerated, for an appropriate use and to maximize clinical benefits, it is important to know potential side effects and conditions that may lead to an increased risk of adverse events. The aim of this ANMCO document is to briefly report clinical evidence that support SGLT2-i use in patients with heart failure and provide practical indications for clinical implementation.

Endothelial function is impaired in first-degree relatives (FDRs) of patients with type 2 diabetes. Many states characterized by endothelial dysfunction are associated with increased cardiovascular sympathetic outflow. In this study, we investigated endothelial and autonomic nervous system (ANS) functioning in FDRs and tested the hypothesis that in basal condition, impaired endothelial function is associated with impaired cardiovascular ANS regulation. Flow-mediated endothelium-dependent and -independent vasodilation of the brachial artery was measured with high-resolution ultrasound in 27 otherwise healthy FDRs (14 men and 13 women; mean age 32 years) with normal oral glucose tolerance and in 15 age- and gender-matched control subjects. Cardiovascular ANS regulation was investigated by means of spectral analysis of heart rate and systolic blood pressure (SBP) variability. Baroreflex sensitivity was assessed by the spontaneous baroreflex sequences technique. Flow-mediated endothelium-dependent vasodilation was 9.4+/-1.0% in FDRs and 17.0+/-2.3% in control subjects (P=0.001). Low-frequency oscillations in SBP variability were 8.6+/-2.8 and 2.8+/-0.6 mm Hg in FDRs and controls, respectively (P=0.04). Baroreflex sensitivity was significantly less in FDRs than controls (22.8+/-2.7 versus 37.0+/-5.8, respectively; P=0.01). Change in vessel diameter was inversely correlated with the low-frequency component of SBP variability (r=-0.40; P=0.014). In healthy FDRs of diabetic patients there is a concomitant, possibly related, impairment in endothelial and ANS functioning, which manifests, indirectly, with increase in vascular sympathetic outflow and a depressed baroreflex, vagal, control of heart rate.