Soluble ST2 (sST2) has recently emerged as a promising biomarker in the field of acute cardiovascular diseases. Several clinical studies have demonstrated a significant link between sST2 values and patients’ outcome. Further, it has been found that higher levels of sST2 are associated with an increased risk of adverse left ventricular remodeling. Therefore, sST2 could represent a useful tool that could help the risk stratification and diagnostic and therapeutic work-up of patients admitted to an emergency department. With this review, based on recent literature, we have built sST2-assisted flowcharts applicable to three very common clinical scenarios of the emergency department: Acute heart failure, type 1, and type 2 acute myocardial infarction. In particular, we combined sST2 levels together with clinical and instrumental evaluation in order to offer a practical tool for emergency medicine physicians.

Background: Acute myocardial infarction (AMI) survivors are at risk of major adverse cardiac events and their risk stratification is a prerequisite to tailored therapeutic approaches. Biomarkers could be of great utility in this setting. Methods: We sought to evaluate the utility of the combined assessment of Galectin 3 (Gal-3) and Galectin 3 binding protein (Gal-3bp) for post-AMI risk stratification in a large, consecutive population of AMI patients. The primary outcomes were: Recurrent angina/AMI and all-cause mortality at 12 months after the index event. Results: In total, 469 patients were included. The median Gal-3bp was 9.1 μg/mL (IQR 5.8–13.5 μg/mL), while median Gal-3 was 9.8 ng/mL (IQR 7.8–12.8 ng/mL). During the 12 month follow-up, 34 patients died and 41 had angina pectoris/reinfarction. Gal-3 was associated with all-cause mortality, while Gal-3bp correlated with the risk of angina/myocardial infarction even when corrected for other significant covariates. The final multivariable model for mortality prediction included patients’ age, left ventricular ejection fraction (LVEF), Gal-3, and renal function. The ROC curve estimated for this model has an area under the curve (AUC) of 0.84 (95%CI 0.78–0.9), which was similar to the area under the ROC curve obtained using the GRACE score 1-year mortality. Conclusions: The integrated assessment of Gal-3 and Gal-3bp could be helpful in risk stratification after AMI.

Hyperglycemia is considered one of the main risk factors for atherosclerosis, since high glucose levels trigger multiple pathological processes, such as oxidative stress and hyperproduction of pro-inflammatory mediators, leading to endothelial dysfunction. In this context, recently approved drugs, such as glucagon-like-peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2i), could be considered a powerful tool for to reduce glucose concentration and cardiovascular risk. Interestingly, many patients with type 2 diabetes mellitus (T2DM) and insulin resistance have been found to be deficient in vitamin D. Recent studies pointed out the unfavorable prognostic values of T2DM and vitamin D deficiency in patients with cardiac dysfunction, either when considered individually or together, which shed light on the role of vitamin D in general health status. New evidence suggests that SGLT2i could adversely affect the production of vitamin D, thereby increasing the risk of fractures, which are common in patients with T2DM. Therefore, given the biological effects of vitamin D as an anti-inflammatory mediator and a regulator of endothelial function and calcium equilibrium, these new findings should be taken into consideration as well. The aim of this review is to gather the latest advancements regarding the use of antidiabetic and antiplatelet drugs coupled with vitamin D supplementation to control glucose levels, therefore reducing the risk of coronary artery disease (CAD).

Survivors after a myocardial infarction (MI), especially those with diabetes mellitus (DM), remain at high risk of further events. Identifying and treating factors that may influence survival may open new therapeutic strategies. We assessed the impact on prognosis of DM and hypovitaminosis D (hypovitD), alone or combined. In this prospective, observational study, 1081 patients were enrolled surviving an MI and divided into four groups according to their diabetic and VitD status. The primary end-point was composite of all-cause mortality, angina/MI and heart failure (HF). Secondary outcomes were mortality, HF and angina/MI. During a follow-up of 26.1 months (IQR 6.6–64.5), 391 subjects experienced the primary end-point. Patients with DM or hypovitD had similar rate of the composite end-point. Patients with only hypovitD or DM did not differ regarding components of composite end-point (angina p = 0.97, HF p = 0.29, mortality p = 0.62). DM and VitD deficiency had similarly adjusted risks for primary end-point (HR 1.3, 95%CI 1.05–1.61; HR 1.3, 95% CI 1.04–1.64). The adjusted HR for primary composite end-point for patients with hypovitD and DM was 1.69 (95%CI 1.25–2.29, p = 0.001) in comparison to patients with neither hypoD nor DM. In conclusion, DM and hypovitD, individually and synergistically, are associated with a worse outcome after MI.

Background: Ghrelin may exert positive effects on cardiac structure and function in heart failure (HF) patients. Methods: We assessed ghrelin levels in 266 dilated cardiomyopathy (DCM) patients and in 200 age, gender and body mass index (BMI) matched controls. Further, we evaluated the expression of ghrelin and growth hormone secretagogue-receptor (GHSR) in the myocardium of 41 DCM patients and in 11 controls. Results: DCM patients had significantly lower levels of total, acylated and unacylated ghrelin when compared to controls (p < 0.05 for all). In controls, we observed a negative correlation of ghrelin with age, male gender and BMI. These correlations were lost in the DCM group, except for male gender. Total ghrelin was higher in patients with more recent diagnosis when compared to patients with longer duration of the DCM (p = 0.033). Further, total ghrelin was higher in patients with lower left ventricular systolic function (<40% LVEF, vs. 40% ≤ LVEF < 49% vs. LVEF ≥ 50%: 480.8, vs. 429.7, vs. 329.5 pg/mL, respectively, p = 0.05). Ghrelin prepropeptide was expressed more in DCM patients than in controls (p = 0.0293) while GHSR was expressed less in DCM patients (p < 0.001). Furthermore, ghrelin showed an inverse correlation with its receptor (ρ = −0.406, p = 0.009), and this receptor showed a significant inverse correlation with Interleukin-1β (ρ = −0.422, p = 0.0103). Conclusion: DCM duration and severity are accompanied by alterations in the ghrelin–GHSR system.