(1) Background: This single-center retrospective study aimed to evaluate whether sodium–glucose cotransporter-2 inhibitors (SGLT2-i) therapy may have a nephroprotective effect to prevent contrast-induced acute kidney injury (CI-AKI) in patients with heart failure (HF) undergoing iodinated contrast medium (ICM) invasive procedures. (2) Methods: The population was stratified into SGLT2-i users and SGLT2-i non-users according to the chronic treatment with gliflozins. The primary endpoint was CI-AKI incidence during hospitalization. Secondary endpoints were all-cause mortality and the need for continuous renal replacement therapy (CRRT). (3) Results: In total, 86 patients on SGLT2-i and 179 patients not on SGLT2-i were enrolled. The incidence of CI-AKI in the gliflozin group was lower than in the non-user group (9.3 vs. 27.3%, p < 0.001), and these results were confirmed after propensity matching analysis. Multivariable logistic regression showed that only SGLT2-i treatment was an independent preventive factor for CI-AKI (OR: 0.41, 95% CI: 0.16–0.90, p = 0.045). The need for CRRT was reported only in five patients in the non-SGLT2-i-user group compared to zero patients in the gliflozin group (p = 0.05). (4) Conclusions: SGLT2-i therapy was associated with a lower risk of CI-AKI in patients with HF undergoing ICM invasive procedures.

Purpose: Although biomarkers of myocardial fibrosis and inflammation have been proposed as potential modulators of response to cardiac resynchronization therapy (CRT), their clinical utility and interaction with echocardiographic parameters remain incompletely understood. This study aims to assess the dynamic changes in these biomarkers, their relationship with echocardiographic variables, and their association with structural response to CRT. Methods: We retrospectively evaluated 86 consecutive patients referred for CRT with symptomatic heart failure, left ventricular (LV) ejection fraction ≤ 35%, QRS width ≥ 130 ms and LBBB morphology. We measured sST-2, Gal-3, NTpro-BNP and eGFR at baseline and after 1 year of CRT. An echocardiographic reduction of LV end-systolic volume ≥ 15% was used to define a patient as a responder to CRT. Results: The mean baseline and follow-up values of Gal-3 (responders: 24.1 [16.8;32] ng/mL, non-responders: 30 [20;39.3] ng/mL, p = 0.03) and sST2 (responders: 28.5 [20;36] ng/mL, non-responders: 34.5 [25;37.7] ng/mL, p = 0.03) were lower in responders than non-responders. Responders showed a significant reduction between baseline and follow-up values of ΔGal-3 (−12.1% vs. −2.5%, p = 0.04), ΔsST2 (−30.8% vs. 2.2%, p < 0.001), ΔNT-proBNP (−16.4% vs. 5.2, p = 0.04) and ΔeGFR (6.7 ± 24.3% vs. -6.3 ± 27.9%, p = 0.03). At the multivariate analyses, baseline Gal-3 [cut-off: 38.5 ng/mL, AUC: 0.63, p = 0.03, (OR 7.13 [1.12;45.41], p = 0.03), together with TAPSE > 17.5 mm (OR 10.86 [3.15;37.44], p < 0.001) significantly correlated with the structural response to CRT in several prediction models. Among echocardiographic parameters, TAPSE remained the strongest predictive factor of positive response to CRT at the univariate and multivariate analyses. Conclusions: In patients with heart failure and reduced ejection fraction undergoing CRT, Gal-3 and TAPSE are significantly associated with a positive structural response to CRT.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a heterogeneous clinical entity encompassing multiple ischemic mechanisms, including atherosclerotic plaque disruption, coronary artery spasm, coronary microvascular dysfunction, coronary embolism, and spontaneous coronary artery dissection. Despite the absence of obstructive coronary disease, patients with MINOCA remain at substantial risk of adverse cardiovascular outcomes, underscoring the need for accurate early diagnosis and effective risk stratification. In this context, accumulating evidence indicates that circulating serum biomarkers may provide additional pathophysiological and prognostic insights in patients with a working diagnosis of MINOCA. Moreover, distinct biomarker profiles may help support the differential diagnostic evaluation between MINOCA and other causes of acute myocardial injury, such as myocardial infarction with obstructive coronary arteries, myocarditis, and Takotsubo syndrome. This narrative review summarizes current evidence on serum biomarkers in MINOCA, highlights their potential role in guiding tailored diagnostic strategies, and discusses future perspectives toward biomarker-driven precision medicine in patients presenting with acute myocardial injury.